ArticlePDF AvailableLiterature Review

The Photobiology of Lutein and Zeaxanthin in the Eye


Abstract and Figures

Lutein and zeaxanthin are antioxidants found in the human retina and macula. Recent clinical trials have determined that age- and diet-related loss of lutein and zeaxanthin enhances phototoxic damage to the human eye and that supplementation of these carotenoids has a protective effect against photoinduced damage to the lens and the retina. Two of the major mechanisms of protection offered by lutein and zeaxanthin against age-related blue light damage are the quenching of singlet oxygen and other reactive oxygen species and the absorption of blue light. Determining the specific reactive intermediate(s) produced by a particular phototoxic ocular chromophore not only defines the mechanism of toxicity but can also later be used as a tool to prevent damage.
This content is subject to copyright. Terms and conditions apply.
Review Article
The Photobiology of Lutein and Zeaxanthin in the Eye
Joan E. Roberts and Jessica Dennison
Department of Natural Sciences, Fordham University, New York City, NY 10023, USA
Correspondence should be addressed to Joan E. Roberts;
Received  August ; Accepted  November 
Copyright ©  J. E. Roberts and J. Dennison. is isan open access article distributed under the CreativeCommons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium,provided the original work is properly cited.
Lutein and zeaxanthin are antioxidants found in the human retina and macula. Recent clinical trials have determined that age-
and diet-related loss of lutein and zeaxanthin enhances phototoxic damage to the human eye and that supplementation of these
carotenoids has a protective eect against photoinduced damage to the lens and the retina. Two of the major mechanisms of
protection oered by lutein and zeaxanthin against age-related blue light damage are the quenching of singlet oxygen and other
reactive oxygen species and the absorption of blue light. Determining the specic reactive intermediate(s) produced by a particular
phototoxic ocular chromophore not only denes the mechanism of toxicity but can also later be used as a tool to prevent damage.
1. Introduction
Lutein and zeaxanthin are antioxidants that accumulate in
the lens and retina of the human eye [–]. ese antioxi-
dants protect ocular tissues against singlet oxygen and lipid
peroxide damage []. Unfortunately, beginning with middle
age, antioxidant protection is depleted and this leads to the
formation of age-related cataracts and macular degeneration
Increasing the intake of fruits and vegetables high in
lutein and zeaxanthin [–] has been found to retard age-
related cataracts and macular degeneration []. In addition,
supplementation with lutein and zeaxanthin has been very
eective at restoring these important ocular antioxidants [,
]. e level and distribution of these carotenoids can be
directly and noninvasively measured in the human eye [–
]. Increasing these carotenoids has been found not only to
lower the risk for irreversible blindness [, –] but also to
potentially improve cognitive function in the elderly [–].
Determining the specic reactive intermediate(s) pro-
duced by a particular phototoxic ocular chromophore not
only denes the mechanism of toxicity but can also later be
used as a tool to prevent damage. For instance, lutein and
zeaxanthin prevent singlet oxygen damage [], whereas N-
acetyl cysteine has been shown to be particularly eective
in quenching UV phototoxic damage and inammation [,
]. In this review, we describe the underlying photobiolog-
ical mechanisms involved in the induction of light-induced
damage to the eye and the appropriate and inappropriate
antioxidants to protect against such damage.
2. Ambient Radiation Ocular Damage
e primary factors that determine whether ambient radia-
tion will injure the human eye are the wavelengths emitted
from sunlight or a specic lamp [] and received by ocular
tissues; the intensity of the light; and the age of the recipient.
2.1. Wavelength Emitted from Source. Radiation from the
sun emits varying amounts of UV-C (– nm), UV-B
(– nm), UV-A (– nm), and visible light (–
 nm) []. Most of the UV-C and some short wavelengths
sources emit diering wavelengths of light depending on
their spectral distribution []. UV radiation contains wave-
lengths shorter than visible light; the shorter the wavelength,
the greater the energy and the greater the potential for biolog-
ical damage. However, although the longer wavelengths are
less energetic, they penetrate the eye more deeply [].
2.2. Wavelength Transmission of Light through the Human
Eye. In order for a photochemical reaction to occur in the
eye, the light must be absorbed in a particular ocular tissue.
e primate/human eye has unique ltering characteristics
that determine in which area of the eye each wavelength of
Hindawi Publishing Corporation
Journal of Ophthalmology
Volume 2015, Article ID 687173, 8 pages
Journal of Ophthalmology
Visi bl e
Cornea Lens
400 nm
F : Wavelength transmission of the adult human eye.
light will be absorbed []. All UV radiation of wavelengths
shorter than  nm is ltered by the human cornea. is
means that the shortest, most energetic wavelengths of light
the human lens. Most UV light is absorbed by the adult lens,
but the exact wavelength absorbed depends upon age []
as shown in Figure . e very young human lens transmits
UV radiation to the retina, while the elderly lens lters
out much of the short blue visible light (– nm) []
before it reaches the retina. In adults, the lens absorbs UV-
B and all the UV-A (– nm); therefore only visible
light (> nm) reaches the retina. Transmission also diers
with species; the lenses of mammals other than primates
transmit ultraviolet light longer than  nm to the retina
[]. Aphakia (removal of the lens) and implanted Intraocular
Lenses (IOLs) aer cataract surgery will also change the
wavelength characteristics of light reaching the retina [–
2.3. Intensity and Mechanism. Ocular damage from light
can occur through either an inammatory response or a
photooxidation reaction. Acute exposure to intense radiation,
for example, exposure to sunlight reected from snow (snow
blindness), or from staring at the sun during an eclipse []
or directly staring at an articial light source that emits UV-
sunburn. is induces an inammatory response in the eye.
e initial insult to the tissue provokes a cascade of events that
eventually results in wider damage to the cornea, lens, and/or
retina [, , ].
Chronic exposure to less intense radiation damages the
eye through a photooxidation reaction. In photooxidation
reactions, a chromophore in the eye absorbs light and
produces reactive oxygen species such as singlet oxygen
Figure . e chromophore may be endogenous (natural) or
exogenous (drug, herbal medication, or nanoparticle that has
accumulated in the eye) []. If an ocular pigment is excited
quickly (in picoseconds) goes back to the ground state, it will
safely dissipate the energy received [].
