No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Age-related maculopathy and the impact of blue light hazard
Abstract
The pathogenesis of age-related maculopathy (ARM), the most common cause of visual loss after the age of 60 years, is indeed a complicated scenario that involves a variety of hereditary and environmental factors. The pathological cellular and molecular events underlying retinal photochemical light damage, including photoreceptor apoptosis, have been analysed in experimental animal models. Studies of age-related alterations of the retina and photoreceptors, the accumulation of lipofuscin in retinal pigment epithelium (RPE) cells, and the formation of drusen have greatly contributed to our knowledge. A new concept of an inflammatory response to drusen has emerged, suggesting immunogenic and systemic reactions in Bruch's membrane and the subretinal space. Oxidative stress and free radical damage also impact on the photoreceptors and RPE cells in the ageing eye. Based on the photoelectric effect, a fundamental concept in quantum physics, the consequences of high-energy irradiation have been analysed in animal models and cell culture. Short-wavelength radiation (rhodopsin spectrum), and the blue light hazard (excitation peak 440 nm), have been shown to have a major impact on photoreceptor and RPE function, inducing photochemical damage and apoptotic cell death. Following cataract surgery, there is a dramatic change in ocular transmittance. In aphakic or pseudophakic eyes (with clear intraocular lenses), high-energy (blue) and ultraviolet-A radiation strikes the retina. Epidemiological data indicate a significantly increased 5-year incidence of late ARM in non-phakic eyes compared with phakic eyes. In recent years, putative prophylactic measures against ARM have emerged. The implantation of 'yellow' intraocular lenses (IOLs) that absorb high-energy blue radiation is, from a theoretical point of view, the most rational approach, and, from a practical point of view, is easy to accomplish. With increasing age, RPE cells accumulate lipofuscin (chromophore A2E). It is noteworthy that the yellow IOL not only protects A2E-laden human RPE cells from blue light (peak 430 nm) damage, but also alleviates the detrimental effects of green (peak 550 nm) and white light. A prophylactic treatment using antioxidants is aimed at counteracting oxidative stress and free radical cellular damage. The Age-Related Eye Disease Study (AREDS), a randomized clinical trial, showed a significantly lower incidence of late ARM in a cohort of patients with drusen maculopathy treated with high doses of antioxidants than in a placebo group. In recent years, considerable progress in retinal research has been achieved, creating a platform for the search for new prophylactic and therapeutic measures to alleviate or prevent photoreceptor and RPE degeneration in ARM.
... Pioneering studies have shown that light intensities two to three times higher than those of normal illumination can result in damage to visual cells in nocturnal animals [35][36][37]. Moreover, a plethora of studies have demonstrated that retinal cells are particularly vulnerable to short-wavelength light, notably blue light [38][39][40], with photoreceptors and the retinal pigment epithelium being among the most affected [37,[41][42][43][44][45]. ...
... In this regard, studies involving rats exposed to full-spectrum white LEDs and blue LEDs (at 460 nm) resulted in free radical production and apoptotic and necrotic photoreceptors, indicating photochemical injury [31,54,[60][61][62]. Moreover, high levels of A2E have been associated with macular degeneration [40]. Additionally, it has been demonstrated that all-trans-retinal leads to the activation of NADPH oxidase, which in turn can increase oxidative stress, trigger RPE apoptosis, and induce an inflammatory response [54]. ...
... Despite these effects, the anti-proliferative properties of blue light may be leveraged for treating certain dermatological conditions, including acne, psoriasis, and precancerous lesions [39,152]. Blue light therapy has shown promising results in acne management [40,153], and positive outcomes have been noted in treatments with topical retinoids for mild skin conditions, such as psoriasis [130][131][132][153][154][155][156][157][158][159][160][161][162]. ...
Visible light refers to the frequencies within the electromagnetic spectrum that humans can see, encompassing radiation with wavelengths falling between 380 nm to 760 nm. The energy of a single photon increases with its frequency. In the retina, photoreceptor cells contain light-sensitive pigments that absorb light and convert it into electrical stimuli through a process known as phototransduction. However, since the absorption spectrum of photoreceptors closely aligns with blue light (ranging from 400 to 500 nm), exposure to high light intensities or continuous illumination can result in oxidative stress within these cells, leading to a loss of their functionality. Apart from photoreceptor cells, the retina also houses photosensitive ganglion cells, known as intrinsically photosensitive retinal ganglion cells (ipRGCs). These cells relay information to the suprachiasmatic nucleus in the brain, playing a crucial role in modulating melatonin secretion, which in turn helps in synchronizing the body’s circadian rhythms and responses to seasonal changes. Both, ipRGCs and skin possess a peak sensitivity to blue wavelengths, rendering them particularly susceptible to the effects of excessive blue light exposure. This study delves into the consequences of excessive illumination and/or prolonged exposure to blue light on retinal function and explores its implications for human health.
... Given the gradual shift in teaching media, what concerns the general public is whether such eLearning would impose threats on eyes, by noting blue enriched white light to be hazardous to retina and macula etc [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. Taking retinal damage for example, Ham et al. revealed the photochemical sensitivity of retina to light to increase with the decrease of wavelength, explaining why retina is more vulnerable to the short wavelength blue light [8]. ...
... To explore if some of the threats can be quantified, a few studies were carried out about the effect of wavelength on photoretinitis [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. The threat was quantified via the use of a permissible exposure-limit [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38]. ...
Projectors have become one major medium in modern teaching, with large area-size displays emerging as an alternative. What concerns the general public is whether such eLearning would impose threat on eyes, by noting blue enriched white light to be hazardous to retina and else. Especially, little was known about their permissible viewing time under a certain viewing clarity. We had hence carried out a quantitative study with the use of a blue-hazard quantification spectrometer to determine the permissible viewing time when using a projector and a large size TV screen for displaying. Surprisingly, the large TV screen could permit a much longer viewing time, meaning which is more eye-friendly. It is plausibly because its resolution is much higher than that of the projector. Two dilemmas were observed in such eLearning; those sitting in the front would suffer a much higher illuminance, leading to a much shorter viewing time, while those sitting in the back would need a far much larger font size to see clearly. To ensure both viewing clarity and a sufficiently long permissible viewing time, orange text on black background is suggested to replace the defaulted black text on white background. The permissible viewing time could hence drastically increase from 1.3 to 83 h at 2 m by viewing a 30 pt font for the TV and from 0.4 to 54 h for the projection. At 6 m, the permissible viewing time was increased from 12 to 236 h for the TV and from 3 to 160 h for the projection, based on a viewable 94 pt font. These results may help educators and other e-display users to wisely apply the display tools with safety.
... Blue light is visible light with a wavelength of 400-2500 nm, also known as high-energy visible light [1], which is the band with the shortest wavelength and highest energy in the visible spectrum [2]. The main sources of blue light are sunlight and electronic screens; although luminous LED screens and fluorescent lamps can also serve as additional sources of blue light [3]. ...
... Thereafter, ELISA and WB were carried out, and the three doses were detected using COL-I and MMP-1 indexes to establish a blue-light-damage cell model. Figure 2. Ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-profiles of the standards (1) and LACCE (2). The letters in the profiles represent the follow leontopodic acid A, (b) leontopodic acid B. Figure 3). ...
Leontopodium alpinum is an important source of raw material for food, medicine, and modern cosmetics. The purpose of this study was to develop a new application for protection against blue light damage. To investigate the effects and mechanism of action of Leontopodium alpinum callus culture extract (LACCE) on blue light damage, a blue-light-induced human foreskin fibroblast damage model was established. The contents of collagen (COL-I), matrix metalloproteinase 1 (MMP-1), and opsin 3 (OPN3) were detected using enzyme-linked immunosorbent assays and Western blotting. The calcium influx and reactive oxygen species (ROS) levels were measured via flow cytometry and the results showed that the LACCE (10–15 mg/mL) promoted the production of COL-I, inhibited the secretion of MMP-1, OPN3, ROS and calcium influx, and may play a role in inhibiting the activation of blue light on the OPN3-calcium pathway. Thereafter, high-performance liquid chromatography and ultra-performance liquid chromatography–tandem mass spectrometry were used to quantitatively analyze the contents of nine active ingredients in the LACCE. The results indicated that LACCE has an anti-blue-light-damage effect and provides theoretical support for the development of new raw materials in the natural food, medicine, and skin care industries.
... Most of the current LED backlight screens can be adjusted for color temperature, and the difference in spectral distribution at different color temperatures is considerable (Feng et al., 2015;Zhu et al., 2017). In terms of the impact of the physical properties of VDT light, it has been found that the percentage of blue light from LED backlight screens increases with color temperature (Algvere et al., 2006) and that the blue light hazard factor also increases rapidly with color temperature. Ma et al. (2017) conducted a screen spectrum test on three mainstream models of LED computers, and the spectrum was generally in the visible range of 400-780 nm. ...
... How to create a light environment conducive to the "learning to learn" effect also needs to be explored. Therefore, it is important to accurately and comprehensively study the photobiological effects of the light environment in the VDT workspace, so as to identify the correlation between its key influences on the effect of "learning to learn" (Algvere et al., 2006). ...
In recent years, the role of video games in enhancing brain plasticity and learning ability has been verified, and this learning transfer is known as the “learning to learn” effect of video game training. At the same time, against the background of healthy lighting, the influence of non-visual effects of light environment on the human rhythmic system has been gradually confirmed. As a special operation form of Visual Display Terminal (VDT) operation, video game training has a high dependence on VDT equipment and the VDT screen, and the background usually has a huge difference in brightness. Compared with the light environment of ordinary operation space, the light environment of VDT operation space is more complex. This complex light environment's non-visual effects cause human emotions, alertness, fatigue, cognitive ability, and other changes, which may affect the efficiency of the “learning to learn” effect of video game training. This article focuses on the impact of the light environment in the VDT workspace on the “learning to learn” effect of video game training. It first traces the factors that trigger the “learning to learn” effect of video game training, that is, the improvement of people's attention, perception, and cognitive ability. Then, the influencing mechanism and the evaluation method of the VDT workspace space light environment on the human rhythm system are discussed based on the basic theory of photobiological effect. In addition, the VDT display lighting light time pattern, photophysical properties, regulation, and protection mechanism on the human rhythm system are studied to demonstrate the VDT workspace light environment's special characteristics. Finally, combined with the progress of artificial lighting technology and the research results of health lighting, given the “learning to learn” effect of video game training, some thoughts on the design of the light environment of the workplace and future research directions are presented.
... In most of the studies, it was suggested that cataract surgery may increase the development and progression of AMD (9)(10)(11)(12)(13)(14). This phenomenon was attributed to increased light toxicity, increased inflammation, and post-operative cystoid macular edema after cataract surgery (15). However, there is still ongoing debate about whether cataract surgery has any effect on the progression of AMD (14). ...
... Cataract surgery may increase the development and progression of AMD (9,(12)(13)(14). This phenomenon was attributed to increased inflammation, increased light toxicity, and postoperative cystoid macular edema after cataract surgery (15). However, there is a debate about the relationship between cataract surgery and the progression of AMD (12). ...
Objectives:
The aim of the study was comparison of wet-type age-related macular degeneration in phakic and pseudophakic patients in terms of anatomical and functional success based on the real-life data of Türkiye.
Methods:
The multicenter retrospective real-life study data of the. retinal study group were used in this study. Among 867 eyes of 867 patients were included in the study. Patients were divided into two groups according to the status of the lens; phakic group and pseudophakic group. The follow-up period of the two groups, the number of injections at the 1st, 2nd, and 3rd years, and changes in the central macular thickness (CMT, μ) and visual acuity (VA, logMAR) of the patients at the beginning, 6th, 12th, 24th, and 36th months were examined.
Results:
In our study, the number of injections in the 1st, 2nd, and 3rd years, respectively, was 4.2±2.0, 1.8±1.9, and 1.0±1.7 in the phakic group, and 3.9±2.0, 1.7±1.9, and 0.8±1.4 in the pseudophakic group. When the two groups were compared in terms of the number of injections, there was a statistically significant difference in the 1st year, but there was no significant difference in the 2nd and 3rd years (p=0.001, p=0.350, and p=0.288, respectively). There was no statistically significant difference between the groups in terms of CMT in the baseline, 6th, 12th, 24th, and 36th months (p=0.991, p=0.327, p=0.652, p=0.599, and p=0.873, respectively). Although there was no difference in VA between groups at the beginning (p=0.052), the phakic group showed statistically better VA in controls at 3rd, 6th, 12th, 24th, and 36th months (p=0.001, p=0.001, p=0.000, p=0.000, and p=0.003, respectively).
Conclusion:
Differences in the number of injections and visual results between phakic and pseudophakic patients in wet type AMD may necessitate the creation of different treatment and follow-up protocols.
