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Human visual system is exposed to high levels of natural and artificial lights of different spectra and intensities along lifetime. Light-emitting diodes (LEDs) are the basic lighting components in screens of PCs, phones and TV sets; hence it is so important to know the implications of LED radiations on the human visual system. The aim of this study was to investigate the effect of LEDs radiations on human retinal pigment epithelial cells (HRPEpiC). They were exposed to three light-darkness (12 h/12 h) cycles, using blue-468 nm, green-525 nm, red-616 nm and white light. Cellular viability of HRPEpiC was evaluated by labeling all nuclei with DAPI; Production of reactive oxygen species (ROS) was determined by H2DCFDA staining; mitochondrial membrane potential was quantified by TMRM staining; DNA damage was determined by H2AX histone activation, and apoptosis was evaluated by caspases-3,-7 activation. It is shown that LED radiations decrease 75-99% cellular viability, and increase 66-89% cellular apoptosis. They also increase ROS production and DNA damage. Fluorescence intensity of apoptosis was 3.7% in nonirradiated cells and 88.8%, 86.1%, 83.9% and 65.5% in cells exposed to white, blue, green or red light, respectively. This study indicates three light-darkness (12 h/12 h) cycles of exposure to LED lighting affect in vitro HRPEpiC.
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Photochemistry and Photobiology, 2013, 89: 468473
Effects of Light-emitting Diode Radiations on Human Retinal Pigment
Epithelial Cells In Vitro
Eva Chamorro*
1
, Cristina Bonnin-Arias
1
, María Jesús Pérez-Carrasco
2
, Javier Muñoz de Luna
3
,
Daniel Vázquez
3
and Celia Sánchez-Ramos
1,2
1
Neuro-Computing and Neuro-Robotics Research Group, Universidad Complutense de Madrid, Madrid, Spain
2
Optometry and Vision Department, Escuela Universitaria de Óptica, Madrid, Spain
3
Optics Department, Escuela Universitaria de Óptica, Madrid, Spain
Received 26 June 2012, accepted 30 August 2012, DOI: 10.1111/j.1751-1097.2012.01237.x
ABSTRACT
Human visual system is exposed to high levels of natural and
articial lights of different spectra and intensities along
lifetime. Light-emitting diodes (LEDs) are the basic lighting
components in screens of PCs, phones and TV sets; hence it
is so important to know the implications of LED radiations
on the human visual system. The aim of this study was to
investigate the effect of LEDs radiations on human retinal
pigment epithelial cells (HRPEpiC). They were exposed to
three lightdarkness (12 h/12 h) cycles, using blue-468 nm,
green-525 nm, red-616 nm and white light. Cellular viability
of HRPEpiC was evaluated by labeling all nuclei with DAPI;
Production of reactive oxygen species (ROS) was determined
by H2DCFDA staining; mitochondrial membrane potential
was quantied by TMRM staining; DNA damage was deter-
mined by H2AX histone activation, and apoptosis was evalu-
ated by caspases-3,-7 activation. It is shown that LED
radiations decrease 7599% cellular viability, and increase
6689% cellular apoptosis. They also increase ROS produc-
tion and DNA damage. Fluorescence intensity of apoptosis
was 3.7% in nonirradiated cells and 88.8%, 86.1%, 83.9%
and 65.5% in cells exposed to white, blue, green or red light,
respectively. This study indicates three lightdarkness (12 h/
12 h) cycles of exposure to LED lighting affect in vitro
HRPEpiC.
INTRODUCTION
Biologic chromophores of retinal pigment epithelium (RPE) cells
can absorb the electromagnetic visible light radiation (380780 nm).
But this luminous energy, necessary for the visual process, can cause
a toxic effect, especially the most energetic radiations of the visible
spectrum: the violet and blue (400500 nm) (1). Short wavelength
light can penetrate through tissues to the cells and their organelles,
inducing the generation of reactive oxygen species (ROS) in RPE
mitochondria and even apoptosis, potentially caused by ROS-dam-
aged mitochondrial DNA (2).