Tri p l et
Ocular chromophore
ground state
F : Photooxidation.
3. Age and Endogenous Singlet
Oxygen Chromophores
As the eye ages, chromophores which were once protective of
to produce singlet oxygen is measured as a quantum yield.
Quantum yield measures the amount of an excited state
produced by an amount of light energy used. e higher the
number is, the more ecient the chromophore is at making a
specic reactive oxygen species. For instance, a chromophore
strong oxidant, while a chromophore with a Quantum Yield
for Singlet Oxygen of . produces negligible amounts of
singlet oxygen.
3.1. Lens. e primary function of the human lens is to focus
light undistorted onto the retina. Although the transmission
properties of most of the components of the eye are stable, the
transmission properties of the lens change throughout life.
e lens is clear for the rst  years of life and then gradually
develops yellow chromophores (-hydroxy kynurenine and
its glucoside). ese are endogenous protective agents which
absorb UV radiation and safely dissipate its energy [].
As long as these chromophores are present, neither UV-
A nor UV-B radiation reaches the retina, and in this way, the
adult human retina is protected against normal levels of UV
radiation []. However, children are at particular risk for UV
damage to the retina because UV is directly transmitted to
their retinas [].
Aer middle age the protective chromophores -
hydroxykynurenine and its glucoside are enzymatically
converted into the phototoxic chromophores xanthurenic
acid and xanthurenic glucoside [, ]. ese xanthurenic
derivatives absorb UV radiation, form triplet states, and
produce singlet oxygen [, ] with a quantum yield of ..
ese endogenous singlet oxygen photosensitizers cross-link
lens protein [] and induce apoptosis in lens epithelial
cells []. ere is also an increase in N-formylkynurenine
[, ] in the lens; it is also an endogenous singlet oxygen
photosensitizer. ese quantum yields are seen in Table .
All of these phototoxic tryptophan derivatives are respon-
sible for UV-A-induced damage to certain target genes [].
With aging there is also a decrease in the production of
antioxidants and antioxidant enzymes in the lens, which
would normally quench these reactive oxygen species and
Journal of Ophthalmology
T : Quantum yields for singlet oxygen for lenticular chro-
Xanthurenic NFK
Singlet oxygen . .
-OH Kyn Kynurenine
Singlet oxygen None .
prevent damage to the lens. As a result of the increase
in phototoxic chromophores concomitant with the loss of
antioxidant protection, both the lens epithelial cells and lens
proteins are injured, which results in the eventual clouding of
the lens, commonly known as a cataract [].
Phototoxic reactions, whether they are caused by endoge-
nous or exogenous singlet oxygen photosensitizers, can cause
a modication of certain amino acids (histidine, tryptophan,
and cysteine) [] and/or a covalent attachment of a sensitizer
to cytosol lens proteins. In either case, the physical properties
of the protein are changed, leading to aggregation and nally
opacication (cataractogenesis). e covalently bound chro-
mophore may now act as an endogenous sensitizer of singlet
oxygen, producing prolonged sensitivity to light. Since there
is little turnover of lens proteins this damage is cumulative.
Any modication in the clarity of the lens impairs both vision
and circadian function [] and has a dramatic eect on
retinal function.
3.2. Retina. eyoungretinaisatparticularriskfordamage
from UV exposure because the young lens has not as
yet synthesized the yellow chromophores that prevent UV
transmission to the retina [, ]; UV damage to the eye is
cumulative and may increase the possibility of developing eye
disorders (macular degeneration) later in life [].
In addition to UV damage, short-wavelength blue visible
light ( nm) damages the retinas of those over  years of
age through a photooxidation reaction with an accumulated
chromophore, lipofuscin [, –].
Lipofuscin is a heterogeneous material composed of a
mixture of lipids, proteins, and various uorescent com-
pounds. It is mainly derived from the chemically modi-
ed residues of incompletely digested photoreceptor outer
segments []. Photoreceptor cells (rods and cones) shed
their outer segments (disc shedding) daily to be nally
phagocytosed (digested) by RPE cells. is RPE phagocytosis
[, ] releases lipofuscin. With age, the rates of lipofuscin
formation and disposal become unbalanced [, ], resulting
in lipofuscin accumulation in the RPE [, ].
In response to short blue visible light ( nm), lipo-
fuscin eciently produces singlet oxygen and lipid peroxy
radicals; there is also some production of superoxide and
hydroxyl radicals [–]. Lipofuscin is autouorescent, and
in previous studies [] it was hypothesized that the main
phototoxic component of lipofuscin was AE [N-retinylidene-
duced by the condensation of phosphatidylethanolamine
with two moles of all-trans-RAL [trans-retinal]. However,
current studies have proven that, rather than being a pho-
tooxidative agent, AE forms the basis of a natural protective
T : Quantum yields for singlet oxygen for retinal chro-
Lipofuscin trans-Retinal AE
Singlet oxygen . . .
mechanism that removes the strong singlet oxygen photo-
sensitizer all-trans- RAL [] and keeps it from damaging
the RPE cells by forming the very weak singlet oxygen
lipofuscin [Φ= .] is relatively high, the quantum eciency
for the generation of singlet oxygen by AE is very low (Φ
= .) [, ]. Table  gives the quantum yields of these
retinal chromophores.
Further in vivo mouse studies [] and human studies
using matrix-assisted laser desorption ionization imaging
mass spectrometry (MALDI IMS) and FT-ICR tandem mass
spectrometry conrm that although AE accumulation in the
retina may be hazardous, the damage done is not through
a photooxidative mechanism [–]. Another mechanism
for AE toxicity to the retina may be the inhibition of
phagolysosomal degradation of photoreceptor phospholipids
[], which would increase the production of lipofuscin
[, ], a blue light singlet oxygen photosensitizer [, ],
survival is dependent on healthy RPE, these primary vision
cells will eventually die, resulting in a loss of (central) vision
(macular degeneration) and other retinopathies. Another
potential toxic mechanism of AE that does not involve light
is the activation of microglial phagocytosis of photoreceptor
cells [, ].