... Animal studies have shown that short-wavelengths can potentially lead to phototoxic retinal damage (Algvere et al., 2006;Wenzel et al., 2005;Ham et al., 1976). In vitro studies of human retinal pigment epithelium (RPE) cells demonstrate that blue-light exposure initiates apoptosis of RPE cells while BLF IOLs reduce this process (Sparrow et al., 2004;Rezai et al., 2008;Tanito et al., 2006). ...
... In the Beaver Dam Eye Study outdoor activity and sun exposure early in life were associated with the development of AMD later in life (Cruickshanks et al., 2001). A similar observation by Taylor et al. showed that patients with higher exposure to blue or visible light over the preceding 20 years were more likely to have geographic atrophy or disciform scarring, which are types of AMD (Algvere et al., 2006;Taylor, 1992). Typical examples of daily activities that may not correlate to "best-corrected visual acuity" but can be considered equally important to patients. ...
Most studies evaluating cataract surgery focus on the primary outcome of early, central, best-corrected visual acuity. However, cataract surgery and intraocular lens (IOL) design have other secondary visual outcomes as well as impacts on various ocular tissues, the visual function, and quality of life. Some of these aspects are more difficult to quantify, or are historically neglected, but might be extremely important to patients. One important development was the addition of blue-light filtering to IOL design. Whether these IOLs truly have the retinal protective qualities they were designed for is disputed, yet other inadvertent desirable and possibly detrimental influences are being examined. Risk of falls, driving accidents, and other injuries decrease following cataract surgery, especially in the elderly, the importance of which cannot be overemphasized. Cataract formation contributes to social isolation and decreases cognitive stimulation in the elderly population, while cataract extraction can reduce the risk of dementia and cognitive decline. Diffractive multifocal and extended depth-of-focus IOLs improve spectacle independence and patient reported outcomes, but positive and negative dysphotopsia may be persistent. Future directions such as using the IOL enabling clear spectacle-free vision at all distances, or intraoperative drug delivery systems show promising preliminary results. It seems inevitable that a higher focus on the secondary outcomes of surgery will increase. We believe that these aspects will become more and more relevant when considering new IOL designs and surgical techniques, a fact that will benefit both the patients and the surgeons.
... It must be considered RP heterogeneity in the disease presentation, which makes identifying typical disease traits a fundamental point for diagnosis and patient care. Lutein and meso-zeaxanthin, forming the Macular pigment (MP), are substances located in the fovea which have been reported to cover a protective role in reducing oxidative stress by partially absorbing the high-energy blue light 9,10 . Consequently, it has been speculated about MP role in protecting against degenerative eye diseases, and its assessment study is necessary for investigating the role of carotenoids and their function 11 ...
This study aimed to analyze Optical Coherence Tomography (OCT) parameters and Macular Pigment Optical Density (MPOD) changes in patients affected by Retinitis pigmentosa (RP). Eighteen eyes of 18 patients suffering from early-stage RP were enrolled in our observational study. 18 eyes of 18 patients age and gender matched were enrolled as controls. Patients were analyzed at baseline by undergoing complete baseline ophthalmologic examination, Spectral-domain Optical Coherence Tomography (OCT), Electroretinogram (ERG) and Heterochromatic Flicker Photometry (HFP). Main outcome measures were Macular Pigment Optical Density (MPOD), Central macular thickness (CMT), Central Choroidal Thickness (CCT) and Choroidal Vascularity Index (CVI). Lower CCT (p = 0.006), CVI (p < 0.001) and MPOD levels (p = 0.038) were found in affected patients, whereas higher CMT was detected in cases compared to healthy controls. Correlation analysis revealed the presence of a negative correlation between BCVA and Age and CMT and BCVA and a positive correlation between CCT and MPOD and CVI and CCT. Retinal and choroidal variations occur in patients affected by early-stage RP regarding functional and anatomical changes.
... Chronic exposure to such light causes photochemical damage in the retina, such as the acceleration of oxidative stress in the degeneration of retinal cells. This could result in the earlier development of chronic eye conditions, including AMD -the numberone cause of blindness among the elderly [4][5]. Neither the cornea nor the lens provides an adequate shield for protection against the harmful effects of blue light. ...
Background: As all of us become more and more dependent on digital devices, the concern about the sight damaging effects associated with blue light exposure has gained attention. The purpose of this study is to investigate whether high-energy visible spectrum particularly in the range 415-455 nm blue light damages the cornea, lens, and retina. Methods:Both in vitro and in vivo models were coupled with a human observational study. For in vitro models, human corneal epithelial cells, lens epithelial cells, as well as retinal pigment epithelial cells were exposed to various intensities of blue light. Adult Sprague-Dawley rats were exposed to blue light for 30 days in vivo. Human subjects were also observed by recording eye strain as well as visual acuity both with and without blue light filtering glasses. Results: Increased oxidative stress, with higher exposure to blue light, led to significantly decreased cell viability from the in vitro study. In vivo studies reported corneal opacity and retinal thinning in some species, most commonly in the high intensities of blue light exposure. Human study results included reduced eye strain and preserved visual acuity from those wearing filters for protection compared with those without. Conclusion: The health risks of prolonged blue light exposure are of large concern, as well as the need for a more intensified research initiative and new ways to reduce its harmful impact on visual welfare in this age of technology.
... Blue light, as one of the three primary colors of light, is indispensable in full-color displays to show colorful pictures, and the screen will inevitably emit a certain amount of blue light. Studies show that continuous exposure to blue light may damage retinal pigment epithelium (RPE) cells, which can lead to visual problems such as ametropia and age-related macular degeneration [3][4][5]. Unfortunately, it is very difficult to avoid blue light hazards while maintaining normal display and lighting quality. Some studies show that the most destructive to RPE cells is the short-wave blue light of 415-455 nm, while the other long-wave blue light is necessary for color balance and human circadian rhythm [6,7]. ...
With the increasing application of display and illumination devices, the injury of blue light to human eyes have attracted more and more attention. The current absorptive anti-blue light films require high preparation temperatures. This study prepared ZnO-Ag nanofilms by sol–gel method at relatively low temperature, 250 °C. The films were further enhanced with SiO2 protective layer under 200 °C to improve the mechanical properties and stability, and the transmittance was investigated. The results showed that the films blocked 50.4% of blue light at wavelengths of 415–455 nm while maintained an impressive average transmittance of 98% for visible light in the range of 500–800 nm. The films had no visual effect on the display quality and the color rendering index increased only from 80.3 to 83.4, but it reduced 25% of blue light-weighted irradiance. Additionally, the films exhibited a high stability when exposed to a high temperature and humid environment (85 °C and 85% RH). Rubbing with a Teflon ball at a load of 0.5 N and a linear speed of 80 mm/min for 30 min did not show significant damage. Finally, the damage to epithelial cells exposed to blue light in the presence of the developed film was greatly alleviated.
Graphical Abstract
... Blue light hazard (BLH) refers to a range of adverse effects on human health resulting from prolonged exposure to short-wavelength light [28,29]. The Circadian Action Factor (CAF) signifies the physiological and behavioral responses generated by the human biological clock in response to the natural variations of the day-night cycle. ...
The optimal laser spectrum for users of all ages is determined by considering the health implications of laser lighting across different age groups. We present a theoretical calculation model for age-related blue light hazard (BLH) and Circadian Action Factor (CAF), establishing optimization criteria that integrate visual and health factors. Health assessments of white laser light source spectra, obtained from the combination of RGB-LDs, were conducted using BLH and CAF at various illumination color temperatures. Based on our proposed comprehensive optimization criteria, white-light laser sources with high luminous efficacy (LER ≥ 330 lm/W), good color rendering (Ra ≥ 70), and color coordinates within the quadrangle region specified by the ANSI C78.377-2008 standard were obtained. This research provides a theoretical foundation for the personalized design and application of high-quality, healthy laser light sources for users of different ages.
... Under IR circumstances, disturbances of oxidative and antioxidative products have been reported in the tissues of liver, skeletal muscle, kidney and brain (22,(98)(99)(100). Additionally, the retina is particularly sensitive to oxidative stress, considering the high oxygen demand and consumption and its high concentration of polyunsaturated fatty acids (PUFA) in the outer segments of photoreceptor (101). Although PUFA are thought to protect against oxidative and inflammatory damage, they may also serve as a substrate for free radicals under special conditions as they provide an available source of electrons (94). ...
Insulin resistance (IR) is becoming a worldwide medical and public health challenge as an increasing prevalence of obesity and metabolic disorders. Accumulated evidence has demonstrated a strong relationship between IR and a higher incidence of several dramatically vision-threatening retinal diseases, including diabetic retinopathy, age-related macular degeneration, and glaucoma. In this review, we provide a schematic overview of the associations between IR and certain ocular diseases and further explore the possible mechanisms. Although the exact causes explaining these associations have not been fully elucidated, underlying mechanisms of oxidative stress, chronic low-grade inflammation, endothelial dysfunction and vasoconstriction, and neurodegenerative impairments may be involved. Given that IR is a modifiable risk factor, it may be important to identify patients at a high IR level with prompt treatment, which may decrease the risk of developing certain ocular diseases. Additionally, improving IR through the activation of insulin signaling pathways could become a potential therapeutic target.
... The native crystalline lens filters ultraviolet (UV) light and reduces transmission of short-wave or "blue" light. 1,2 Although the crystalline lens is highly transparent in children, light transmission gradually decreases with age, especially at shorter wavelengths, as shown by the dotted lines in Figure 1. Transmission of 480-nm light, for instance, is expected to decrease by 72% between the ages of 10 and 80 years. ...
Blue light–filtering (BLF) intraocular lenses (IOLs) are designed to mimic the healthy natural adult crystalline lens. Studies that evaluated the relative merit of ultraviolet-only IOL design (ie, blocking wavelengths <400 nm) versus BLF IOL design (ie, filtering wavelengths ~400–475 nm in addition to blocking wavelengths <400 nm) on protection and function of the visual system suggest that neither design had a deleterious impact on visual acuity or contrast sensitivity. A BLF design may reduce some aspects of glare, such as veiling and photostress. BLF has been shown in many contexts to improve visual performance under conditions that are stressed by blue light, such as distance vision impaired by short-wave dominant haze. Furthermore, some data (mostly inferential) support the notion that BLF IOLs reduce actinic stress. Biomimetic BLF IOLs represent a conservative approach to IOL design that provides no harm for visual acuity, contrast sensitivity, or color vision while improving vision under certain circumstances (eg, glare).
... Blue light has been shown to induce several effects on humans. Specifically, prolonged exposure to blue light can induce dry eyes [3,4], blurred vision [4,5], eye fatigue [6], retinal damage, and age-related macular degeneration [7]. ...
Humans are persistently exposed to massive amounts of blue light via sunlight, computers, smartphones, and similar devices. Although the positive and negative effects of blue light on living organisms have been reported, its impact on learning and memory remains unknown. Herein, we examined the effects of widespread blue light exposure on the learning and memory abilities of blue light-exposed mice. Ten-week-old male ICR mice were divided into five groups (five mice/group) and irradiated with blue light from a light-emitting diode daily for 6 months. After 6 months of blue light irradiation, mice exhibited a decline in memory and learning abilities, assessed using the Morris water maze and step-through passive avoidance paradigms. Blue light-irradiated mice exhibited a decreased expression of the clock gene brain and muscle arnt-like 1 (Bmal1). The number of microglia and levels of M1 macrophage CC-chemokine receptor 7 and inducible nitric oxide synthase were increased, accompanied by a decrease in M2 macrophage arginase-1 levels. Levels of angiopoietin-like protein 2 and inflammatory cytokines interleukin-6, tumor necrosis factor-α, and interleukin-1β were elevated. Our findings suggest that long-term blue light exposure could reduce Bmal1 expression, activate the M1 macrophage/Angptl2/inflammatory cytokine pathway, induce neurodegeneration, and lead to a decline in memory.
... In the Beaver Dam Eye Study, outdoor activity and sun exposure early in life were associated with the development of AMD. 3 Moreover, patients with significantly higher exposure to blue or visible light were more likely to have RPE atrophy or disciform scarring. 4 Blue-light filtering (BLF(intraocular lenses (IOLs(are designed to approximate light filtration of the natural crystalline lens by a chromophore that absorbs shortwavelength light (400-460 nm(. ...
... Ultraviolet radiation is a non-ionizing radiation with wavelengths ranging from (100-400 nm) [1].The ultraviolet spectrum is divided into three bands; UV-A (315-400 nm), UV-B region (280-315 nm) and UV-C (100-280 nm) wavelengths [2]. In the electromagnetic spectrum, the wavelength to which the human eye is most sensitive is visible light (400-700 nm) [3].Sunlight reaches the Earth's surface after being absorbed by 30% of the atmosphere. ...