The human visual system is exposed to a limited number of
natural and articial lights of different spectra and intensities.
Light pollution is increasing exponentially, and energy-efcient
light sources as light-emitting diodes (LEDs) have been devel-
oped as an option to replace the traditional light bulbs. In the
coming years, incandescent light sources will be progressively
replaced by LEDs, and it is estimated that by 1 September 2016
there will be no incandescent lights in Europe (3).
White LEDs present specic spectral and energetic character-
istics compared with that of other domestic light sources, so the
potential risks of these new light sources need to be explored to
answer whether they could be eventually harmful for the eye (3).
The purpose of the work was to study the effects of LED
lighting on RPE cells. Outcome measures included cell viability,
oxidative stress, mitochondrial membrane potential, DNA
damage and apoptosis.
MATERIALS AND METHODS
Cell culture of human RPE. The human retinal pigment epithelial cell
line HRPEpiC (ScienceCell Research Laboratories), was grown in a low-
serum epithelial cell culture medium (ScienceCell Research Laboratories).
After the primary cultures became conuent, the cells were detached
from the culture dish with the use of the Trypsin/EDTA solution (Sigma-
Aldrich). Cells were plated in a 96-well, black clear Imaging Plate
(Becton, Dickinson and Company) with Poly-L-lysine (Sigma-Aldrich)
Coating (density =5000 cells/well). The cells were incubated in a
humidied atmosphere of 5% CO
2
and 95% air at 37°C, and the culture
medium was changed every 24 h, following each light phase.
Light exposure. Illumination was produced by a LED-based system.
The cells plated in the imaging plate were exposed to three lightdark-
ness (12 h/12 h) cycles, using blue light (468 nm), green light (525 nm),
red light (616 nm) or white light in well chambers (light intensity was
5mWcm
2
). Measures of phototoxicity were taken after the last
darkness phase of the total exposure cycle.
Although this value is not very frequent in daylife situations, it can be
found in several cases. Moreover, we chose this value to compare our
results with other studies about this subject (4,5). This value implies
34.150 lux for an incandescent light source or 33.446 lux for a D65
(skylight) light source. It is similar to the horizontal irradiance for a lying
person looking upwards in a clear sky day when the sun is around 37.5°
(6) or a person at 20 cm of a 100 W incandescent lamp (7).
The control group consisted of RPE cells kept in darkness. Figure 1
shows a schematic diagram of the LED lighting irradiation system, and
the spectral irradiance of LED lighting.
Cell viability. The cell nuclei were labeled by incubating the cells
with the nuclear stain 46-diamidine-2-phenylindole dihydrochloride,
DAPI (Sigma-Aldrich), for 1 h. The viable cells were counted under
a BD Pathway 855 uorescence microscope (Becton, Dickinson and
Company), and an analysis of the image data was performed using
Attovision software (Becton, Dickinson and Company) (Table 1).
Measurement of intracellular ROS production. Oxidative stress was
measured using the dye (5-(and-6)chloromethyl-2,7-dichlorodihydrouo-
*Corresponding author email: eva.chamorro@opt.ucm.es (Eva Chamorro)
© 2012 Wiley Periodicals, Inc.
Photochemistry and Photobiology © 2012 The American Society of Photobiology 0031-8655/13
468
rescein diactate acetyl ester H2DCFDA (Invitrogen, Germany) at a nal
concentration of 1:1000 for 30 min at 37°C in darkness. Excess dye was
removed by washing in PBS. Fluorescence intensity was measured in a
BD Pathway 855 Bioimager (Becton, Dickinson and Company) using an
excitation band pass lter at 492495 nm and an emission cutoff lter at
517527 nm.
Measurement of mitochondrial membrane potential (MMP). Mito-
chondrial damage was assessed by using the dye Tetramethylrhodamine,
methyl ester, TMRM (Invitrogen) at a nal concentration of 1:1000 for
30 min at 37°C in darkness. Excess dye was removed by washing in
PBS. Fluorescence intensity was measured in a BD Pathway 855 Bioim-
ager (Becton, Dickinson and Company) using an excitation band pass l-
ter at 549 nm and an emission cutoff lter at 572 nm.