4. Prevention of Damage by
Lutein and Zeaxanthin
Lutein and zeaxanthin are ocular antioxidants of dietary
origin []. ese carotenoids are found in the human lens,
[], retinal pigment epithelium/choroid (RPE/choroid), the
macula, the iris, and the ciliary body []. Recent clinical trials
have determined that age- and diet-related loss of lutein and
zeaxanthin enhances phototoxic damage to the human eye,
while supplementation of these carotenoids has a protective
eect against photoinduced damage to the lens and the
retina. e use of improper carotenoids as an antioxidant (𝛽-
in the AREDS  clinical trial is not only ineective because it
does not pass blood ocular barriers but may be hazardous to
human health [, ].
4.1. Structure of Carotenoids in relation to eir Function
and Location in the Eye. Lutein and zeaxanthin have a -
carbon basal structure, which include a system of conjugated
double bonds (alternating double and single bonds) as shown
in Figure . Chemical structures with extensive conjugated
bonds absorb light in the visible range; lutein and zeaxanthin
absorb blue visible light (– nm).
Carotenoids that are substituted with hydroxyl (-OH)
functional groups are known as xanthophylls. Lutein and
Journal of Ophthalmology
Macular xanthophylls
F : Structures of lutein, zeaxanthin, B-carotene, and lycopene.
zeaxanthin are xanthophylls, and their hydroxyl functional
groups permit both lutein and zeaxanthin and their structural
isomers to cross both blood-ocular and blood-brain barriers.
Other carotenoids (𝛽-carotene and lycopene) contain only
carbon and hydrogen atoms and do not cross the blood-brain
or ocular barriers [].
4.2. Photochemical Mechanism of Protection. Ocular expo-
sure to sunlight, UV, and short blue light-emitting lamps
directed at the human eye can lead to the induction of
cataracts and retinal degeneration. is process is particularly
hazardous aer the age of  because there is a decrease
in naturally protective antioxidant systems and an increase
in UV and visible light-absorbing endogenous phototoxic
chromophores that eciently produce singlet oxygen and
damage is through a photooxidation reaction. In photooxi-
dation reactions, phototoxic chromophores in the eye absorb
light, are excited to a singlet and then a triplet state, and
species which in turn damage the ocular tissues [, ].
e phototoxic reactions damage can be prevented by the
appropriate antioxidant quenchers as shown in Figure .
Lutein and zeaxanthin are naturally accumulating ocular
antioxidants that eciently quench both singlet oxygen and
lipid peroxy radicals []. Zeaxanthin, with  conjugated
double bonds, has a higher ability to quench singlet oxygen
than lutein ( conjugated double bonds) as shown in Figure 
e synergistic action of several ocular antioxidants not
only mimics the natural antioxidant protection of the eye
(xanthophylls, vitamin E, vitamin C, and glutathione) but also
has been found to be most eective. e highly successful
synergistic action of zeaxanthin and vitamin E or vitamin
C indicates the importance of the antioxidant interaction
in ecient protection of cell membranes against oxidative
Ocular chromophore
ground state
Lutein and
F : Photochemical mechanism of protection.
Chemical structures of the three
macular carotenoids
F : e structures of xanthophyll isomers.
damage induced by photosensitized reactions []. Increased
levels of both lutein and zeaxanthin were found to reduce
age-related nuclear cataracts [, ]. Clinical trials with
a combination of lutein, zeaxanthin, and its isomer meso-
zeaxanthin were found to be more protective of the retina
than lutein or zeaxanthin alone [, ]. is is not surprising
as the order of eciency of quenching singlet oxygen is
lutein <zeaxanthin <meso-zeaxanthin <all three combined
[, ]. e structures of these xanthophylls are shown in
Figure .
4.3. Photochemical Mechanism of Prooxidation and Damage
by Antioxidants. Bothluteinandzeaxanthinareveryeec-
tive quenchers of singlet molecular oxygen (1O2) and lipid
peroxy radicals. However, in the process, these carotenoids
are oxidized to their corresponding radical cations. ese
cations must be reduced to regenerate the original carotenoid,
allowing their reuse as an antioxidant. Vitamin E (𝛼-
tocopherol) is an antioxidant that can reduce oxidized
carotenoids, but in turn, this leaves the tocopherol oxidized
[]. However, the oxidized vitamin E can be reduced and
regenerated by vitamin C (ascorbic acid). Vitamin C can then
be further reduced by copper and zinc [, ]. Without this
appropriate combination of oxidizing and reducing agents,
antioxidants become prooxidants and can potentially damage
clinical trial [, ].
Summary. It is essential to determine the specic reactive
intermediate(s) produced by a particular endogenous or
Journal of Ophthalmology
exogenous photosensitizing agent in each compartment of
the eye. is information not only denes the mechanism
of toxicity but can also later be used as a tool to prevent
damage. For instance, singlet oxygen that forms with the
photooxidation of lipofuscin in the aged retina may be
quenched by dietary or supplemental lutein and zeaxanthin,
thereby preventing damage to the human retina. Using the
proper sunglasses to block wavelengths that excite endoge-
nous and exogenous ocular photosensitizers has been shown
to limit the singlet oxygen damage to the eye. In the future,
gene therapy for retinal dystrophies will be initiated. Ocular
imaging techniques using confocal imaging or with adaptive
optics are now available. ese techniques will allow for
direct verication of the physical and metabolic state of
the human eye and accurate and digitalized monitoring
of any therapeutic benet of all new treatments against
blindness including antioxidant supplements such as lutein
and zeaxanthin.
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
e authors thank Drs. Joost vant Erve and Ann Motten of
NIEHS, North Carolina, for help in editing this paper and
[] H. H. Billsten, P. Bhosale, A. Yemelyanov, P. S. Bernstein,
and T. Pol´
ıvka, “Photophysical properties of xanthophylls in
carotenoproteins from human retinas,” Photochemistry and
[] P. S. Bernstein, F. Khachik, L. S. Carvalho, G. J. Muir, D.-
Y. Zhao, and N. B. Katz, “Identication and quantitation of
carotenoids and their metabolites in the tissues of the human
eye,Experimental Eye Research, vol. , no. , pp. –, .
[] F.Khachik,P.S.Bernstein,andD.L.Garland,“Identication
of lutein and zeaxanthin oxidation products in human and
monkey retinas,Investigative Ophthalmology & Visual Science,
vol. , no. , pp. –, .