ARTICLE INFO Polarized lenses are recommended because exposure to intense sunlight damages cellular function and photoreceptor structures in the eyes. Polarized lenses filter all wavelengths of UV radiation and most of the reflected glare due to strong reflections depending on the angle of incidence of sunlight and environmental factors. The wavelength of mineral glass in the horizontal and vertical direction (~550nm) is 16.64% for (CF1) and 13.21% for (CF2). There is a sudden drop of 27.87 at 729nm in CF2 and a sudden increase to 58.80 at 730nm in CF1. Absorbance values at 730nm are 0.21 with a decrease in AF1 and 0.54 with an increase in AF2. CF2 is polarized. To determine how the structure of the lens material affects light transmittance and absorbance, the light transmittances of smoked mineral and organic lenses of the same color are 16.64 for the mineral lens and 22.47 for the organic lens at (~550nm) wavelength. Maximum transmittance is 81.25 for mineral lens and 85.73 for organic lens. For night vision, at (~507nm) wavelength, it is 19.35 for mineral lens and 25.00 for organic lens. At (~550nm) wavelength, absorbance values are 0.78 for mineral lens and 0.62 for organic smoked lens. In the study, the effect of color factor on the light transmittance and absorption of organic smoked, brown and green polarized lenses was investigated. Light transmittance at 550 nm wavelength is 22.47 in smoked, 13.48 in brown and 14.32 in green. Absorbance at 550 nm wavelength is 0.62 in smoked, 0.94 in brown and 0.82 in green lens. Since dark lenses do not allow high light transmission, smoked color should be chosen for good vision in the visible light region. Brown color should be preferred if dark glasses should be used in situations where bright light is intense. In the 507nm wavelength of color polarized lenses, smoked is 25.00, brown is 11.45 and green is 16.94. Smoked should be chosen for night vision.
... Red light has neuroprotective effects that have been demonstrated in several models of retinal disease [14]. Blue radiation belongs to the area of the spectrum close to that of UV rays and can cause a series of alterations and irreversible damage to eye tissue, including age-related macular degeneration [15][16][17]. Blue light seems to be responsible for harmful biological effects not only on the retina but also on human health, including the immune system and skin [18][19][20]. The skin and eye are the only organs of the human body exposed directly to light radiation. ...
Several cell-signaling mechanisms are activated by visible light radiation in human keratinocytes, but the key regulatory proteins involved in this specific cellular response have not yet been identified. Human keratinocytes (HaCaT cells) were exposed to blue or red light at low or high irradiance for 3 days in cycles of 12 h of light and 12 h of dark. The cell viability, apoptotic rate and cell cycle progression were analyzed in all experimental conditions. The proteomic profile, ox-idative stress and mitochondrial morphology were additionally evaluated in the HaCaT cells following exposure to high-irradiance blue or red light. Low-irradiance blue or red light exposure did not show an alteration in the cell viability, cell death or cell cycle progression. High-irradiance blue or red light reduced the cell viability, induced cell death and cell cycle G2/M arrest, increased the reactive oxygen species (ROS) and altered the mitochondrial density and morphology. The proteo-mic profile revealed a pivotal role of Cytoplasmic thioredoxin reductase 1 (TXNRD1) and Aldo-keto reductase family 1 member C3 (AKR1C3) in the response of the HaCaT cells to high-irradiance blue or red light exposure. Blue or red light exposure affected the viability of keratinocytes, activating a specific oxidative stress response and inducing mitochondrial dysfunction. Our results can help to address the targets for the therapeutic use of light and to develop adequate preventive strategies for skin damage. This in vitro study supports further in vivo investigations of the biological effects of light on human keratinocytes.
... In this epidemiological study the risk factor for AMD due to blue light (3.7) was almost as high as reported for smoking (4.0). There has been some research to show that using blue light filtering lenses can improve visual func on (reduce glare and increase contrast) under ar ficial ligh ng [103] and decrease risk of AMD [104,105]. Other research has demonstrated that photobiomodula on with red-NIR can improve visual acuity in people with AMD [106,107]. ...
In Western societies, people spend as much as 87% of their time indoors under artificial lighting. In the past few decades, the spectral quality of our artificial lighting has changed dramatically as the lighting industry develops more energy efficient lighting that primarily aims to decrease the energy demands and increase the intensity of the specific wavelengths (colours) of light needed for vision. We have seen a widespread increase in the use of fluorescent and phosphorbased
white LED bulbs. These lights often produce too much short wavelength, high energy, violetblue light that contributes to photochemical damage in our skin and eyes over time, and not enough of the mid wavelength, blue-turquoise, light that we need to maintain our circadian (sleep-wake) cycle and alertness, nor the long wavelength red and near infrared (NIR) light that we now know has health benefits (activates melatonin antioxidant production in our mitochondria). Furthermore,
these light sources often have wavelength regions (parts of the colour spectrum) that are relatively lower than would be present under natural sun/skylight conditions. While the primary objective of lighting is to provide adequate light for seeing, recently, we have learned that some of these missing wavelengths and or the balance of different parts of the spectrum have important health benefits
(e.g. blue-turquoise and red/NIR). This is perhaps not surprising since we have evolved under a stable sun/skylight for millions of years.
With this knowledge now available to us, we should take a more precautionary approach whenconsidering the spectral characteristics of lights installed in buildings like schools, offices, homes, and care homes for the elderly, where people may spend more than half of their waking hours. The best option would be a light source that: minimizes the high energy short wavelength violet-blue light, has
a relatively good proportion of blue-turquoise light to keep occupants alert and stimulate their sleepwake cycle, has enough red/NIR to promote good health, and is a close match to sun/skylight to allow for any yet unknown benefits of different parts of the spectrum.
... Blue-violet light could cause oxygen-dependent retinal injury, acting on specific chromophores, and N-retinylidene-N-retinylethanolamine (A2E) is considered the most important target molecule. Reactive oxygen species (ROS) initiate the activity of cysteine-dependent proteases, ultimately leading to apoptosis and cell death [28,[31][32][33][34]. Mitochondria from photoreceptors, retinal ganglion cells, and RPE cells are the main targets of blue light-associated oxygen free radicals [35][36][37]. Moreover, photophobia, a common unpleasant symptom in patients with RP, has been described to be caused primarily by SWL in its interaction with S-cones from the retina [38]. ...
Background
The medical community is beginning to recognize that retinitis pigmentosa (RP), due to its disabling progression, eventually leads to a reduction in the patient´s quality of life, a direct economic impact, and an increase in the burden on the health care system. There is no curative treatment for the origin of the disease, and most of the current interventions fail in reducing the associated negative psychological states, such as anxiety and depression, which lead to increased variability of vision and pose a continuous threat to the patient’s independence.
Objective
The aim of this study is to assess the effect of oral melatonin (OM) administration alone and combined with short-wavelength light (SWL)–blocking filters on patients with RP and test their effectiveness in improving the level of stress and sleep problems in many of these patients.
Methods
We have developed a low-cost therapy protocol for patients with RP with sleep disorders and negative psychological stress. Patients will be randomized to receive a combined intervention with SWL-blocking filters and OM, SWL-blocking filters alone, or OM alone. There will also be a nonintervention arm as a control group. This study will be conducted across 2 retinal units in patients with RP with sleep disorders and high perceived stress and anxiety score reports. Patients will be assessed in the preintervention period, weekly during the 4 weeks of intervention, and then at 6 months postintervention. The primary outcomes are the differences in changes from baseline to postintervention in hormone release (α-amylase, cortisol, and melatonin) and sleep quality, as measured with the visual analog scale. Secondary outcome measures include clinical macular changes, as measured with optical coherence tomography and optical coherence tomography angiography; retinal function, as measured using the visual field and best-corrected visual acuity; sleep data collected from personal wearables; and several patient-reported variables, such as self-recorded sleep diaries, quality of life, perceived stress, and functional status.
Results
This project is still a study protocol and has not yet started. Bibliographic research for information for its justification began in 2020, and this working group is currently seeking start-up funding. As soon as we have the necessary means, we will proceed with the registration and organization prior to the preliminary phase.
Conclusions
In this feasibility randomized clinical controlled trial, we will compare the effects of SWL blocking alone, administration of OM alone, and a combined intervention with both in patients with RP. We present this study so that it may be replicated and incorporated into future studies at other institutions, as well as applied to additional inherited retinal dystrophies. The goal of presenting this protocol is to aid recent efforts in reducing the impact of sleeping disorders and other psychological disorders on the quality of life in patients with RP and recovering their self-autonomy. In addition, the results of this study will represent a significant step toward developing a novel low-cost therapy for patients with RP and validating a novel therapeutic target.
International Registered Report Identifier (IRRID)
PRR1-10.2196/49196
... 9 Blue light is a high-energy and highfrequency light; prolonged exposure can result in photophobia, ocular pain, cataract, and age-related macular degeneration. 3,30,36,45,53,56 Using a B6 mouse blue light exposure model, strong (mice housed in mirrored-wall boxes) and acute (3 hours blue light exposure has been shown to increase corneal mechanical sensitivity, tear secretion, and photophobia, immediately after illumination or within 3 days of recovery). 36 Hence, blue light exposure may be used as a pathogenic factor for establishing an animal model of ocular neuropathic pain. ...
... However, most LEDs emissions contain blue light (400-500 nm), which can lead to severe retinal damage and upset biorhythms [7,8]. Furthermore, there is sufficient evidence to prove that the long-term cumulative damage of blue light to human eyes is the chief culprit of age-related macular degeneration (AMD), one of the main diseases causing blindness in developed countries [9,10]. Therefore, LEDs without any blue emission ("blue-free") have gradually attracted extensive attention. ...
To fabricate a ZnO-related light-emitting diode (LED) with zero emission at blue wavelengths (“blue-free”), an ingenious strategy is employed. Specifically, for the first time to the best of our knowledge, a natural oxide interface layer, possessing remarkable visible emission potential, is introduced into the Au/i-ZnO/n-GaN metal–insulator–semiconductor (MIS) structure. The unique Au/i-ZnO/interface layer/n-GaN structure successfully eliminated the harmful blue emissions (400–500 nm) from the ZnO film, and the remarkable orange electroluminescence is mainly attributed to the impact ionization process of the natural interface layer at high electric field. It is worth mentioning that the device achieved ultra-low color temperature (2101 K) and excellent color rendering index (92.8) under electrical injection, indicating that the device could fulfill the requirements of electronic display systems and general illumination, and might even play unexpected roles in special lighting domains. The results obtained provide a novel and effective strategy for the design and preparation of ZnO-related LEDs.
... While the screen protector consistently provided a percent reduction in blue light intensity, the effect this has on ocular or general health is unknown. Reducing blue light intensity may provide benefits of better sleep and protection against retinal diseases such as macular degeneration, but further research is needed to investigate this potential health risk [14][15][16][17] . ...
... The cornea and lens absorb ultraviolet (UV) light below 400 nm, whereas the visible light component (380-780 nm) of optical radiation can penetrate the retina. In particular, blue light (400-500 nm) is known to cause retinal damage due to its relatively high energy [30,31]. A2E is a prominent constituent of lipofuscin that enhances cellular sensitivity to light radiation. ...
Retinal pigment epithelial (RPE) cell dysfunction is a key driving force of AMD. RPE cells form a metabolic interface between photoreceptors and choriocapillaris, performing essential functions for retinal homeostasis. Through their multiple functions, RPE cells are constantly exposed to oxidative stress, which leads to the accumulation of damaged proteins, lipids, nucleic acids, and cellular organelles, including mitochondria. As miniature chemical engines of the cell, self-replicating mitochondria are heavily implicated in the aging process through a variety of mechanisms. In the eye, mitochondrial dysfunction is strongly associated with several diseases, including age-related macular degeneration (AMD), which is a leading cause of irreversible vision loss in millions of people globally. Aged mitochondria exhibit decreased rates of oxidative phosphorylation, increased reactive oxygen species (ROS) generation, and increased numbers of mitochondrial DNA mutations. Mitochondrial bioenergetics and autophagy decline during aging because of insufficient free radical scavenger systems, the impairment of DNA repair mechanisms, and reductions in mitochondrial turnover. Recent research has uncovered a much more complex role of mitochondrial function and cytosolic protein translation and proteostasis in AMD pathogenesis. The coupling of autophagy and mitochondrial apoptosis modulates the proteostasis and aging processes. This review aims to summarise and provide a perspective on (i) the current evidence of autophagy, proteostasis, and mitochondrial dysfunction in dry AMD; (ii) current in vitro and in vivo disease models relevant to assessing mitochondrial dysfunction in AMD, and their utility in drug screening; and (iii) ongoing clinical trials targeting mitochondrial dysfunction for AMD therapeutics.