Immunocytochemical detection of histone H2AX and activated cas-
pase-3 and -7. DNA damage and apoptosis were evaluated by immuno-
cytochemistry, evaluating the activation of histone H2AX and caspases-3
and -7. At given time periods, cells were washed with phosphate-buffered
saline, (PBS; Sigma-Aldrich) and xed with 4% paraformaldehyde
(Sigma-Aldrich) for 1 h. Cells were suspended in 0.3% Triton X-100-
PBS (Sigma-Aldrich) in a 3% bovine serum albumin (BSA; Sigma-
Aldrich) 1% (wt/vol) in PBS for 30 min to suppress. The cells were then
incubated in 2.5% PBS +BSA containing either a combination of 1:400
diluted antiphospho-histone H2AX (Abcam, UK) and 1:400 anticaspase-3
rabbit antibody (Cell Signaling Technology). The cells were then incu-
bated for 1 h and washed twice with PBS, and resuspended in 1:400
diluted goat antimouse Alexa Fluor 633 conjugated (Invitrogen) and
1:400 diluted goat antirabbit Alexa Fluor 488 (Invitrogen) for 30 min at
room temperature in darkness. After three washing steps, the uorescence
of the samples was measured in the Pathway 855 automated uorescence
microscope (Becton, Dickinson and Company) using an excitation band
pass lter at 632 nm and an emission cutoff lter at 647 nm for caspase-
3, -7 detection. For histone H2AX detection, an excitation band pass lter
at 488 nm and an emission cutoff lter at 594 nm were used.
Statistical analysis. Every experiment was repeated three times. The
values were given as mean ±SD. Data were analyzed using an unpaired
two-tailed t-test by Statgraphics version Centurion XVI.I. A Pvalue less
than 0.05 was considered statistically signicant.
RESULTS
Cell viability
Nonirradiated RPE cells grew properly, but the irradiation inhib-
ited the growth of RPE cells. The difference in the cell number
of RPE cells irradiated by blue, green or white LED lighting and
nonirradiated was statistically very signicant (P<0.01). Maxi-
mum damage was observed in cells exposed to blue LED light-
ing. In the experiments, 99%, 88% and 75% of the irradiated
cells became nonviable after their exposure to blue, green or
white light. Red light caused a slight decrease of number of RPE
cells. However, the difference in cell number of RPE cells irradi-
ated by red light and not irradiated was statistically insignicant
(Figs. 2A, 3A and 4A).
Measurement of intracellular ROS production
Low level production of reactive oxygen species was observed
in RPE cells maintained in darkness. However, a signicant
increase in the level of ROS was observed after three lightdark-
ness cycles (12 h/12 h) with blue light, green light or red light.
Nonincrease of cellular cytoplasm uorescence was detected in
cells exposed to white LED lighting in comparison with non
irradiated cells (Figs. 2B, 3B and 4B).
Measurement of mitochondrial membrane potential
After three lightdarkness cycles of irradiation, no signicant
effect on mitochondrial membrane potential was detectable
compared to control cells for any of the different LED lighting
(Figs. 2C, 3C and 4C).
Effects of light on DNA damage of RPE
Signicant DNA damage was observed for light-exposed RPE
cells. The uorescence microscopic data for all irradiated RPE
Figure 1. Schematic diagram of the LED lighting irradiation system and
spectral irradiance of the different LED lighting sources: blue, green, red
and white light.
Table 1. Cell viability, reactive oxygen species ROS production, mitochondrial membrane potential, DNA damage and apoptosis of cultured RPE irradi-
ated with blue, green, red and white LED lighting. Values indicate uorescence intensity, mean ±SD.