[] K. J. Yeum, A. Taylor, G. Tang, and R. M. Russell, “Measurement
of carotenoids, retinoids, and tocopherols in human lenses,
Investigative Ophthalmology & Visual Science,vol.,no.,pp.
–, .
[] R. Edge, D. J. McGarvey, and T. G. Truscott, “e carotenoids
as anti-oxidants—a review,Journal of Photochemistry and
Photobiology B: Biology, vol. , no. , pp. –, .
[] J.M.Nolan,J.Stack,O.O’Donovan,E.Loane,andS.Beatty,
“Risk factors for age-related maculopathy are associated with a
relative lack of macular pigment,Experimental Eye Research,
[] J. M. Humphries and F. Khachik, “Distribution of lutein,
zeaxanthin, and related geometrical isomers in fruit, vegetables,
wheat, and pasta products,Journal of Agricultural and Food
“Separation, identication, and quantication of carotenoids
in fruits, vegetables and human plasma by high performance
liquid chromatography,Pure and Applied Chemistry,vol.,
no. , pp. –, .
[] J. M. Seddon, U. A. Ajani, R. D. Sperduto et al., “Dietary
carotenoids, vitamins A, C, and E, and advanced age-related
macular degeneration. Eye Disease Case-Control Study Group,
–, .
[] O.Sommerburg,J.E.E.Keunen,A.C.Bird,andF.J.G.M.
van Kuijk, “Fruits and vegetables that are sources for lutein
and zeaxanthin: the macular pigment in human eyes,British
Journal of Ophthalmology, vol. , no. , pp. –, .
[] J. A. Mares-Perlman, A. I. Fisher, R. Klein et al., “Lutein and
zeaxanthin in the diet and serum and their relation to age-
related maculopathy in the ird National Health andNutrition
Examination Survey,American Journal of Epidemiology,vol.
, no. , pp. –, .
[] S. Beatty, U. Chakravarthy, J. M. Nolan et al., “Secondary
outcomes in a clinical trial of carotenoids with coantioxidants
versus placebo in early age-related macular degeneration,
[] R. A. Bone, J. T. Landrum, L. H. Guerra, and C. A. Ruiz,
“Lutein and zeaxanthin dietary supplements raise macular
pigment density and serum concentrations of these carotenoids
in humans,Journal of Nutrition,vol.,no.,pp.,
[] J. L. Dennison, J. Stack,S. B eatty, and J. M. Nolan, “Concordance
of macular pigment measurements obtained using customized
heterochromatic icker photometry, dual-wavelength autouo-
rescence, and single-wavelength reectance,Experimental Eye
Research, vol. , pp. –, .
[] P.S.Bernstein,D.-Y.Zhao,M.Sharifzadeh,I.V.Ermakov,and
W. Gellermann, “Resonance Raman measurement of macular
carotenoids in the living human eye,Archives of Biochemistry
and Biophysics,vol.,no.,pp.,.
[] P. S. Bernstein, D.-Y. Zhao, S. W. Wintch, I. V. Ermakov, R. W.
McClane, and W. Gellermann, “Resonance Raman measure-
ment of macular carotenoids in normal subjects and in age-
related macular degeneration patients,Ophthalmology,vol.,
[] S.Sabour-Pickett,J.M.Nolan,J.Loughman,andS.Beatty, “A
the macular carotenoids for age-related macular degeneration,
Molecular Nutrition and Food Research,vol.,no.,pp.
, .
[] J. A. Mares-Perlman, A. E. Millen, T. L. Ficek, and S. E.
Hankinson, “e body of evidence to support a protective
role for lutein and zeaxanthin in delaying chronic disease.
Overview,Journal of Nutrition,vol.,no.,pp.SS,
[] E.Y.Chew,T.E.Clemons,J.P.SanGiovannietal.,“Secondary
analyses of the eects of lutein/zeaxanthin on age-related mac-
ular degeneration progression: AREDS report no. ,JAMA
zeaxanthin for the treatment of age-related cataract: AREDS
randomized trial report no. ,JAMA Ophthalmology,vol.,
Journal of Ophthalmology
[] E. J. Johnson, “A possible role for lutein and zeaxanthin in
cognitive function in the elderly,e American Journal of
Clinical Nutrition, vol. , no. , pp. S–S, .
[] J. M. Nolan, E. Loskutova, A. N. Howard et al., “Macular
pigment, visual function, and Macular disease among subjects
with Alzheimer’s disease: an exploratory study,Journal of
Alzheimer’s Disease,vol.,no.,pp.,.
[] J. Feeney,C. Finucane, G. M. Sav va et al.,“Low macular pigment
optical density is associated with lower cognitive performance
in a large, population-based sample of older adults,Neurobiol-
ogy of Aging,vol.,no.,pp.,.
[] E. M. Busch, T. G. M. F. Gorgels, J. E. Roberts, and D. van
Norren, “e eects of two stereoisomers of N-acetylcysteine
on photochemical damage by UVA and blue light in rat retina,
Photochemistry and Photobiology,vol.,no.,pp.,
[] J. E. Roberts, “Update on the positive eects of light in humans,
Photochemistry and Photobiology,vol.,no.,pp.,
[] J. E. Roberts, “Ultraviolet radiation as a risk factor for cataract
and macular degeneration,” Eye and Contact Lens,vol.,no.,
[] J. E. Roberts, “Screening for ocular phototoxicity,International
Journal of Toxicology,vol.,no.,pp.,.
[] M.Norval,A.P.Cullen,F.R.deGruijletal.,“eeectson
actions with climate change,Photochemical & Photobiological
[] L.Fenton,J.Ferguson,andH.Moseley,“Analysisofenergysav-
ing lamps for use by photosensitive individuals,Photochemical
and Photobiological Sciences, vol. , no. , pp. –, .
[] J. E. Roberts, “Ocular photoxicity,Journal of Photochemistry
and Photobiology B: Biology,vol.,no.-,pp.,.
[] R. A. Weale, “Age and the transmittance of the human crys-
talline lens,e Journal of Physiology,vol.,pp.,
[] A. Bachem, “Ophthalmic ultraviolet action spectra,American
Journal of Ophthalmology,vol.,no.,pp.,.