... 9 Blue light is a high-energy and highfrequency light; prolonged exposure can result in photophobia, ocular pain, cataract, and age-related macular degeneration. 3,30,36,45,53,56 Using a B6 mouse blue light exposure model, strong (mice housed in mirrored-wall boxes) and acute (3 hours blue light exposure has been shown to increase corneal mechanical sensitivity, tear secretion, and photophobia, immediately after illumination or within 3 days of recovery). 36 Hence, blue light exposure may be used as a pathogenic factor for establishing an animal model of ocular neuropathic pain. ...
To elucidate the physiological, cellular, and molecular mechanisms responsible for initiating and sustaining ocular neuropathic pain, we created a blue-light-exposure model in C57BL/6 mice. Mice were exposed to 12 h of blue or white light followed by 12 h of darkness. Before blue light exposure, baseline tear secretion, stability, and ocular hyperalgesia were assessed by measuring hyper- or hypo-osmotic solution-induced eye wiping, wind-induced eye closing, and cold-induced eye blinking. At 1 day post-blue light exposure, alterations in hypotonic/hypertonic-induced eye-wiping, and tear film abnormalities were observed. Eye-wiping behaviors were abolished by topical anesthesia. The cold-stimulated eye-blinking and wind-stimulated eye-closing behaviors began after day 3 and their frequency further increased after day 9. Blue-light exposure reduced the density of nerve endings, and increased their tortuosity, the number of beadlike structures, and the branching of stromal nerve fibers, as assessed by whole-mount confocal microscopy. Blue-light exposure also increased TRPV1, but not TRPV4 staining intensity of corneal-projecting neurons in the trigeminal ganglia, as detected by Fluorogold retrograde labeling and immunohistochemistry. TRPV1 and substance P expression was increased, whereas CGRP expression deceased at the mRNA level in isolated corneal projecting neurons. Hence, our blue-light exposure B6 mouse model for assessing tearing and ocular hyperalgesia is useful for studying ocular pain and its underlying mechanisms. Blue-light-induced alterations in tearing and ocular hyperalgesia may be related to the elevated expression of TRPV1, SP, and/or the suppressed expression of CGRP at the ocular surface.
... 80,90,91 A LED display on smartphones is an example of BL emitter. Blue light harms photoreceptors and pigmented epithelium cells, 92 and the reviewed fNIRS study suggests the negative impact of BL on reading comprehension. 63 In the reviewed studies, BL increased total hemoglobin concentrations when the participants were exposed to light emitted by a color-filtered white lightbulb, but it remained constant under LED illumination. ...
Near-infrared (NIR) spectroscopy, also known as functional NIR spectroscopy (fNIRS), is a tool for measuring the hemodynamic response of the prefrontal cortex (PFC) by using NIR light, enabling a noninvasive indirect neural activity assessment. The application of fNIRS in emotion recognition or the differential diagnosis of psychiatric disorders of depressive patients, including major depressive disorder, bipolar disorder and schizophrenia, has previously been reported. Although the use of fNIRS has gradually expanded in cognitive neuroscience studies, few researchers have focused on the effects of light exposure in fNIRS studies. In addition, to the best of our knowledge, there are no scoping reviews of fNIRS studies on light exposure. Because light is an important topic in cognitive neuroscience and psychiatry, we evaluated fNIRS studies on light exposure in humans. We reviewed 10 papers in their entirety. Bright light (BR) modulates fear, and the color differences showed no significance in 1 study, whereas other studies delved extensively into the effects of colored light, finding some individual hemodynamic responses. In our study, we highlighted that the effects of natural light have not been studied using fNIRS. Light is becoming a critical topic in cognitive neuroscience and psychiatry, and fNIRS is critical for improving public health and managing psychiatric disorders.
... With the widespread adoption of organic light-emitting diode and light-emitting diode-backlit displays, concerns have been expressed regarding their short wavelength blue light emission [112] and the potential of such emissions to cause health issues [113][114][115][116]. It is well established that high intensity blue light can cause damage to the retina [3] and ocular surface [4], but current understanding is that the low intensity blue light produced by digital displays is insufficient to cause phototoxicity, even following prolonged periods of use [112]. ...
Eye strain when performing tasks reliant on a digital environment can cause discomfort, affecting productivity and quality of life. Digital eye strain (the preferred terminology) was defined as "the development or exacerbation of recurrent ocular symptoms and/or signs related specifically to digital device screen viewing". Digital eye strain prevalence of up to 97% has, due to no previously agreed definition/diagnostic criteria and limitations of current questionnaires, failed to differentiate such symptoms from those arising from non-digital tasks. Objective signs such as blink rate or critical flicker frequency changes are not 'diagnostic' of digital eye strain nor validated as sensitive. The mechanisms attributed to ocular surface disease exacerbation are mainly reduced blink rate and completeness, partial/uncorrected refractive error and/or underlying binocular vision anomalies, together with the cognitive demand of the task and differences in position, size, brightness and glare compared to an equivalent non-digital task. In general, interventions are not well established; patients experiencing digital eye strain should be provided with a full refractive correction for the appropriate working distances. Improving blinking, optimizing the work environment and encouraging regular breaks may help. Based on current, best evidence, blue-light blocking interventions do not appear to be an effective management strategy. More and larger clinical trials are needed to assess artificial tear effectiveness for relieving digital eye strain, particularly comparing different constituents; a systematic review within the report identified use of secretagogues and warm compress/humidity goggles/ambient humidifiers as promising strategies, along with nutritional supplementation (such as omega-3 fatty acid supplementation and berry extracts).
... The beginning of the new millennium has seen a change in the type of IOLs being implanted in a patient's eye-from the classic clear ultraviolet light-filtering IOLs to the yellow-tinted blue light-filtering IOLs. The reason behind it is that the latter prevents the blue light exposure of the retina, especially abundant in A2E with aging, and as such, prevents DNA damage and cell apoptosis mediated by singlet oxygen, which is wavelength dependent [59][60][61][62]. Studies performed by Sparrow et al. and Yanagi et al. [60,63] showed the inhibition of vascular endothelial growth factor (VEGF) production as well as a protective role of the blue-blocking IOL on RPE cells, while Obana et al. [64], by performing Raman spectroscopy, highlighted a reduction in macular pigment optical density (MPOD) in the clear IOL group. ...
Light is a fundamental aspect of our lives, being involved in the regulation of numerous processes in our body. While blue light has always existed in nature, with the ever-growing number of electronic devices that make use of short wavelength (blue) light, the human retina has seen increased exposure to it. Because it is at the high-energy end of the visible spectrum, many authors have investigated the theoretical harmful effects that it poses to the human retina and, more recently, the human body, given the discovery and characterization of the intrinsically photosensitive retinal ganglion cells. Many approaches have been explored, with the focus shifting throughout the years from examining classic ophthalmological parameters, such as visual acuity, and contrast sensitivity to more complex ones seen on electrophysiological assays and optical coherence tomographies. The current study aims to gather the most recent relevant data, reveal encountered pitfalls, and suggest future directions for studies regarding local and/or systemic effects of blue light retinal exposures.
... In this context, BL can harm the retina via ROS accumulation and DNA damage, especially when the repair mechanisms of the eye for BL weaken due to aging [14,15]. The extent of damage can be even greater if crystalline lenses are removed by cataract surgery, allowing more BL to reach the retina [16]. The combination of light exposure, elevated metabolic activity, accumulation of oxidized lipoproteins, and decreased antioxidant functions during aging make retinal tissues even more vulnerable to oxidative stress [17,18]. ...
Awareness toward the risks of blue light (BL) exposure is rising due to increased use of BL-enriched LEDs in displays. Short-wave BL (400–500 nm) has a high photochemical energy, leading to the enhanced production of reactive oxygen species (ROS). BL potentially plays a role in causing dry eye, cataracts, and age-related macular degeneration (AMD). The effect of BL on retinal pigment epithelium cells (RPEs) or photoreceptors has been extensively investigated. In contrast, only a few studies have investigated the effects of BL exposure on Müller cells (MCs). This is mainly due to their lack of photosensitive elements and the common assumption that their reaction to stress is only secondary in disease development. However, MCs perform important supportive, secretory, and immune functions in the retina, making them essential for retinal survival. Increased oxidative stress is a key player in many retinal diseases such as AMD or glaucoma. We hypothesize that increased oxidative stress can also affect MCs. Thus, we simulated oxidative stress levels by exposing primary porcine MCs and human MIO-M1 cells to BL. To confirm the wavelength-specificity, the cells were further exposed to red (RL), purple (PL), and white light (WL). BL and WL exposure increased ROS levels, but only BL exposure led to apoptosis in primary MCs. Thus, BL accounted for the harmful part of WL exposure. When cells were simultaneously exposed to BL and RL (i.e., PL), cell damage due to BL could be partly prevented, as could the inhibition of p53, demonstrating the protective effect of RL and p53 dependency. In contrast, BL hardly induced apoptosis in MIO-M1 cells, which is likely due to the immortalization of the cells. Therefore, enhanced oxidative stress levels can significantly harm MC function, probably leading to decreased retinal survival and, thus, further enhancing the progression of retinal diseases. Preventing the cell death of these essential retinal cells represents a promising therapy option to enhance retinal survival.
... Remarkably, retinal damage is often the most common, but also relatively serious in the process of light damage to the eye [7]. Recent studies found the case of a 13-year-old boy looking at a green diode laser with an average output of 154 MW reflected in a mirror. ...
Background:
Light-induced retinal damage is a serious vision-threatening disease, resulting from unsuitable laser irradiation, high-power light and sustaining light exposure. Therefore, effectively evaluate the morphological and functional of retinal damage is urgently needed. Now, we mainly reported three patients suffered from typical light irradiations.
Case summary:
Patient 1 suffered from old laser pointer irradiation and followed with amblyopia treatment. Patient 2 suffered from acute high-energy light irradiation. Patient 3 suffered from sustaining optical fiber irradiation. Detailed morphological and functional examinations of the retina revealed that the lesions of the three patients had many similar characteristics, such as macular morphological changes, patent pattern visual monitoring amplitude or peak time abnormalities, multi-fucus electroretinograms macular central amplitude density decreased.
Conclusion:
In conclusion, light-induced retinopathy has many common features, which can help clinical medical staff to diagnose retinal photodamage diseases.
To investigate the laser-based displays that can offer the light source with a high level of photobiological safety and are suitable for users of different ages, this research optimizes the light source of the three-primary laser-based displays from its peak wavelength and the fractions of radiant flux. The non-linear program based on genetic algorithm is used to set the color gamut coverage over 90% and the correlated color temperature at 6500 K. Find suitable peak wavelength and fractions of radiant flux with the premise of less than the blue light hazard (BLH) caused by the D65 light source to the 1 year, and select the result with the maximum circadian action factor (CAF) as the optimization for each age. Meanwhile, this research explores the effect that a change in the peak wavelength and fractions of radiant flux near the optimal results on CAF and BLH in different age groups. It provides reference for the design of health consideration laser displays for different age users in the daily working environment.
5-aminolevulinic acid (ALA) is used during resection of malignant gliomas due to its fluorescence properties and has been shown to render resection more effective than resection without ALA guidance. The aim of this narrative review is to categorize the adverse effects of ALA relevant to anesthesia providers. Intraoperative hypotension, porphyria-related side effects, alterations in blood chemistry and coagulation, photosensitivity, and increased levels of liver enzymes have all been reported. We also sought to examine the impact of dosage and timing of oral administration on efficacy of ALA and on these side effects. Twenty-seven studies met our inclusion criteria of patients undergoing craniotomy for glioma resection using ALA and occurrence of at least one adverse effect. The results of these studies showed that there was heterogeneity in levels of intraoperative hypotension, with some reporting an incidence as high as 32%, and that hypotension was associated with antihypertensive medication use. Clinical symptoms of porphyria, such as gastrointestinal disturbance, were less commonly reported. Photosensitivity of the skin after 5-ALA administration was well documented particularly in patients exposed to light; however, adverse effects on the eye were not adequately studied. Elevation in liver enzymes was a common finding postoperatively but was often clinically insignificant. The timing of oral administration presents practical issues for the preoperative management of patients undergoing resection with ALA. We provide guidance for perioperative management of patients who receive ALA for brain tumor resection. Controlled studies with adequate statistical power are required to further understand and prevent the adverse effects of ALA.
We develop a new type of violet-light-excitable Eu ²⁺ :Sr 8 CaLu(PO 4 ) 7 phosphor with tunable green–yellow emissions and high photoluminescence quantum yields above 70% via Na ⁺ alloying-induced local structural modification.