Control Blue light Green light Red light White Light
Viability (FU) 855 ±403 10 ±2* 99 ±114* 339 ±1 217 ±108*
ROS (FU) 593 ±78 737 ±19* 855 ±30* 1004 ±49* 656 ±26
MMP (FU) 634 ±19 620 ±39 823 ±30 780 ±128 770 ±18
DNA damage (FU) 131 ±41 2537 ±589* 2258 ±738* 1920 ±286* 2697 ±493*
Apoptosis (%) 3.7 ±0.02 86.1 ±0.03* 83.9 ±0.05* 65.5 ±0.07* 88.8 ±0.02*
*P<0.05 compared to the control.
Photochemistry and Photobiology, 2013, 89 469
cells show the increased degradation of nucleic acids in compari-
son with the control cells. Maximum damage was showed to
cells exposed to blue LED lighting (Figs. 2D, 3D and 4D).
Detection of apoptosis
The percentage of apoptotic cells was increased on light-exposed
RPE cells in comparison with RPE cells maintained in darkness.
The death of nonirradiated RPE cells reached a frequency of
3.7%. However, cell death was 86%, 84%, 66% and 89% for
blue, green, red and white-irradiated RPE, respectively (Figs. 2E,
3E and 4E).
DISCUSSION
Epidemiological studies suggest an association between visible
light exposure and increased risk of advanced age-related macu-
lar degeneration (AMD). Visible light can affect the retina and
RPE by photochemical, thermal and mechanical mechanism (8).
Photochemical damage occurs when the incident radiation has
a wavelength in the high energy portion of the visible spectrum.
An electron in an excited state can return to the inhibited state
dissipating the extra energy. One way to dissipate this energy is
to break a bond in another molecule through a direct exchange
of electron or direct exchange of hydrogen producing reactive
oxygen species (ROS) (2,4,9). A proposed mechanism of cell
damage induced by light is the oxidative process (10). The outer
layers of the retina are continuously exposed to high levels of
oxygen due to the abundant blood supply of the choriocapillaries
(1,3). The formation of ROS at the level of the RPE leads to cell
damage with the subsequent degeneration of photoreceptors (11).
Noell (1980) was the rst to observe that the action spectrum of
retinal damage induced by light was similar to the action spec-
trum of rhodopsin (scotopic sensitivity), thus suggesting that rho-
dopsin or its photoproducts were acting as mediators in the
retinal damage (8,12). Subsequent studies have supported this
mechanism (13,14).
Experimental evidence has demonstrated that the retina and
RPE are much more sensitive to blue light damage than red or
green light (9,15,16). Most research works have been focused
on evaluating the response of the retina to light from conven-
tional lighting sources as halogen or uorescent. It has been
speculated that LED lighting radiation may cause ocular damage
(3), however, the potential risks of these new light sources has
not been explored. In this study, we have demonstrated that
LED lighting can damage RPE cells. The results of this study
clearly show that LED lighting radiation decreases by 7599%
the cellular viability and increases by 6689% the cellular apop-
tosis, as well as there is an increase in the production of ROS
and DNA damage.
These results are consistent with previous reports that sug-
gest that visible light of conventional light sources could cause
Figure 2. Representative images of effects of LED lighting on human retinal pigment epithelial cells in vitro. HRPEpiC cells were exposed to blue,
green, red and white LED lighting (irradiated cells) or maintained in darkness (control) for three lightdarkness cycles (12 h/12 h). (A) Cellular viability
of HRPEpic cells determined by labeling all nuclei with DAPI. (B) ROS production determined by the H2DCFDA staining and uorescence micros-
copy; an increase of uorescence in cells indicates oxidative stress. (C) Mitochondrial membrane potential determined by the TMRM staining and uo-
rescence microscopy. Reduction or absence of uorescence indicates decrease of MMP. (D) DNA damage determined by the activation of H2AX
histone. (E) Apoptosis determined by the activation of caspases-3,-7. The white arrows indicate apoptotic cells.