[] F. M. Barker, G. C. Brainard, and P. Dayhawbarker, “Trans-
mittance of the human lens as a function of age,Investigative
Ophthalmology & Visual Science,vol.,no.,p.,.
[] I. Alexander, F. M. Cuthbertson, G. Ratnarajan et al., “Impact of
cataract surgery on sleep in patients receiving either ultraviolet-
blocking or blue-ltering intraocular lens implants,Investiga-
tive Ophthalmology and Visual Science,vol.,no.,pp.
, .
[] C. Schmoll, A. Khan, P. Aspinall et al., “New light for old eyes:
comparing melanopsin-mediated non-visual benets of blue-
light and UV-blocking intraocular lenses,British Journal of
Ophthalmology, vol. , no. , pp. –, .
[] P. L. Turner and M. A. Mainster, “Circadian photoreception:
ageing and the eye’s important role in systemic health,British
Journal of Ophthalmology,vol.,no.,pp.,.
[] D. H. Sliney, “Exposure geometry and spectral environment
determine photobiological eects on the human eye,Photo-
chemistry and Photobiology,vol.,no.,pp.,.
[] R. S. Klein, V. P. Werth, J. C. Dowdy, and R. M. Sayre,
Analysis of compact uorescent lights for use by patients with
photosensitive conditions,Photochemistry and Photobiology,
vol. , no. , pp. –, .
[] D. H. Sliney, “Optical radiation safety of medical light sources,
Physics in Medicine and Biology, vol. , no. , pp. –, .
[] M. T. Magone and S. M. Whitcup, “Mechanisms of intraocular
inammation,Chemical Immunology,vol.,pp.,.
[] J. W. Streilein, “Ocular immune privilege: the eye takes a dim
but practical view of immunity and inammation,Journal of
Leukocyte Biology,vol.,no.,pp.,.
[] J. Dillon and S. J. Atherton, “Time resolved spectroscopic stud-
ies on the intact human lens,Photochemistry and photobiology,
[] J. Dillon, “e photophysics and photobiology of the eye,
Journal of Photochemistry and Photobiology B: Biology,vol.,
no. -, pp. –, .
[] J. E. Roberts, E. L. Finley, S. A. Patat, and K. L. Schey,
“Photooxidation of lens proteins with xanthurenic acid: a
putative chromophore for cataractogenesis,Photochemistry
and Photobiology, vol. , no. , pp. –, .
[] G. iagarajan, E. Shirao, K. Ando, A. Inoue, and D. Bala-
subramanian, “Role of xanthurenic acid -O-𝛽-D-glucoside, a
novel uorophore that accumulates in the brunescent human
eye lens,Photochemistry and Photobiology,vol.,no.,pp.
–, .
[] J. E. Roberts, J. F. Wishart, L. Martinez, and C. F. Chignell,
“Photochemical studies on xanthurenic acid,Photochemistry
and Photobiology,vol.,no.,pp.,.
[] D. Balasubramanian, “Photodynamics of cataract: an update on
endogenous chromophores and antioxidants,Photochemistry
and Photobiology, vol. , no. , pp. –, .
[] M. Ehrensha, B. Zhao, U. P. Andley, R. P. Mason, and J.
E. Roberts, “Immunological detection of N-formylkynurenine
in porphyrin-mediated photooxided lens 𝛼-crystallin,Photo-
chemistry and Photobiology, vol. , no. , pp. –, .
[] C. M. Krishna, S. Uppuluri, P. Riesz, J. S. Zigler Jr., and D.
Balasubramanian, “A study of the photodynamic eciencies of
some eye lens constituents,” Photochemistry and Photobiology,
[] U. P. Andley, Z. Song, E. F. Wawrousek, and S. Bassnett, “e
molecular chaperone 𝛼A-crystallin enhances lens epithelial cell
growth and resistance to UVA stress,e Journal of Biological
[] J. E. Roberts, “e photodynamic eect of chlorpromazine,
promazine, and hematoporphyrin on lens protein,Investigative
Ophthalmology & Visual Science,vol.,no.,pp.,
[] J. E. Roberts, Photobiology of the Lens in Photobiology
Photobiological Sciences, ,
[] W. K. Noell, “Possible mechanisms of photoreceptor damage by
light in mammalian eyes,Vi sion Rese arch,vol.,no.,pp.
–, .
[] H. R. Taylor, S. West, B. Munoz, F. S. Rosenthal, S. B. Bressler,
and N. M. Bressler, “e long-term eects of visible light on the
eye,Archives of Ophthalmology,vol.,no.,pp.,.
[] A. R. Wielgus, R. J. Collier, E. Martin et al., “Blue light induced
AE oxidation in rat eyes—experimental animal model of dry
AMD,Photochemical & Photobiological Sciences, vol. , no. ,
[] A. R. Wielgus, C. F. Chignell, P. Ceger, and J. E. Roberts,
“Comparison of AE cytotoxicity and phototoxicity with all-
trans-retinal in human retinal pigment epithelial cells,Photo-
chemistry and Photobiology,vol.,no.,pp.,.
Journal of Ophthalmology
[] B. M. Kevany and K. Palczewski, “Phagocytosis of retinal rod
and cone photoreceptors,Physiology,vol.,no.,pp.,
[] R. W. Young, “e renewal of photoreceptor cell outer seg-
[] D. H. Anderson, S. K. Fisher, and R. H. Steinberg, “Mammalian
cones: disc shedding, phagocytosis, and renewal,Investigative
Ophthalmology and Visual Science,vol.,no.,pp.,
[] M. L. Katz, “Incomplete proteolysis may contribute to lipof uscin
accumulation in the retinal pigment epithelium,Advances in
Experimental Medicine and Biology,vol.,pp.,.
[] M. L. Katz, L. M. Rice, and C.-L. Gao, “Reversible accumulation
of lipofuscin-like inclusions in the retinal pigment epithelium,
Investigative Ophthalmology & Visual Science,vol.,no.,pp.
–, .
[] C.K.Dorey,G.Wu,D.Ebenstein,A.Garsd,andJ.J.Weiter,“Cell
loss in the aging retina. Relationship to lipofuscin accumulation
and macular degeneration,” Investigative Ophthalmology &
Visual Sc ience,vol.,no.,pp.,.