Short wavelength light emissions from digital devices have been the subject of various investigations in recent years, in relation to the possible damage that can be caused to the retina. In hospital work environments, the use of video terminals is now common and healthcare professionals are exposed both to the screens of medical and generic monitors. Since current European legislation on occupational health establishes exposure limit values to blue light exposure in terms of radiance, by following the most current technical reports and international guidelines a method was defined for the evaluation of the blue light radiance emitted by monitors. In addition, since blue light filtering glasses are common among the population, quantitative measurements were performed on a sample of them, in order to better quantify the exposure levels of health workers who regularly wear them. It is the intention of the authors to present a metrologically correct standard of measurement, which can be easily implemented for the assessment of the blue light hazard in a healthcare environment.
Age-related macular degeneration (AMD) is one of an increasing number of diseases that causes irreversible impairment and loss of vision in the elderly. AMD occurs by oxidative stress-mediated apoptosis of retinal pigment epithelium cells. The onset of AMD may be positively correlated with the exposure to blue light. We screened food-derived carotenoids for cytoprotective action against blue light irradiation using human ARPE-19 retinal pigment epithelium cells. This study revealed that blue light irradiation triggered apoptosis and oxidative stress in all-trans-retinal (atRAL)-exposed ARPE-19 cells by generating singlet oxygen (1O2), leading to significant cell death. We found that astaxanthin, a potent anti-oxidative xanthophyll abundant in several marine organisms including microalgae, salmon, and shrimp, significantly suppresses blue light-induced apoptotic cell death of atRAL-exposed ARPE-19 cells by scavenging 1O2. Mechanistic studies using the blue-light irradiated cells also demonstrated that the cytoprotective effects of astaxanthin can be attributed to scavenging of 1O2 directly. Our results suggest the potential value of astaxanthin as a dietary strategy to prevent blue light-induced retinal degeneration including AMD.
Human eyes’ protection becomes more and more important due to the increasing dependence on screens and lighting sources. In this work, a narrowband blue light photodetector based on CH
NH
PbBrCl
single crystal and its filterless application in blue light hazard detection has been reported. It is found that the photodetector is only sensitive to light between 400 and 500 nm, eliminating the influence of other light photons. Then the relationship between the blue light weighted radiance and photocurrent can be described as a numerical function, through which the blue light hazard level can be detected. By introducing the back-end circuits, the photodetector has been applied to a portable blue light hazard detection system, which can detect and display the blue light hazard level of illuminations. Thus, this photodetector and its application may have potential applications in the future healthcare field.
Purpose:
To measure the macular pigment optical density in first-degree relatives of patients with age-related macular degeneration and compare it with a healthy control group.
Methods:
One hundred and twenty-eight healthy subjects who were first-degree relatives of age-related macular degeneration patients were included in the study (Group 1). As the control group, 74 healthy subjects were included in the study (Group 2). The right eyes of all cases were included in the study. Macular pigment optical density was measured with a commercially available device (MPSII®, Elektron Technology, Switzerland) using technology based on heterochromatic flicker photometry. Central foveal thickness and subfoveal choroidal thickness were measured with spectral-domain optical coherence tomography. Values were compared between the two groups.
Results:
There were 54 males and 74 females in Group 1 and 32 males and 42 females in Group 2. The mean ± SD ages of Group 1 and Group 2 were 49.0 ± 7.6 and 41.8 ± 8.6, respectively. Mean ± SD macular pigment optical density values of Group 1 and Group 2 were 0.43 ± 0.09 and 0.47 ± 0.12 (p = 0.048), mean ± SD central foveal thickness were 208 ± 19 and 216 ± 8 µm (p = 0.014), and mean ± SD subfoveal choroidal thickness were 232 ± 29 and 250 ± 21 µm (p = 0.002), respectively.
Conclusion:
The macular pigment optical density values were significantly lower in the first-degree relatives of patients with age-related macular degeneration than in the control group. Macular pigment optical density may be a marker for the development of age-related macular degeneration in the future in the first-degree relatives of age-related macular degeneration patients. Further prospective studies with a larger number of participants will be needed to confirm our results moreover, to clarify its benefit as an early diagnostic biomarker.
Age-related macular degeneration (AMD) is a retinal degenerative disorder prevalent in the elderly population, which leads to the loss of central vision. The disease progression can be managed, if not prevented, either by blocking neovascularization (“wet” form of AMD) or by preserving retinal pigment epithelium and photoreceptor cells (“dry” form of AMD). Although current therapeutic modalities are moderately successful in delaying the progression and management of the disease, advances over the past years in regenerative medicine using iPSC, embryonic stem cells, advanced materials (including nanomaterials) and organ bio-printing show great prospects in restoring vision and efficient management of either forms of AMD. This review focuses on the molecular mechanism of the disease, model systems (both cellular and animal) used in studying AMD, the list of various regenerative therapies and the current treatments available. The article also highlights on the recent clinical trials using regenerative therapies and management of the disease.
Background: Blue light causes retinal photoreceptor damage via oxidative and endoplasmic reticulum (ER) stress. A previous study showed that blueberry stem extract (BStEx) and its active components have cytoprotective effects against blue-light-induced photoreceptor cell damage by suppressing oxidative stress. This study demonstrated the inhibitory effect of BStEx against blue light-induced ER stress in photoreceptor cells. Methods: The photoreceptor cells treated with BStEx or the antioxidant N-Acetyl-L-cysteine (NAC) as a positive control were used and then exposed to blue light. The cytoprotective effects of BStEx and NAC were evaluated using CCK-8. The ER stress-related protein expression changes over time, and its levels were measured after each exposure time to blue light in photoreceptor cells treated with BStEx or NAC. Results: BStEx and NAC showed protective effects against blue-light-induced photoreceptor morphological abnormalities and cell damage. Although blue light triggered ER stress factors such as BiP, PERK, ATF6, eIF2α, ATF4, and CHOP, which in turn stimulated cell cycle arrest factors p53 and p21 and upregulation of apoptosis-inducing factors caspase-3. However, BStEx suppressed the increase in expression of BiP, ATF4, ATF6, CHOP, p53, p21, and caspase-3, but not mitochondrial apoptotic factors Bax and cytochrome c. Furthermore, the antioxidant NAC showed similar suppressive effects on BStEx. Conclusion: Our findings suggest that blue light-induced ER stress is primarily caused by oxidative stress, and BStEx might suppress ER stress via an antioxidant effect. The antioxidant NAC contributes to the cell proliferative capacity and suppression of apoptosis in photoreceptor cells.
IntroductionExposure to blue light has seriously increased in our environment since the arrival of light emitting diodes (LEDs) and, in recent years, the proliferation of digital devices rich in blue light. This raises some questions about its potential deleterious effects on eye health. The aim of this narrative review is to provide an update on the ocular effects of blue light and to discuss the efficiency of methods of protection and prevention against potential blue light-induced ocular injury.Methods
The search of relevant English articles was conducted in PubMed, Medline, and Google Scholar databases until December 2022.ResultsBlue light exposure provokes photochemical reactions in most eye tissues, in particular the cornea, the lens, and the retina. In vitro and in vivo studies have shown that certain exposures to blue light (depending on the wavelength or intensity) can cause temporary or permanent damage to some structures of the eye, especially the retina. However, currently, there is no evidence that screen use and LEDs in normal use are deleterious to the human retina. Regarding protection, there is currently no evidence of a beneficial effect of blue blocking lenses for the prevention of eye diseases, in particular age-related macular degeneration (AMD). In humans, macular pigments (composed of lutein and zeaxanthin) represent a natural protection by filtering blue light, and can be increased through increased intake from foods or food supplements. These nutrients are associated with lower risk for AMD and cataract. Antioxidants such as vitamins C, E, or zinc might also contribute to the prevention of photochemical ocular damage by preventing oxidative stress.Conclusion
Currently, there is no evidence that LEDs in normal use at domestic intensity levels or in screen devices are retinotoxic to the human eye. However, the potential toxicity of long-term cumulative exposure and the dose-response effect are currently unknown.
Background:
Computer vision syndrome is a group of eye and vision-related problems that result from prolonged computer use. The worldwide pandemic of coronavirus disease-2019 (COVID-19) lockdown has led to an increase in the digital screen exposure as jobs as well as academic learning have majorly shifted online. This has caused an increase in digital eye strain (DES) globally. The aims and objectives of this study were to compare the knowledge, attitude, and practices among medical and nonmedical professionals with regard to DES in a background of COVID-19 lockdown.
Materials and methods:
A cross-sectional, observational, online questionnaire-based research survey analysis was conducted among medical professionals with age- and sex-matched nonmedical professionals. Responses were collected over a week and analyzed. The level of significance was set at a P < 0.05. Statistical Package for the Social Sciences software version 23.0 was used for the result analysis.
Results:
Our study included 353 (50.4%) medical and 347 (49.6%) nonmedical personnel. It was noted that 266 (75.4%) of medical professionals and 268 (77.2%) of nonmedical professionals experienced eye problems after prolonged digital screen exposure. A significant proportion of respondents experienced an increase in symptoms following COVID-19 lockdown with 140 (52.6%) being medical professionals and 163 (60.8%) nonmedical professionals (P = 0.015).
Conclusions:
DES is a preventable lifestyle-associated disorder. Awareness among the masses can reduce the adverse effects. Proper lighting, adequate viewing distance, voluntary blinking, and using lubricating eye drops are a few ways to reduce the chances of DES. Further studies are needed to formulate standardized guidelines for the management of DES.
Long-term light exposure, especially in the spectrum of blue light, frequently causes excessive oxidative stress in dry age-related macular degeneration (AMD). Here, to gain insight into the underlying mechanism, we focused on mitochondrial dynamics alterations under long-term exposure to blue light in mouse and retinal cells. Six-month-old C57BL/6 mice were exposed to blue light (450 nm, 800 lx) for 2 weeks. The phenotypic changes in the retina were assayed using haematoxylin-eosin staining and transmission electron microscopy. Long-term blue light exposure significantly thinned each retinal layer in mice, induced retinal apoptosis and impaired retinal mitochondria. A retinal pigment epithelial cell line (ARPE-19) was used to verify the phototoxicity of blue light. Flow cytometry, immunofluorescence and MitoSox Red probe experiments confirmed that more total and mitochondria-specific ROS were generated in the blue light group than in the control group. Mito-Tracker Green probe showed fragmented mitochondrial morphology. The western blotting results indicated a significant increase in DRP1, OMA1, and BAX and a decrease in OPA1 and Bcl-2. In conclusion, long-term exposure to blue light damaged the retinas of mice, especially the ONL and RPE cells. There was destruction and dysfunction of mitochondria in RPE cells in vivo and in vitro. Mitochondrial dynamics were disrupted with characteristics of fusion-related obstruction after blue-light irradiation.
Blue light causes retinal damage that can lead to ocular diseases such as age-related macular degeneration. In this study, we determined the protective effect of blueberry stem extract (BStEx) and active components on blue light-emitting diode (LED) light-induced retinal photoreceptor cell damage in vitro. Photoreceptor cells cultured in the presence of BStEx or components were exposed to blue light to induce cell damage. BStEx, fractions of BStEx containing proanthocyanidins, chlorogenic acid, catechin, and epicatechin prevented the cell damage and/or inhibited the generation of reactive oxygen species (ROS). Furthermore, BStEx reduced apoptosis and cell death, and inhibited the phosphorylation of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase leading to cellular apoptosis induced by blue light exposure. These findings suggest that BStEx and components exert a protective effect against blue light-induced photoreceptor cell damage through the inhibition of MAPK phosphorylation and ROS production.
The zero‐dimensional perovskite‐like derivative Cs3Cu2X5 (X = Cl, Br, I) with self‐trapped excitons (STEs) photoluminescence (PL) has attracted tremendous interest in the field of optoelectronics. Nonetheless, it is challenging for Cs3Cu2Br5 material to attain full visible spectrum emission and prevent light‐induced photochemical damage to the retina (blue light hazard) in applications. Herein, Mn2+ is chosen as the dopant to alloy into Cs3Cu2X5 via a one‐step solid state synthesis method. Significantly, the series of Mn2+‐doped show the emission peak of 460 nm STEs and the emission peak of 550 nm Mn2+. More importantly, the high energy absorption of Mn2+ facilitates the transfer of exciton energy, contributing to a reduction in blue emission peak at 460 nm. Simultaneously, ≈17.5% of Mn2+ is alloyed into the Cs3Cu2X5lattice to induce the energy transfer channels from the Cs3Cu2X5 host to the Mn2+ guest to lead to the emission of Mn2+, which broadens emission spectrum (400–620 nm) and realizes 80% reduction of the blue emission peak at 460 nm. Additionally, a white light‐emitting diodes can decrease the blue emission band via 71.45% and an ultrahigh color rendering index (CRI) of 94.5 is produced using the 17.5% Mn2+: Cs3Cu2X5 perovskite‐like derivative powder material. This article introduces that Mn2+ is alloyed into the lattice of Cs3Cu2Br5, which brings new yellow emission at 550 nm and the emission peak at 460 nm is reduced by 80%. Furthermore the color rendering index of the white light‐emitting diode produced by 17.5% Mn‐doped Cs3Cu2Br5 is 94.5 and the blue band (400–480 nm) decreases by 71.45%.