470 Eva Chamorro et al.
Figure 3. Effects of monochromatic LED lighting on human retinal pig-
ment epithelial cells in vitro. HRPEpiC cells were exposed to blue, green
and red LED lighting (irradiated cells) or maintained in darkness (con-
trol) for three lightdarkness cycles (12 h/12 h). The graph displays
mean uorescence intensity radios of irradiated cells versus non irradiated
controls. Bars represent mean ±SD from n=35 experiments. The
asterisk (*) indicates signicant differences as compared to controls
(P<0.05, Studentst-test). (A) Cellular viability of HRPEpic cells deter-
mined by labeling all nuclei with DAPI. (B) ROS production determined
by the H2DCFDA staining and uorescence microscopy. (C) Mitochon-
drial membrane potential determined by the TMRM staining and uores-
cence microscopy. (D) DNA damage determined by the activation of
H2AX histone. (E) Apoptosis determined by the activation of caspases-3,
-7 is observed as a pink coloration around DAPI-stained cells.
Figure 4. Effects of white LED lighting on human retinal pigment epithe-
lial cells in vitro. HRPEpiC cells were exposed to white LED lighting (irra-
diated cells) or maintained in darkness (control) for three lightdarkness
cycles (12 h/12 h). The graph displays mean uorescence intensity radios
of irradiated cells versus non irradiated controls. Bars represent mean ±SD
from n=35 experiments. The asterisk (*) indicates signicant differences
as compared to controls (P<0.05, Studentst-test). (A) Cellular viability
of HRPEpic cells determined by labeling all nuclei with DAPI. (B) ROS
production determined by the H2DCFDA staining and uorescence micros-
copy. (C) Mitochondrial membrane potential determined by the TMRM
staining and uorescence microscopy. (D) DNA damage determined by the
activation of H2AX histone. (E) Apoptosis determined by the activation of
caspases-3, -7 is observed as a pink coloration around DAPI-stained cells.
Photochemistry and Photobiology, 2013, 89 471
cell damage. Sparrow et al. (5) analyzed human RPE cells irra-
diated with blue light (430 nm, 8 mW cm
2
), green light
(550 nm, 8 mW cm
2
) and white light (246 mW cm
2
). The
light was delivered from a tungsten halogen source for 20 min
and it was observed that illuminated RPE cells remained viable.
In another study, Godley et al. exposed conuent cultures of
human primary retinal epithelial cells to visible light (390
550 nm at 2.8 mW cm
2
) of a metal halide lamp for 09h
and analyzed cell viability and ROS production. Cells main-
tained in the absence of blue light exposure showed no
decrease in viability, no mitochondrial or nuclear DNA damage
and low level production of ROS; however, blue light-irradiated
cells showed an increasing loss of viability (ca 10%), time-
dependent increase in the levels of ROS and maximal mito-
chondrial DNA damage 3 h after exposure with evidence of
some repair mechanism (1).
On the other hand, Chu et al. studied changes on viability of
RPE as a result of blue and red halogen light irradiation. Early
passages of human RPE cells were exposed to blue light
(460 nm, 0.4 mW cm
2
) and red light (640 nm, 1 mW cm
2
)
for 48 h. Cell viability was not signicantly affected by blue-
light irradiation or red-light irradiation at low doses (17). Later
on, Youn et al. investigated light-induced retinal damage in
human RPE cells exposed to specic narrow wavebands of blue
light obtained using interference lters and an arc lamp system
(400 nm at an irradiance of 1.555 mW cm
2
, 420 nm at an irra-
diance of 1.466 mW cm
2
and 435.8 nm at an irradiance of
1.351 mW cm
2
) for 312 h. Cells exposed to 400 nm light
showed decrease in cell viability, degradation of mitochondria
and nucleic acids damage; however, no alterations were observed
for 420 and 435.8 nm light-exposed RPE cells (18).
Of relevance is the research carried out by Roehlecke et al. in
which they evaluated the in vitro response of RPE cells exposed
to blue LED lighting. Cells were irradiated with 405 nm light at
an output power of 0.3 or 1 mW cm
2
for 3, 24 or 72 h. The
data showed a signicantly stimulated ROS production and a
decrease of mitochondrial membrane potential after 24 h of
exposure to blue light, but no apoptosis or viability changes were
evidenced. They used low doses of light for up to 72 h without
a repair time, to establish an in vitro model system in which light
irradiation induced mild stress without causing cell death (2).