[] M. Boulton, F. Docchio, P. Dayhaw-Barker, R. Ramponi, and R.
Cubeddu, “Age-related changes in the morphology, absorption
and uorescence of melanosomes and lipofuscin granules of the
retinal pigment epithelium,Vision R es earch,vol.,no.,pp.
–, .
of lipofuscin in human retinal pigment epithelial cells,Free
Radical Biology & Medicine,vol.,no.,pp.,.
[] K.Reszka,G.E.Eldred,R.H.Wang,C.Chignell,andJ.Dillon,
“e photochemistry of human retinal lipofuscin as studied by
EPR,Photochemistry and photobiology,vol.,no.,pp.
, .
[] M. R´
ozanowska, J. Jarvis-Evans, W. Korytowski, M. E. Boulton,
J. M. Burke, and T. Sarna, “Blue light-induced reactivity of
retinal age pigment: in vitro generation of oxygen-reactive
–, .
[] M. R´
ozanowska, J. Wessels, M. Boulton et al., “Blue light-
induced singlet oxygen generation by retinal lipofuscin in non-
polar media,Free Radical Biology & Medicine,vol.,no.-,
pp. –, .
[] J. R. Sparrow, C. A. Parish, M. Hashimoto, and K. Nakanishi,
AE, a lipofuscin uorophore, in human retinal pigmented
epithelial cells in culture,Investigative Ophthalmology and
Visual Sc ience, vol. , no. , pp. –, .
[] A. Maeda, T. Maeda, M. Golczak et al., “Involvement of all-
trans-retinal in acute light-induced retinopathy of mice,e
[] A. Broniec, A. Pawlak, T. Sarna et al., “Spectroscopic properties
andreactivityoffreeradicalformsofAE,Free Radical Biology
&Medicine, vol. , no. , pp. –, .
[] A. R. Wielgus and J. E. Roberts, “Retinal photodamage by
endogenous and xenobiotic agents,Photochemistry and Photo-
[] J. E. Roberts, B. M. Kukielczak, D.-N. Hu et al., “e role of AE
in prevention or enhancement of light damage in human retinal
pigment epithelial cells,Photochemistry and Photobiology,vol.
Ablonczy, “Spatial localization of AE in the retinal pigment
epithelium,Investigative Ophthalmology and Visual Science,
vol. , no. , pp. –, .
[] Z.Ablonczy,D.B.Gutierrez,A.C.Grey,K.L.Schey,andR.K.
Crouch, “Molecule-specic imaging and quantitation of AE in
the RPE,Advances in Experimental Medicine and Biology,vol.
, pp. –, .
[] Z. Ablonczy, D. Higbee, D. M. Anderson et al., “Lack of
correlation between the spatial distribution of AE and lipo-
fuscin uorescence in the human retinal pigment epithelium,
Investigative Ophthalmology & Visual Science,vol.,no.,pp.
–, .
[] S. C. Finnemann, L. W. Leung, and E. Rodriguez-Boulan, “e
lipofuscin component AE selectively inhibits phagolysoso-
mal degradation of photoreceptor phospholipid by the retinal
pigment epithelium,Proceedings of the National Academy of
Sciences of the United States of America,vol.,no.,pp.
, .
[] L. Feeney-Burns and G. E. Eldred, “e fate of the phagosome:
conversion to ‘age pigment’ and impact in human retinal pig-
ment epithelium,Transactions of the Ophthalmological Societies
of the United Kingdom,vol.,part,pp.,.
[] L.Zhao,M.K.Zabel,X.Wangetal.,“Microglialphagocytosis
of living photoreceptors contributes to inherited retinal degen-
eration,EMBO Molecular Medicine,vol.,no.,pp.,
AE accumulation inuences retinal microglial activation and
complement regulation,Neurobiolog y of Aging,vol.,no.,
[] A.Perry,H.Rasmussen,andE.J.Johnson,“Xanthophyll(lutein,
zeaxanthin) content in fruits, vegetables and corn and egg
products,” Journal of Food Composition and Analysis,vol.,no.
, pp. –, .
[] K.-J. Yeum, F. Shang, W. Schalch, R. M. Russell, and A.
Taylor, “Fat-soluble nutrient concentrations in dierent layers
of human cataractous lens, Current Eye Research,vol.,no.,
pp. –, .
[] Age-Related Eye Disease Study Research Group, “A random-
ized, placebo-controlled, clinical trial of high-dose supplemen-
tation with vitamins C and E, beta carotene, and zinc for age-
related macular degeneration and vision loss: AREDS report no.
,Archives of Ophthalmology (Chicago, Ill),vol.,no.,pp.
–, .
[] R. Straight and J. D. Spikes, “Photosensitized oxidation of
biomolecules,” in Singlet Oxygen,A.A.Frimer,Ed.,pp.,
[] J. Widomska and W. K. Subczynski, “Why has nature chosen
lutein and zeaxanthin to protect the retina?” Journal of Clinical
& Experimental Ophthalmology, vol. , article , .
detecting singlet oxygen production,Nature,vol.,no.,
[] F. B¨
ohm, R. Edge, and T. G. Truscott, “Interactions of dietary
carotenoids with singlet oxygen (O) and free radicals: poten-
tial eects for human health,Acta Biochimica Polonica,vol.,
no. , pp. –, .
[] P. F. Conn, W. Schalch, and T. G. Truscott, “e singlet oxygen
and carotenoid interaction,Journal of Photochemistry and
Photobiology B: Biology,vol.,no.,pp.,.
Journal of Ophthalmology
[] M. Wrona, M. R´
ozanowska, and T. Sarna, “Zeaxanthin in
combination with ascorbicacid or 𝛼-to copherol protects ARPE-
 cells against photosensitized peroxidation of lipids,Free
Radical Biology & Medicine,vol.,no.,pp.,.
zeaxanthin and the risk of age-related nuclear cataract among
the elderly Finnish population,British Journal of Nutrition,vol.
, no. , pp. –, .
[] C.-J. Chiu and A. Taylor, “Nutritional antioxidants and age-
related cataract and maculopathy,Experimental Eye Research,
vol. , no. , pp. –, .