In this study we incorporated a PffBT4T-2OD:PC71BM bulk-heterojunction (BHJ) active layer in the layer structure ITO/ZnO/BHJ/MoO3/Ag, obtaining high-performance organic photodiodes (OPDs) for application in blue-light hazard (BLH) detection. The high crystallinity of PffBT4T-2OD resulted in the OPD displaying high performance even when the thickness of the BHJ layer was up to 850 nm. The efficient OPD suppressed charge injection (from the metal contacts), thereby providing state-of-the-art performance: external quantum efficiencies of greater than 70% (380-710 nm), a value of Jd of 1.18 × 10⁻⁹ A cm⁻² (-2 V), and high detectivity [2.9 × 10¹³ Jones, -2 V (710 nm)]. The observed ultra-high cut-off frequency [>800 kHz (at 530 nm), with rise/fall times of less than 350 ns at reverse biases of less than -3 V] exceeded that of a silicon photodiode and made the system suitable for use in image photosensors and medical monitoring. The wide linear dynamic range (LDR, 530 nm) of the OPD (139 dB at -1 V, from 2.2 × 10⁻⁴ to 2.5 × 10⁻¹¹ A cm⁻²) encompassed the mesopic and scotopic vision regimes. Combined with the design of a BLH filter, we calculated the environmental BLH weighted irradiation power density [WDBLH = CB × JSC (current density of diode)] to evaluate the BLH effect for various light sources and commercially available lenses; here CB (12.69, reported herein) is a corrective constant for BLH photodetectors. Finally, our design allowed ready determination of the ratio of blue-violet and blue-green light.
Andy Sanders takes a look at the published evidence for the impact on ocular and visual health.
Background:
Observational and experimental data suggest that antioxidant and/or zinc supplements may delay progression of age-related macular degeneration (AMD) and vision loss.
Objective:
To evaluate the effect of high-dose vitamins C and E, beta carotene, and zinc supplements on AMD progression and visual acuity.
Design:
The Age-Related Eye Disease Study, an 11-center double-masked clinical trial, enrolled participants in an AMD trial if they had extensive small drusen, intermediate drusen, large drusen, noncentral geographic atrophy, or pigment abnormalities in 1 or both eyes, or advanced AMD or vision loss due to AMD in 1 eye. At least 1 eye had best-corrected visual acuity of 20/32 or better. Participants were randomly assigned to receive daily oral tablets containing: (1) antioxidants (vitamin C, 500 mg; vitamin E, 400 IU; and beta carotene, 15 mg); (2) zinc, 80 mg, as zinc oxide and copper, 2 mg, as cupric oxide; (3) antioxidants plus zinc; or (4) placebo.
Main outcome measures:
(1) Photographic assessment of progression to or treatment for advanced AMD and (2) at least moderate visual acuity loss from baseline (> or =15 letters). Primary analyses used repeated-measures logistic regression with a significance level of.01, unadjusted for covariates. Serum level measurements, medical histories, and mortality rates were used for safety monitoring.
Results:
Average follow-up of the 3640 enrolled study participants, aged 55-80 years, was 6.3 years, with 2.4% lost to follow-up. Comparison with placebo demonstrated a statistically significant odds reduction for the development of advanced AMD with antioxidants plus zinc (odds ratio [OR], 0.72; 99% confidence interval [CI], 0.52-0.98). The ORs for zinc alone and antioxidants alone are 0.75 (99% CI, 0.55-1.03) and 0.80 (99% CI, 0.59-1.09), respectively. Participants with extensive small drusen, nonextensive intermediate size drusen, or pigment abnormalities had only a 1.3% 5-year probability of progression to advanced AMD. Odds reduction estimates increased when these 1063 participants were excluded (antioxidants plus zinc: OR, 0.66; 99% CI, 0.47-0.91; zinc: OR, 0.71; 99% CI, 0.52-0.99; antioxidants: OR, 0.76; 99% CI, 0.55-1.05). Both zinc and antioxidants plus zinc significantly reduced the odds of developing advanced AMD in this higher-risk group. The only statistically significant reduction in rates of at least moderate visual acuity loss occurred in persons assigned to receive antioxidants plus zinc (OR, 0.73; 99% CI, 0.54-0.99). No statistically significant serious adverse effect was associated with any of the formulations.
Conclusions:
Persons older than 55 years should have dilated eye examinations to determine their risk of developing advanced AMD. Those with extensive intermediate size drusen, at least 1 large druse, noncentral geographic atrophy in 1 or both eyes, or advanced AMD or vision loss due to AMD in 1 eye, and without contraindications such as smoking, should consider taking a supplement of antioxidants plus zinc such as that used in this study.
Oxidative stress can cause cancer. Our aim was to establish whether antioxidant supplements reduce the incidence of gastrointestinal cancer and mortality.
With the Cochrane Collaboration methodology, we reviewed all randomised trials comparing antioxidant supplements with placebo for prevention of gastrointestinal cancers. We searched electronic databases and reference lists (February, 2003). Outcome measures were incidence of gastrointestinal cancers, overall mortality, and adverse effects. Outcomes were analysed with fixed-effect and random-effects model meta-analyses and were reported as relative risk with 95% CIs.
We identified 14 randomised trials (n=170,525). Trial quality was generally high. Heterogeneity of results was low to moderate. Neither the fixed-effect (relative risk 0.96, 95% CI 0.88-1.04) nor random-effects meta-analyses (0.90, 0.77-1.05) showed significant effects of supplementation with beta-carotene, vitamins A, C, E, and selenium (alone or in combination) versus placebo on oesophageal, gastric, colorectal, pancreatic, and liver cancer incidences. In seven high-quality trials (n=131727), the fixed-effect model showed that antioxidant significantly increased mortality (1.06, 1.02-1.10), unlike the random-effects meta-analysis (1.06, 0.98-1.15). Low-quality trials showed no significant effect of antioxidant supplementation on mortality. The difference between the mortality estimates in high-quality and low-quality trials was significant (Z=2.10, p=0.04 by test of interaction). beta-carotene and vitamin A (1.29, 1.14-1.45) and beta-carotene and vitamin E (1.10, 1.01-1.20) significantly increased mortality, whereas beta-carotene alone only tended to increase mortality (1.05, 0.99-1.11). In four trials (three with unclear or inadequate methodology), selenium showed significant beneficial effect on the incidence of gastrointestinal cancer.
We could not find evidence that antioxidant supplements can prevent gastrointestinal cancers; on the contrary, they seem to increase overall mortality. The potential preventive effect of selenium should be studied in adequate randomised trials.
A sequence variation in the pigment epithelial protein RPE65 has been shown to correlate with RPE65 protein levels, rhodopsin regeneration kinetics and light damage susceptibility in different mouse strains. Here, we tested whether such a correlation can also be found in rats. We examined four rat strains for RPE65 protein levels and the Rpe65 gene sequence. In two strains, we additionally determined Rpe65 mRNA levels, rhodopsin regeneration and light damage susceptibility (LDS).RPE65 protein levels were higher in Lewis and Brown Norway rats compared to Wistar and Long Evans. The albino strains Wistar and Lewis were investigated further. Lewis had higher Rpe65 mRNA levels than Wistar. Sequence analysis of the coding region of the Rpe65 cDNA revealed no relevant sequence variations in the two strains. Content and regeneration of rhodopsin were comparable in both strains. However, Wistar rats were more susceptible to light damage than Lewis. We conclude that lower RPE65 protein levels in Wistar may have been caused by decreased gene expression and not by a sequence variation as suggested for mice. In rats, RPE65 may not be a limiting factor for rhodopsin regeneration. Since LDS in rats did not directly correlate with RPE65 protein levels and rhodopsin regeneration, other yet unidentified (genetic) factors may account for the susceptibility differences observed in rats.
The human retina is a unique component of the nervous system in that throughout life it is continuously exposed to optical radiation between 400 and 1400 nm. The physiology of the ageing retina and the regression in visual performance with age cannot therefore be studied in isolation, or discriminated, from the life long cumulative effects of radiant exposure. This paper describes the spectrum of age related changes in the retina as they merge imperceptibly between declining visual function and overt pathology.
Purpose:
Vascular endothelial growth factor (VEGF) is a potent and specific angiogenic growth factor, in vitro and in vivo, that may be associated with the development of intraocular neovascularization. In the current study, the authors analyze the expression of VEGF in subfoveal fibrovascular membranes from patients with age-related macular degeneration.
Methods:
Surgically removed subfoveal fibrovascular membranes from 18 eyes were analyzed for the expression of VEGF mRNA and protein using in situ hybridization and immunohistochemistry, respectively.
Results:
Most specimens expressed both VEGF mRNA and protein. The VEGF mRNA expression was particularly high in areas with a marked inflammatory response, in which the expression was concentrated to cells resembling fibroblasts and to surrounding inflammatory cells. VEGF protein expression was seen in fibrovascular parts of the membranes and was predominantly localized to the cytoplasm of fibroblastlike cells. In some of these membranes, strong VEGF protein immunoreactivity also was concentrated to extracellular matrix foci within the fibrovascular stroma.
Conclusions:
Results indicate that VEGF may be of pathogenetic importance for the development of the choroidal neovascularization (age-related macular degeneration) and also may implicate a role of fibroblasts of presumable choroidal origin in this process.
Eyes of pigmented rabbits were exposed (3.5 hours) to light from a xenon lamp, passing IR filters, fiber optics and various test filters (IOL or potential IOL materials). Retinal irradiance was 60-70 mW/cm2, i.e. below the level for thermal damage. Neuroretinal and pigment epithelial (PE) function and appearance were assessed by DC electroretinography and opthalomoscopy before exposure, and one day and four to six days thereafter. A yellow (blue light absorbing) filter (not disturbing color vision) was found to protect the PE and neuroretina against photochemical light damage (mainly 'the blue light hazard') significantly better than a Perspex CQ (clear PMMA) material. On the contrary, a combination of Perspex and a neutral density filter, equal to the yellow filter regarding total irradiance transmitted, did not protect significantly better than Perspex. The yellow filter protected the PE significantly better than a UV filter. These findings may be important when developing IOL materials.
objective. To investigate the role of macrophages in the development of laser-induced choroidal neovascularization (CNV) by selective depletion with liposomal clodronate (Cl2MDP-LIP).
methods. Laser photocoagulation was used to induce CNV in wild-type C57BL/6J mice. Animals were treated with intravenous (IV) and/or subconjunctival (SC) Cl2MDP-LIP or PBS-LIP at the following time points: 2 days before, immediately after, 2 days before and immediately after, or 2 days after laser injury. CNV responses were compared on the basis of en masse volumetric measurements and fluorescein angiography after laser photocoagulation. Macrophages were identified by immunostaining for F4/80, and vascular endothelial growth factor (VEGF) expression was quantified by ELISA.
results. Macrophages invaded the site of laser injury within 1 day of photocoagulation and peaked at 3 days. IV Cl2MDP-LIP significantly decreased the volume of CNV and angiographic leakage when administered 2 days before and/or immediately after laser injury, but not when administered 2 days after injury. SC Cl2MDP-LIP significantly decreased lesion volume when coadministered with IV PBS-LIP but not IV Cl2MDP-LIP. IV Cl2MDP-LIP was significantly more beneficial when administered 2 days before laser injury than immediately after, but combining SC Cl2MDP-LIP with IV treatment eliminated this difference. Reduction in CNV volume correlated with VEGF protein levels and number of infiltrating macrophages.
conclusions. Generalized macrophage depletion reduced the size and leakage of laser-induced CNV and was associated with decreased macrophage infiltration and VEGF protein. These findings define the role of the macrophage as a critical component in initiating the laser-induced CNV response.
Using histochemical staining techniques and electron microscopy, the authors have examined the histochemical properties and ultrastructure of Bruch's membrane in 30 human eyes with an age range of 1 to 95 years. The results analyzed in three age groups (0–30 years, 31–60 years, and older than 60 years) show that there is a progressive accumulation of lipids in Bruch's membrane with relation to age. Differences were found in the specific types of lipids in individual eyes. Five eyes stained for neutral lipids alone, four stained predominantly for phospholipids, and nine stained intensely for both neutral lipids and phospholipids. The deposits were associated with the progressive destruction of the native architecture of Bruch's membrane but no correlation was identified between specific inclusions in Bruch's membrane with a particular lipid. These results are significant to age-related macular disease (ARMD), and the lipid rich barrier in Bruch's membrane is implicated as a cause of photoreceptor dysfunction and pigment epithelial detachment.