It has been suggested that cells may adapt themselves to the
light-induced stress and therefore survive (2) so in the present
study we have exposed cells to three lightdarkness cycles
(12 h/12 h) instead of continuous light.
It is relevant that ROS production was the highest in cells
irradiated with the red light, not correlating with DNA damage
or apoptosis where blue and green light produce more phototoxic
effects.
From this we can infer that ROS are not the only elements
responsible for cell damage and apoptosis. Other photosensitive
molecules have been studied, mitochondrial respiratory chain
enzymes (13,19,20), melanin (21) and products of intermediate
intermedia genes (10,11,14). However, our results regarding
ROS must be considered with caution since the presence of
photosensitizers such as riboavin in the culture medium can
inuence on light-dependent ROS generation (2224).
Summing up, three lightdarkness cycles (12 h/12 h) expo-
sure to LED lighting affect the growth of RPE cells, produce
cellular stress increasing ROS levels accompanying an increase
of DNA damage and apoptotic cells. Future investigation will
determine the intensities and wavelengths of LED lighting which
are lethal and nonlethal for ocular tissues, as well as the effect of
optical lters in RPE cell protection. This information will be
necessary to develop appropriate normative for this growing
industry eld.
AcknowledgementThis work has been supported in part by Fundación
Mapfre (Spain).
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Photochemistry and Photobiology, 2013, 89 473
... In contrast, white LED (411-777 nm) when applied at a dose of light of 5.17 J/cm 2 was able to improve the periocular wrinkles of female patients 40 . The oxidative stress activates multiple signaling pathways including mitogen-activated protein kinase cascades that are responsible to causes retinal pigment epithelium damage 55 . ...
... In general, it has been suggested that the cytotoxicity of LEDs is related to the increase of cell apoptosis, production of reactive oxygen species (ROS), lipid peroxidation and DNA damage 3,55 . Mitochondria have also been identified as a target for the toxicity of LED illumination 15,23,56,57 , which could be related to the induction of apoptosis. ...
... Concerning the DNA damage, it is important to note that DNA damage would be expected as a consequence of mitochondrial impairment and ROS production caused by LED irradiation independently of the wavelength used 25 . However, reports on genotoxicity are scarce and sometimes contradictory 25,55,67 . Considering that these radiations may promote DNA modifications, they can become potentially mutagenic and cause malignancy in human cells, so, this aspect should be explored in the future. ...
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The pandemic and lockdown caused by COVID-19 accelerated digitalization. Personal digital devices, emitting high-energy light, namely in the blue wavelength, have raised concerns about possible harmful effects on users’ eyes. Scientific research history has shown a relationship between exposure to blue light and changes in ocular structures. The main goal of this review is to examine frequent and prolonged exposure to blue radiation from computers, tablets and smartphones and its consequences on vision and ocular structures. Bibliographic research was carried out on changes induced by blue light in ocular structures, the cornea, the crystalline lens and the retina based on the following scientific databases: BioOne Complete™; Google Scholar™; Paperity™; PubMed™; and ScienceOpen™. The most significant studies on blue light and ocular damage were selected and reviewed. The most relevant bibliographic data were analyzed and summarized and some gaps in the theme of blue light from digital devices were identified. The experimental need to acquire additional new data is suggested. The hypothesis that continued use of digital devices enriched with blue light may interfere with the biological tissues of the cornea, crystalline lens, or retina is not clarified in the available scientific evidence. Therefore, additional studies are needed to answer this problem.
... Several studies have explored the cellular and molecular mechanisms of blue-light toxicity by modeling the aging retina with RPE cells loaded with A2E, a derivative of the visual pigment that accumulates in this epithelium with age [23,24,[34][35][36]. While these studies demonstrated the toxicity of blue light, we refined the most harmful range as extending from 400 to 455 nm, with peak toxicity between 415 and 455 nm, applying 10 nm narrow-band light exposure [18,21]. ...