[] K. O. Akuo, J. M. Nolan, A. N. Howard et al., “Sustained sup-
plementation and mon itored response with dieri ng carotenoid
formulations in early age-related macular degeneration,Eye,
[] B. Li, F. Ahmed, and P. S. Bernstein, “Studies on the singlet
oxygen scavenging mechanism of human macular pigment,
Archives of Biochemistry and Biophysics,vol.,no.,pp.
, .
[] T. G. Truscott, “Synergistic eects of antioxidant vitamins,
Bibliotheca Nutritio et Dieta, no. , pp. –, .
[] e Age-Related Eye Disease Study  (AREDS) Research
Group, “Lutein + zeaxanthin and 𝜔- fatty acids for age-related
macular degeneration,e Journal of the American Medical
[] H.Sies,W.Stahl,andA.R.Sundquist,“Antioxidantfunctions
of vitamins. Vitamins E and C, beta-carotene, and other
carotenoids,Annals of the New York Academy of Sciences,vol.
, pp. –, .
[] S. Y. Cohen, “Vitamins for prevention of age related macular
degeneration: ecacy and risk,Bulletin de la Soci´
... ROS and other reactive species can be formed by ocular photosensitizers in the human eye, such as the by-products of retinal or, possibly, trans-retinal itself [11,75]. Such by-product accumulation also increases with age [11]. ...
... ROS and other reactive species can be formed by ocular photosensitizers in the human eye, such as the by-products of retinal or, possibly, trans-retinal itself [11,75]. Such byproduct accumulation also increases with age [11]. ...
... It is noteworthy that a mix of zeaxanthin, meso-zeaxanthin, and lutein was more effective in protecting the retina than either lutein or zeaxanthin alone. This outcome is consistent with a descending singlet-oxygen quenching efficiency in the order of all three combined > meso-zeaxanthin > zeaxanthin > lutein (summarized in [75]). Leaf carotenoids can quench singlet oxygen either by the transfer of excitation energy and subsequent loss of this energy as heat or by a chemical mechanism involving oxidation of the carotenoid [16,17]. ...
Full-text available
A synthesis is provided of the roles of the carotenoids zeaxanthin and/or lutein in opposing (i) photodamage in plants, (ii) photodamage to the human eye as well as cognitive dysfunction and a host of human diseases and disorders, and (iii) damage to extremophile microorganisms in the most inhospitable environments on earth. Selected examples are used to examine microenvironments and basic biological structures with which these xanthophylls associate as well as the effect of the organisms’ external environment. An overview is presented of the multiple principal mechanisms through which these xanthophylls can directly or indirectly impact organisms’ internal redox (oxidant/antioxidant) balance that provides input into the orchestration of growth, development, and defense in prokaryotic microorganisms, plants, and humans. Gaps in the research are identified, specifically with respect to the need for further in vivo assessment of the mechanisms.
... Carotenoids are a family of terpenoid pigments rich in fruits and vegetables and are related to several potential health benefits because of their antioxidant and anti-inflammatory properties [1][2][3][4][5]. Lutein is one of the main carotenoids that can selectively accumulate in the eye, macula and retina in particular, and is known for eye protection effects, especially against photoinduced damage [6][7][8]. This is mainly because lutein is capable of quenching singlet oxygen and other reactive oxygen species and absorbing blue light [6]. ...
... Lutein is one of the main carotenoids that can selectively accumulate in the eye, macula and retina in particular, and is known for eye protection effects, especially against photoinduced damage [6][7][8]. This is mainly because lutein is capable of quenching singlet oxygen and other reactive oxygen species and absorbing blue light [6]. Abundant epidemiological evidence has suggested that lutein intake is positively correlated with a lower risk of age-related macular degeneration and cataracts [9][10][11]. ...
... All simulated saliva fluid (SSF), simulated gastric fluid (SGF) and simulated intestinal fluid (SIF) solutions were prepared according to the INFOGEST method. Specifically, SSF was comprised of 15.1 mmol/L potassium chloride (KCL), 3.7 mmol/L potassium dihydrogen phosphate (KH 2 PO 4 ), 13.6 mmol/L sodium bicarbonate (NaHCO 3 ), 0.15 mmol/L magnesium chloride hexahydrate (MgCl 2 (H 2 O) 6 ) and 0.06 mmol/L ammonium carbonate ((NH 4 ) 2 CO 3 ); SGF was comprised of 6.9 mmol/L KCL, 0.9 mmol/L KH 2 PO 4 , 25 mmol/L NaHCO 3 , 47.2 mmol/L NaCl, 0.1 mmol/L MgCl 2 (H 2 O) 6 and 0.5 mmol/L (NH 4 ) 2 CO 3 ; SIF was comprised of 6.8 mmol/L KCL, 0.8 mmol/L KH 2 PO 4 , 85 mmol/L NaHCO 3 , 38.4 mmol/L NaCl and 0.33 mmol/L MgCl 2 (H 2 O) 6 . To start, 5 g of cut noodle samples were mixed with 3.5 mL SSF, 0.5 mL salivary a-amylase (1500 U/mL) solution, 25 uL CaCl 2 (0.3 M) and 975 uL deionized water, and were incubated in the water bath at 37 • C, 85 rpm for 2 min. ...
Full-text available
Inadequate intake of lutein is relevant to a higher risk of age-related eye diseases. However, lutein has been barely incorporated into foods efficiently because it is prone to degradation and is poorly bioaccessible in the gastrointestinal tract. Microfluidics, a novel food processing technology that can control fluid flows at the microscale, can enable the efficient encapsulation of bioactive compounds by fabricating suitable delivery structures. Hence, the present study aimed to evaluate the stability and the bioaccessibility of lutein that is encapsulated in a new noodle-like product made via microfluidic technology. Two types of oils (safflower oil (SO) and olive oil (OL)) were selected as a delivery vehicle for lutein, and two customized microfluidic devices (co-flow and combination-flow) were used. Lutein encapsulation was created by the following: (i) co-flow + SO, (ii) co-flow + OL, (iii) combination-flow + SO, and (iv) combination-flow + OL. The initial encapsulation of lutein in the noodle-like product was achieved at 86.0 ± 2.7%. Although lutein’s stability experienced a decreasing trend, the retention of lutein was maintained above 60% for up to seven days of storage. The two types of device did not result in a difference in lutein bioaccessibility (co-flow: 3.1 ± 0.5%; combination-flow: 3.6 ± 0.6%) and SO and OL also showed no difference in lutein bioaccessibility (SO: 3.4 ± 0.8%; OL: 3.3 ± 0.4%). These results suggest that the types of oil and device do not affect the lutein bioaccessibility. Findings from this study may provide scientific insights into emulsion-based delivery systems that employ microfluidics for the encapsulation of bioactive compounds into foods.