The effect of continuous bright light on the retina of albino rats was studied. It was found that after several hours of exposure the electroretinogram (ERG) deteriorated. However, this phenomenon was found to be reversible. Evidence is presented to show that the deterioration and recovery of the ERG is related to tissue damage and regeneration. Support is given to the theory that the mediating factor in the light damage is chronic visual pigment bleaching.
• Objective.
—To investigate the relationship of sunlight exposure with age-related maculopathy. This was investigated in the population-based Beaver Dam Eye Study.
Design.
—In this cross-sectional population-based study, questionnaire data about sunlight exposure were obtained. Stereoscopic color fundus photographs were graded to determine the presence of age-related maculopathy.
Participants.
—People aged 43 through 84 years who resided in Beaver Dam, Wis, between 1987 and 1988 were examined between 1988 and 1990.
Results.
—Light exposure was not associated with early age-related maculopathy in women. In men, after adjusting for age, the amount of time spent outdoors in summer was associated with increased retinal pigment (odds ratio [OR], 1.44; 95% confidence interval [CI], 1.01 to 2.04). Wearing eyeglasses was inversely associated with increased retinal pigment (OR, 0.75; 95% CI, 0.58 to 0.97), and the use of hats and sunglasses was inversely associated with soft indistinct drusen (OR, 0.61; 95% CI, 0.38 to 0.98). The amount of leisure time spent outdoors in summer was significantly associated with exudative macular degeneration (OR, 2.26; 95% CI, 1.06 to 4.81) and late maculopathy (OR, 2.19; 95% CI, 1.12 to 4.25). There were no associations between estimated ambient UV-B exposure and age-related maculopathy.
Conclusions.
—These data suggest that exposure to sunlight may be associated with age-related maculopathy. However, longitudinal studies of these associations are needed.
Objective
To examine the association between ocular factors and the incidence and progression of age-related maculopathy.
Participants
A population of 3684 adults (43-86 years of age at baseline) living in Beaver Dam, Wis, studied at baseline and 5 years later.
Methods
Standardized protocols for refraction and determination of iris color, administration of a questionnaire, and slitlamp and retroillumination photographs of the lenses to determine cataract type and stereoscopic color fundus photographs to determine presence and severity of age-related maculopathy. Standard univariate and multivariate analyses were performed.
Main Outcome Measures
Incidence and progression of age-related maculopathy.
Results
After controlling for age, eyes that had undergone cataract surgery before baseline were more likely to have progression of age-related maculopathy (odds ratio, 2.71; 95% confidence interval [CI], 1.69-4.35) and to develop signs of late age-related maculopathy (odds ratio, 2.80; 95% CI, 1.03-7.63) than were eyes that were phakic at baseline. These relationships remained after controlling for other risk factors in multivariate analyses. There was no relationship of nuclear cataract, cortical cataract, or iris color to the incidence and progression of age-related maculopathy.
Conclusion
These findings indicate a relationship between cataract surgery and increased risk of progression of age-related maculopathy.
purpose. When the pyridinium bisretinoid A2E, an age-related fluorophore in the retinal pigment epithelium (RPE), is irradiated with blue light, photochemical events are initiated that can ultimately provoke cell death. This study was designed to determine whether DNA is a target of the cellular damage.
methods. ARPE-19 cells accumulated A2E before exposure to blue light. DNA damage was assayed in individual cells by alkaline gel electrophoresis (comet assay), with and without the addition of the repair enzymes formamidopyrimidine N-glycosylase (Fpg), endonuclease III (endo III) and T4-endonuclease V (T4-endo V) to characterize DNA lesions. Damage was quantified as comet tail moment. The base lesion 8-oxo-deoxyguanosine (8-oxo-dG) was detected by immunoperoxidase and histochemical methods. The singlet oxygen quencher, sodium azide, was tested for its ability to reduce DNA damage, and cell viability was quantified.
results. DNA damage was induced in A2E-containing RPE exposed to 430-nm illumination. The extent of damage, measured as tail moment, was proportional to exposure duration and was reduced by preincubation with sodium azide. The detection of FPG- and endo III–sensitive DNA lesions revealed the presence of oxidized purine and pyrimidine bases, whereas labeling with specific antibody and binding of fluorescein-labeled avidin indicated that guanine bases were oxidatively modified to 8-oxo-dG. The ability of the cells to repair the DNA damage declined as the severity was increased, and kinetic studies disclosed rapid and slow stages of repair.
conclusions. DNA is one of the cellular constitutents that can be damaged by the interaction of A2E and blue light. At least some of the DNA lesions are oxidative base modifications.
purpose. Drusen are variably sized extracellular deposits that form between the retinal pigmented epithelium (RPE) and Bruch’s membrane. They are commonly found in aged eyes, however, numerous and/or confluent drusen are a significant risk factor for age-related macular degeneration. The purpose of this study was to investigate the impact of drusen on overlying cells of the retina.
methods. Tissue containing retina and RPE/choroid was dissected from human donor eyes, embedded in agarose, and sectioned at 100 μm using a vibratome. Sections were immunostained with a panel of antibodies that labeled glial cells, first-, second-, and third-order retinal neurons and processed for confocal microscopy.
results. Retinal cells that overlie both soft and hard drusen exhibited numerous structural and molecular abnormalities. Normally detectable only in the outer segments of rod photoreceptors, rod opsin immunolabeling was also observed in the inner segment, cell body, axon, and axon terminal of photoreceptors that overlie drusen. Labeling with this antibody also revealed the deflection and shortening of rod inner and outer segments. Cone photoreceptors displayed similar structural abnormalities, as well as a decrease in cone opsin immunoreactivity. Drusen-associated abnormalities in the synaptic terminals of photoreceptor cells were also observed. In addition, an increase in intermediate filament protein immunoreactivity (vimentin and glial fibrillary acidic protein) was observed within Müller glial cells in areas of retina overlying drusen. Both soft and hard drusen were associated with a similar spectrum of effects in both macular and extramacular regions. Second- and third-order neurons, including bipolar, horizontal, amacrine, and ganglion cells all appeared unaffected. The structural and molecular abnormalities observed in photoreceptors and Müller glial cells were confined to retinal regions directly overlying and immediately adjacent to drusen; more distant retinal regions appeared unperturbed. Remarkably, significant abnormalities were observed over small subclinical drusen.
conclusions. Retinal cells overlying both soft and hard drusen exhibit structural and molecular abnormalities indicative of photoreceptor degeneration and Müller glial activation. These abnormalities resemble the degenerative effects common to many forms of retinal degeneration, but are confined to areas directly overlying drusen. This suggests that photoreceptor cell function is compromised as a consequence of drusen formation.
Background: Delineation of the morphologic aspects of age-related macular degeneration (ARMD) is helpful in correlation with the clinical features and may contribute to understanding the pathogenesis. Methods: All eyes on file in the Eye Pathology Laboratory, Wilmer Institute, with the known features of ARMD were analyzed according to age, sex, and race. Methods included routine sections in the macula, stepped-serial and serial sections, and electron microscopy and two-dimensional reconstruction in selected cases. Results: There were 760 eyes with ARMD from 450 patients. Only 5.3% of these patients were black. Nodular drusen were observed in 6.2% of eyes (n = 47), basal laminar deposits in 54.7%, basal linear deposits in 27.6%, neovascularization in 38.2%, and disciform scars in 40.8%. Three types of soft drusen were identified and were observed in 28.0%. The mean diameter of the disciform scar was 3.73 mm, and mean thickness was 0.27 mm. In disciform scars greater than 0.2 mm in thickness, only approximately 25% of the surface of the scar had some remaining photoreceptor cells. Serous or hemorrhagic detachments were observed in 10.4% of eyes. Retinal pigment epithelial (RPE) atrophy without disciform scars was observed in 24.6% of eyes. Areolar atrophy was the most common feature observed in eves of black patients. Conclusion: This comprehensive histopathologic evaluation provides the tabulation of the various morphologic features of ARMD. Basal laminar deposit and basal linear deposit, but not nodular drusen, are important positive associations with choroidal neovascularization, disciform scarring, and visual loss. Preservation of photoreceptor cells was seen only over disciform scars 0.2 mm thickness or less.
The retina represents a paradox, in that, while light and oxygen are essential for vision, these conditions also favour the formation of reactive oxygen species leading to photochemical damage to the retina. Such light damage seems to be multi-factorial and is dependent on the photoreactivity of a variety of chromophores (e.g., vitamin A metabolites, lipofuscin, melanin, flavins, porphyrins, carotenoids) endogenous to the retina. The aim of this article is to provide a detailed review of our current understanding of the photochemistry and photobiology of these chromophores and to consider how they may contribute to retinal ageing and pathology.
A number of studies have suggested that both genetic and environmental factors play a role in age-related macular degeneration (AMD). In this study, the authors evaluated five fibulin genes in a large series of patients with AMD. The fibulins are a recently identified family of six extracellular matrix proteins that have roles in the assembly and stabilization of supramolecular extracellular-matrix-complexes. The authors studied 402 unrelated patients with AMD and 429 control subjects from the same clinic population. DNA samples were screened for sequence variations in five members of the fibulin gene family. Amino acid-altering sequence variations were found in all five fibulin genes, many of which were observed only in patients with AMD. Seven of the 402 patients with AMD had amino acid-altering sequence variations in the fibulin 5 gene, whereas none were observed among 429 control subjects (P < .01). Additionally, these seven patients all had small, circular drusen, which are commonly referred to as basal laminar or cuticular drusen. In this study, missense mutations in the fibulin 5 gene were found in 1.7 percent of patients with AMD. Many variations in other fibulin genes were also found in these patients. The authors conclude that the evolutionary conservation of the affected residues suggests that several of these variations may also be involved in AMD.—Valerie Biousse
PurposeTo assess whether cataract surgery in older persons increases risk for the development of late-stage age-related maculopathy (ARM).
By its action on rhodopsin, light triggers the well-known visual transduction cascade, but can also induce cell damage and death through phototoxic mechanisms e a comprehensive understanding of which is still elusive despite more than 40 years of research. Herein, we integrate recent experimental findings to address several hypotheses of retinal light damage, premised in part on the close anatomical and metabolic relationships between the photoreceptors and the retinal pigment epithelium. We begin by reviewing the salient features of light damage, recently joined by evidence for retinal remodeling which has implications for the prognosis of recovery of function in retinal degenerations. We then consider select factors that influence the progression of the damage process and the extent of visual cell loss. Traditional, genetically modified, and emerging animal models are discussed, with particular emphasis on cone visual cells. Exogenous and endogenous retinal protective factors are explored, with implications for light damage mechanisms and some suggested avenues for future research. Synergies are known to exist between our long term light environment and photoreceptor cell death in retinal disease. Understanding the molecular mechanisms of light damage in a variety of animal models can provide valuable insights into the effects of light in clinical disorders and may form the basis of future therapies to prevent or delay visual cell loss.
A central measure of the qualtiy of a hypothesis is its ability to explain known observations. Although some elements of senescence and ischemia theories may be operative, the oxidative injury model as we propose above seems to explain injury model as we propose above seems to explain the observed aspects of CNV, and geographic atrophy, in ARMD. Each of the aspects of the proposed theory is biologically plausible and has been based on experimental data, some of which are related to the eye and some to other fields such as atherosclerosis and cancer research. There are still a number of questions that face all of those diseases in terms of prevention and treatment. Although aging, in part may be the result of an accumulation of genetic defects that do not necessarily inhibit reproduction, there is increasing evidence that much of the aging phenotype is also the result of oxidatives stress and the induced cellular adaptation responses. A principle risk factor for degenerative aspects of aging appears to be life itself. Aging is a problem that has challenged biologists and philosophers for centuries. Aging has deterministic and stochastic aspects, something that most ancient of philosophers knew. Clearly, there are numerous factors involved, and many of these are coded into our genetic structure. Certainly, genes are powerful navigators of our face, but the course can be modified by our interventions. ARMD affects the quality of life, particularly in aged people who may have other infirmities. We are closing in on a workable hypothesis for CNV in ARMD; it is easily conceivable that there will be a viable theory in the next few years. The next step is to identify points of attack on the process so that ARMD may be prevented or cured.
An abstract is unavailable. This article is available as HTML full text and PDF.
An abstract is unavailable. This article is available as HTML full text and PDF.
Purpose: Experimental and epidemiological studies suggest that low antioxidant intake may be associated with the occurrence of neovascular age-related macular degeneration (AMD).
Methods: We investigated this hypothesis further with a case-control study involving 72 case and 66 control patients attending the Ophthalmology Department of the University Hospital in Nijmegen. Data were collected by interview on antioxidant intake (i.e. in fruit and vegetables), cigarette smoking, sunlight exposure and familial predisposition. Antioxidant intake was calculated according to the method described in the Framingham Eye Study. Logistic regression analysis was used to estimate odds ratios (OR) and 95% confidence intervals (CI).