... Filtering out blue light has already been reported to provide retinal protection both clinically, using blue-light-filtering IOL [35,[40][41][42][43], and in vitro, using broadband blue-lightfiltering lenses or IOL [34,36,[44][45][46]. However, broadband filters have major limitations for permanent wear due to alterations in color vision and non-visual retinal functions (peak at 480 nm). ...
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Blue light accelerates retinal aging. Previous studies have indicated that wavelengths between 400 and 455 nm are most harmful to aging retinal pigment epithelia (RPE). This study explored whether filtering these wavelengths can protect cells exposed to broad sunlight. Primary porcine RPE cells loaded with 20 µM A2E were exposed to emulated sunlight filtered through eye media at 1.8 mW/cm2 for 18 h. Filters selectively filtering out light over 400–455 nm and a dark-yellow filter were interposed. Cell damage was measured by apoptosis, hydrogen peroxide (H2O2) production, and mitochondrial membrane potential (MMP). Sunlight exposure increased apoptosis by 2.7-fold and H2O2 by 4.8-fold, and halved MMP compared to darkness. Eye Protect SystemTM (EPS) technology, filtering out 25% of wavelengths over 400–455 nm, reduced apoptosis by 44% and H2O2 by 29%. The Multilayer Optical Film (MOF), at 80% of light filtered, reduced apoptosis by 91% and H2O2 by 69%, and increased MMP by 73%, overpassing the dark-yellow filter. Photoprotection increased almost linearly with blue-violet light filtering (400–455 nm) but not with total blue filtering (400–500 nm). Selective filters filtering out 25% (EPS) to 80% (MOF) of blue-violet light offer substantial protection without affecting perception or non-visual functions, making them promising for preventing light-induced retinal damage with aesthetic acceptance for permanent wear.
... With rapid urbanization and the ubiquitous adoption of digital devices (e.g., computers, smartphones), the widespread application of screen-based activities has raised particular concerns about the undesirable impact of excessive digital display use on ocular health (5)(6)(7). Overexposure to blue light predisposes the photoreceptors and retinal pigment epithelium (RPE) cells to cumulative photochemical damage by oxidative stress, inflammatory responses, and mitochondrial apoptosis (8,9). Although the blue light emitted from electronic devices is well below safe viewing limits and it is not intense enough to induce acute damage in the retina (10), the long-term exposure to the low-illuminance artificial light may have chronic, cumulative effects on eye health. ...
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... The widespread and rapid replacement of most lamps and luminaires by products incorporating LEDs started around 2010 and provided an incentive for most research teams to use LEDs to investigate the mechanisms of light-induced retinal damage in biological experiments, both in vivo (see for instance Shang et al., 2017) and in vitro (see for instance Chamorro et al., 2013). Such studies used narrow band LEDs (coloured LEDs) instead of filtered lamps or lasers that were commonly used before the advent of LEDs. ...
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... Además, el ojo humano está equipado con mecanismos naturales de protección, como el cristalino y el pigmento macular, que filtran parte de la luz azul antes de que alcance los fotorreceptores de la retina. A pesar de esto, se ha cuestionado si la luz azul emitida por las pantallas podría afectar negativamente la salud visual y se ha sugerido que se debería "ayudar" al ojo en la tarea de filtrar la luz azul mediante filtros especiales en gafas o sobre los propios dispositivos (Chamorro et al., 2013). No obstante, es importante señalar que los experimentos que resucitaron esta hipótesis presentaban errores metodológicos significativos, lo que compromete la validez científica de utilizar filtros para este propósito. ...
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A medida que la tecnología redefine la educación a través de las Tecnologías de la Información y Comunicación (TIC), el aumento en el uso de pantallas digitales genera inquietudes sobre sus posibles efectos sobre la salud visual. Al analizar la evidencia científica, este trabajo desmonta mitos y aclara conceptos erróneos. No se trata del objeto observado en sí, sino factores conductuales como la distancia, la iluminación y las pausas, además del tiempo al aire libre, los responsables de los problemas visuales. Las pantallas como herramientas educativas no presentan mayores riesgos que los materiales impresos cuando se usan adecuadamente. En este panorama tecnológico en constante evolución, es crucial fomentar la alfabetización digital y el uso equilibrado de las TIC, empoderando a estudiantes y educadores para aprovechar al máximo los beneficios que estas herramientas modernas pueden ofrecer.
... Retina is much more sensitive to short wavelengths such as blue light [7]. Potential injuries from light exposure depend on several factors. ...
... The biological effects of light radiation belonging to the visible spectrum were studied especially on retinal cells for both blue and red light [10][11][12][13]. Red light has neuroprotective effects that have been demonstrated in several models of retinal disease [14]. ...
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... In some cases, the procedure may also result in the patient having to remain in the hospital for a longer period of time, experiencing heat, having loose stools, becoming dehydrated, and perhaps causing damage to the retina. There is a decrease in cellular viability and an increase in cellular apoptosis that occurs in vitro when human retinal pigment epithelial cells (HRPEpiC) are subjected to three light-darkness cycles (12 h/12 h) of radiation [10]. ...
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To evaluate the in vitro response of retinal pigment epithelial (RPE) cells to a nonlethal dose of blue light. The human RPE cell line ARPE-19 was irradiated with blue light (405 nm) at an output power of 1 mW/cm(2) or 0.3 mW/cm(2). The following parameters were studied: metabolic activity; apoptosis; reactive oxygen species (ROS) production; mitochondrial membrane potential (MMP); ultrastructural changes of mitochondria; production of advanced glycation endproducts (AGEs); and stress-related cellular proteins. Nonlethal doses of blue light irradiation significantly reduced ARPE-19 metabolic activity and MMP while increasing intracellular ROS levels and expression of stress-related proteins heme oxygenase-1 (HO-1), osteopontin, heat shock protein 27 (Hsp-27), manganese superoxide dismutase (SOD-Mn), and cathepsin D. Blue light irradiation also induced ultrastructural conformation changes in mitochondria, resulting in the appearance of giant mitochondria after 72 h. We further found enhanced formation of AGEs, particularly N(epsilon)-(carboxymethyl) lysine (CML) modifications, and a delay in the cell cycle. ARPE-19 cells avoid cell death and recover from blue light irradiation by activating a host of defense mechanisms while simultaneously triggering cellular stress responses that may be involved in RPE disease development. Continuous light exposure can therefore detrimentally affect metabolically stressed RPE cells. This may have implications for pathogenesis of age-related macular degeneration.
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A GROWING body of literature attests to the deleterious effects of long term exposure to light1-8. To define more critically the differences between thermal and photochemical effects, we have exposed the retinae of rhesus monkeys to eight monochromatic laser lines from 1,064-441.6 nm. Thermal damage to the retina is to be expected for the 1,064-nm line since the photopigments are not involved and energy absorption takes place predominantly in the melanin granules of the pigment epithelium and the choroid. Although data on pathogenesis are not yet available, we found some interesting differences in retinal sensitivity in going from the near infrared to the blue wavelengths in the visible spectrum.
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The present study demonstrates narrowband short-wavelengths radiation- (400, 420, and 435.8 nm) induced cellular damage of cultured human retinal pigment epithelial cells using in vitro biological assays to determine wavelengths that are responsible for photochemical lesions of the retina. This work involved the exposure of retinal pigment epithelial (RPE) cells (ARPE-19) to narrowband light of three different wavelengths (400, 420, and 435.8 nm) using a xenon arc lamp and interference filters. Cellular viability, mitochondrial distribution, and nucleic acid (both DNA and RNA) damage were quantified after various energy levels of exposure, using the Alamar blue assay, and confocal laser scanning microscopy with two fluorescent stains (Rhodamine 123 and Acridine Orange). The results clearly show that 400 nm light radiation can cause significant dose-dependent decreases in RPE cell viability as well as degradations of DNA/RNA and mitochondria in RPE cells, while 420 and 435.8 nm light radiation cause no cellular damage. While further evaluations may be needed to assess specificity and confounding factors of these assessment tools, the results may be a matter for consideration in future IOL design efforts.
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