Results: The prevalence rate of AMD in patients with low antioxidant intake and low lutein intake (dichotomized at the median value) was about twice as high as that in patients with high intake: OR = 1.7, 95% CI (0.8–3.7), and OR = 2.4, 95% CI (1.1–5.1). Further specification of intake data into quartiles of antioxidant intake and lutein/zeaxanthine intake showed a clear dose–response relationship.
Conclusion: The effect of dietary antioxidants upon macular health warrants preventive studies.
Apoptosis is a genetically regulated form of cell death. Individual cells show condensed nuclear chromatin and cytoplasm, and biochemical analysis reveals fragmentation of the DNA. Ensuing cellular components, apoptotic bodies, are removed by macrophages or neighboring cells. Genes involved in the regulation of apoptosis as well as stimuli and signal transduction systems, are only beginning to be understood in the retina. Therefore, we developed a new in vivo model system for the investigation of events leading to apoptosis in the retina and the pigment epithelium. We induced apoptosis in retinal photoreceptors and the pigment epithelium of albino rats by exposure to 3000 lux of diffuse, cool white fluorescent light for short time periods of up to 120 minutes. Animals were killed at different time intervals during and after light exposure. The eyes were enucleated and the lower central retina was processed for light- and electron microscopy. DNA fragmentation was analysed in situ by TdT-mediated dUTP nick-end labeling (TUNEL) or by gel electrophoresis of total retinal DNA. We observed that the timing of apoptosis in the photoreceptors and pigment epithelium was remarkably different, the pigment epithelium showing a distinct delay of several hours before the onset of apoptosis. In photoreceptors, apoptosis was induced within 90 minutes of light exposure, with the morphological appearance of apoptosis preceding the fragmentation of DNA. In the pigment epithelium, the morphological appearance of apoptosis and DNA fragmentation were coincident. Different regulative mechanisms may lead to apoptotic cell death in the retinal photoreceptors and pigment epithelium. This in vivo model system will allow measurement of dose-responses, a potential spectral dependence and the molecular background of apoptotic mechanisms in the retina.
Experimental models and observational studies suggest that vitamin E supplementation may prevent cardiovascular disease and cancer. However, several trials of high-dosage vitamin E supplementation showed non-statistically significant increases in total mortality.
To perform a meta-analysis of the dose-response relationship between vitamin E supplementation and total mortality by using data from randomized, controlled trials.
135,967 participants in 19 clinical trials. Of these trials, 9 tested vitamin E alone and 10 tested vitamin E combined with other vitamins or minerals. The dosages of vitamin E ranged from 16.5 to 2000 IU/d (median, 400 IU/d).
PubMed search from 1966 through August 2004, complemented by a search of the Cochrane Clinical Trials Database and review of citations of published reviews and meta-analyses. No language restrictions were applied.
3 investigators independently abstracted study reports. The investigators of the original publications were contacted if required information was not available.
9 of 11 trials testing high-dosage vitamin E (> or =400 IU/d) showed increased risk (risk difference > 0) for all-cause mortality in comparisons of vitamin E versus control. The pooled all-cause mortality risk difference in high-dosage vitamin E trials was 39 per 10,000 persons (95% CI, 3 to 74 per 10,000 persons; P = 0.035). For low-dosage vitamin E trials, the risk difference was -16 per 10,000 persons (CI, -41 to 10 per 10,000 persons; P > 0.2). A dose-response analysis showed a statistically significant relationship between vitamin E dosage and all-cause mortality, with increased risk of dosages greater than 150 IU/d.
High-dosage (> or =400 IU/d) trials were often small and were performed in patients with chronic diseases. The generalizability of the findings to healthy adults is uncertain. Precise estimation of the threshold at which risk increases is difficult.
High-dosage (> or =400 IU/d) vitamin E supplements may increase all-cause mortality and should be avoided.
The photopathology of retinal lesions produced by extended exposure (1000 sec) to low corneal power levels (62 microW) of blue light (441 nm) was investigated by light microscopy in 20 rhesus eyes over an interval ranging from 1 hr to 90 days after exposure. Results indicate a nonthermal type of photochemical lesion originating in the retinal pigment epithelium and leading to a histological response with hypopigmentation which requires 48 hr to appear. This type of lesion helps to explain solar retinitis and eclipse blindness and has significance for aging and degenerative changes in the retina.
The photoreceptor synapses of albino rats show considerable pathologic changes following fluorescent light exposure. The changes in the synapses and in the lamellar membranes of the outer segments occur and progress simultaneously. Membranes proliferate in the paramitochondrial zone of the rod synaptic spherule and fine budding of the smooth endoplasmic reticulum occurs in the cone pedicle within one hour's exposure to the brightness of 500 foot candles. Proliferating paramitochondrial membranes have no cytochrome c oxidase activity and degenerate together with mitochondria by further exposure. The cone pedicles remain relatively intact in photically damaged retina.
Exposure to constant light causes extensive rod photoreceptor damage but spares the photopic system in albino rats. The rod branch of the dark-adaptation curve shows considerable elevation in threshold; the cone branch is hardly affected. Longer exposure and chromatic adaptation suggest that there are three cone mechanisms with peaks near wavelengths of 450,520, and 560 nanometers.
The histologic manifestations of rhodopsin-mediated versus short-wavelength classes of retinal phototoxicity were compared after spectral exposures of the albino rat retina. Animals were exposed to wave-bands of light centered at the peak of rhodopsin absorbance (green, 500 nm) or in the ultraviolet A (UVA; 360 nm). Intensity-damage curves generated for each wave-band indicated that UVA light was 50-80 times more effective than green light at causing photoreceptor cell losses. Examination of early ultrastructural changes in rod inner segments, outer segments, and retinal pigment epithelium revealed a remarkable degree of similarity between UVA and green light-induced damage. Furthermore, the two classes of damage were indistinguishable in terms of post-exposure recovery from threshold damage and regional distribution of photoreceptor cell loss along the vertical meridian. The finding of essentially identical histologic manifestations for the two classes of damage raises the possibility that they share a common biochemical etiology or pathway of cell destruction.
Using histochemical staining techniques and electron microscopy, the authors have examined the histochemical properties and ultrastructure of Bruch's membrane in 30 human eyes with an age range of 1 to 95 years. The results analyzed in three age groups (0-30 years, 31-60 years, and older than 60 years) show that there is a progressive accumulation of lipids in Bruch's membrane with relation to age. Differences were found in the specific types of lipids in individual eyes. Five eyes stained for neutral lipids alone, four stained predominantly for phospholipids, and nine stained intensely for both neutral lipids and phospholipids. The deposits were associated with the progressive destruction of the native architecture of Bruch's membrane but no correlation was identified between specific inclusions in Bruch's membrane with a particular lipid. These results are significant to age-related macular disease (ARMD), and the lipid rich barrier in Bruch's membrane is implicated as a cause of photoreceptor dysfunction and pigment epithelial detachment.
The impact of aging on cell loss in the human retina was examined in foveal and temporal equatorial regions in eyes from 35 donors with ages spanning a 78-yr period from the second to the ninth decade of life. Equatorial cones and retinal pigment epithelial cells (RPE) decreased at uniform rates from the second to the ninth decade, 16 and 14 cells/mm2/yr, respectively. Equatorial rods and cells in the ganglion cell layer (GCL) showed nonuniform rate decreases with age. The rates of rod and GCL cell loss were faster between the second and fourth decades (970 and 9 cells/mm2/yr, respectively) than between the fourth and ninth decades (570-330 and 6-3 cells/mm2/yr). The rod and GCL cell densities at the temporal equator maintained a constant ratio (rods-GCL cell ratio = 103 +/- 0.4, mean +/- standard deviation) and the same reduction slope ratio at different times during aging. Thus, the equatorial rod and GCL cell losses were correlated statistically. The ratio of equatorial photoreceptors to RPE cells showed no significant change with age, suggesting parallel loss of these closely apposed cells. At the foveal center, the variability of cone density between individuals in each decade grouping was large (1.7- to threefold). No significant differences were found in cone or RPE cell densities at the foveal center from the second to ninth decade, suggesting that the densities of foveal cones and RPE cells were stable throughout this period. Foveal RPE density was significantly higher than equatorial RPE density in each age group. No significant difference was found between the equatorial photoreceptor-RPE ratio and foveal cone-RPE ratio in any age group. Cells in the GCL in the fovea decreased by approximately 16% from the second to the sixth decade. These results indicated that (1) rod photoreceptors and cells in the GCL were more vulnerable to loss during aging than cones; (2) photoreceptors and RPE cells showed parallel changes during aging; and (3) the photoreceptor loss accompanying aging was less pronounced in the fovea than in the peripheral retina.
A computerized, television-based, imaging fundus reflectometer was used to obtain estimates of the spatial distribution of macular pigment (xanthophylls) from seven normal subjects. Digitized images of the bleached macula of each subject were acquired at illuminating wavelengths from 462 to 697 nm. An analysis of spectral reflectances indicated that differences in short-wavelength reflectance between the foveal center and parafovea were influenced by spatial variations in melanin and oxyhemoglobin absorption as well as by the distribution of macular pigment. To provide an estimate of the spatial distribution of macular pigment alone, we have corrected fundus images obtained at 462 nm for the effect of melanin and oxyhemoglobin absorption. The spatial variation in macular pigment double density across the horizontal and vertical meridians of the retina was well described by Gaussian functions. The peak double densities for the individual subjects ranged from 0.22 to 0.45 and the standard deviations of the Gaussian functions averaged approx. 1 degree.
The effects of moderate increments in the intraocular pressure on blood flow rates in the various tissues of the eye were studied in monkeys. Blood flow rates were determined with radioactively labelled microspheres, 15 μm in diam. One eye had its spontaneous intraocular pressure while the other eye had its pressure stabilized at a higher level. The mean values for the intraocular pressures in the two eyes were 13 and 41 cm H2O respectively. In eyes with spontaneous intraocular pressure mean blood flow through the retina, the iris, the ciliary body, and the choroid were 25, 17, 89, and 607 mg/min respectively. Blood flow through the ciliary processes was 222 and through the ciliary muscle 153 g/min/00 g tissue respectively. In eyes with increased intraocular pressure there were statistically significant reductions in blood flow through the choroid and through the prelaminar part of the optic nerve by 29 and 30% of the mean blood flow through control eyes respectively. The changes in blood flow through the retina, the iris, the ciliary processes and the ciliary muscle were not statistically significant. They ranged from a reduction by 8% to an increase by 19% in eyes with increased intraocular pressure. The results suggest that even moderate increments in intraocular pressure cause clear reductions in the blood flow through the choroid and through the prelaminar part of the optic nerve, while blood flow through the retina outside the optic disc and through the different parts of the anterior uvea is efficiently autoregulated. It is suggested that the susceptibility of the optic disc to increments in intraocular pressure is due to the deficient autoregulation of blood flow through the optic disc, which in turn might be explained by the choroidal origin of the optic disc vessels which interferes with normal autoregulatory mechanisms.
Exposure of adult, albino rats to fluorescent and incandescent illuminance causes photoreceptor degeneration, which is followed by active phagocytosis of the fragmented cells. Male and female rats from 3 wk of age to adulthood were exposed to a lighting schedule and an elevated environmental temperature known to induce receptor destruction in adult animals; control groups were exposed to cyclic lighting and room temperature. Retinas of 3 and 4 wk old experimental animals were apparently unaffected by light exposure. Outer and inner segments were fragmented and receptor nuclei were pyknotic in localized areas of the central retina of some 5 and most 6 wk old rats; areas of focal damage were more severe in 7 wk old rats. At 8 wk of age, the reduction in average thickness of the outer nuclear layer (ONL) first became statistically significant. Thereafter, photoreceptor destruction and reduction in OLN thickness became progressively more severe as the rats aged. Reduction in the overall thickness of the retina as a result of light exposure was not as impressive as the effect on the ONL. Photoreceptor damage apparently was not influenced by the animal's gender.
Selective loss of sensitivity to blue and green parts of the spectrum following intermittent, repeated exposures to intense spectral lights persists longer than 3 yr following blue lights and between 18 and 40 days following green lights. The “blue-blindness” involves complete and sole loss of the response of the short-wavelength responsive cones. The “green-blindness” involves complete and sole loss of response of middle-wavelength sensitive cones. Histo-pathology of cones in a “blue-blinded” retina in comparison with cytochemical labeling of short-wavelength cones, reveals that they follow a similar distribution: are sparse in the foveola. reach a peak of about 16% of the cones near 1 and fall to 8–12% of the cones at 7. Continuous as distinct from intermittent exposures to similar blue lights produces a wholly different picture of gross pigment-epithelial damage with little photoreceptor degeneration.