... Noteworthy, lutein has been described as protective for both macula and the entire retina, most probably due to its ability to work as a "scavenger" in preventing the formation of free radicals (reactive oxygen species) [15]. Furthermore, the lutein's property to absorb light at 446 nm (blue region) might appear of great utility also during EDM manipulation, as the blue light was found to trigger reactive oxygen species generation at least in retinal tissue (mainly by photoreceptors) [23]. ...
Full-text available
Purpose The study aims to evaluate the usefulness of lutein/trypan blue vital dye for the staining of corneal tissues and endothelium–Descemet membrane (EDM) for Descemet membrane endothelial keratoplasty (DMEK). Methods Sixteen human corneal tissues (Eye Bank, Rome, Italy) were used. Corneal endothelium was tested at 25 s (T0), 1 min (T1), 2 min (T2), and 4 min (T4) from dye addition. Staining intensity and cell counting were compared. Stripped EDM was analyzed for selected apoptotic (AP, caspases, BCL2, BAX) and differentiation (VEGF-A, TGF-β1RI, SMAD3/7, SMA) targets and changes in target expression. Protein extracts were analyzed through SDS-PAGE/IB. Results Although trypan blue staining produced the same color intensity of lutein/trypan blue dye in half the time, lutein/trypan blue reached a good and adequate color intensity at T4, which persisted even on excised and washed EDM grafts. Lutein/trypan blue-stained EDM showed a reduced number of blue-stained cells and AP immunoreactivity was significantly reduced in the same samples. An increased BCL2 transcript and a reduced BAX transcript were detected in lutein/trypan blue-stained EDM. No significant changes were observed for the main effector caspases (3/9) upon both treatments and the target genes representative of endothelial cell trans-differentiation (TGF-β1RI, SMAD3/7, SMA). A trend in vascular endothelial growth factor (VEGF-A) regulation was observed in lutein/trypan blue-treated EDM grafts. Conclusion Obtained results suggest that lutein/trypan blue dye deserves attention in the DMEK field and support the potential routine use of this dye as a valid alternative to trypan blue for all procedures devoted to the assessment of endothelial cell viability and visualization of EDM graft before DMEK grafting.
... One of the important classes of nutritionally beneficial components is carotenoids [64]. About more than 90% of the carotenoids produced by rice comprise lutein and zeaxanthin. ...
Full-text available
This review investigates black rice's photochemistry, functional properties, food applications, and health prospects. There are different varieties of black rice available in the World. The origins of this product can be traced back to Asian countries. This rice is also known as prohibited rice, emperor's rice, and royal's rice. Black rice is composed of different nutrients including fiber, protein, carbohydrates, potassium, and vitamin B complex. It contains an antioxidant called anthocyanin as well as tocopherols. Antioxidants are found mostly in foods that are black or dark purple. Due to its nutritious density, high fiber level, and high antioxidant content, black rice is a good alternative to white and brown rice. Utilizing black rice in various foods can enhance the nutritional value of food and be transformed into functional food items. Many non-communicable diseases (NCDs) can be prevented by eating black rice daily, including cancer cells, atherosclerosis, hypertension, diabetes, osteoporosis, asthma, digestive health, and stroke risk. This review aim is to discuss the role of nutritional and functional properties of black rice in the formation of functional food against different non-communicable diseases.
... Compared with longer wavelengths of visible light, short blue wavelengths are higher in energy and generate reactive oxygen species (ROS). 91,92 Zeaxanthin can provide stronger oxidant defense than L during photooxidation, 93 while lutein has a greater capacity to absorb shortwavelength light irradiation in lipid membranes. 94 Compared with other carotenoids (eg, lycopene or b-carotene), L and Z are more effective in scavenging ROS and can also reduce phospholipid peroxidation. ...
Full-text available
Lutein, zeaxanthin, and meso-zeaxanthin are three xanthophyll carotenoid pigments that selectively concentrate in the center of the retina. Humans cannot synthesize lutein and zeaxanthin, so these compounds must be obtained from the diet or supplements, with meso-zeaxanthin being converted from lutein in the macula. Xanthophylls are major components of macular pigments that protect the retina through the provision of oxidant defense and filtering of blue light. The accumulation of these three xanthophylls in the central macula can be quantified with non-invasive methods, such as macular pigment optical density (MPOD). MPOD serves as a useful tool for assessing risk for, and progression of, age-related macular degeneration, the third leading cause of blindness worldwide. Dietary surveys suggest that the dietary intakes of lutein and zeaxanthin are decreasing. In addition to low dietary intake, pregnancy and lactation may compromise the lutein and zeaxanthin status of both the mother and infant. Lutein is found in modest amounts in some orange- and yellow-colored vegetables, yellow corn products, and in egg yolks, but rich sources of zeaxanthin are not commonly consumed. Goji berries contain the highest known levels of zeaxanthin of any food, and regular intake of these bright red berries may help protect against the development of age-related macular degeneration through an increase in MPOD. The purpose of this review is to summarize the protective function of macular xanthophylls in the eye, speculate on the compounds’ role in maternal and infant health, suggest the establishment of recommended dietary values for lutein and zeaxanthin, and introduce goji berries as a rich food source of zeaxanthin.
... Macular carotenoids are naturally occurring antioxidants located in the photoreceptor outer segments, mainly the rods [12,13]. Lutein and zeaxanthin absorb the short wavelength blue and green light and prevent the phototoxic damage to the underlying RPE [14,15]. In eyes with CR, there is disruption of photoreceptor outer segments resulting in the loss of macular carotenoids, lutein and zeaxanthin. ...
Full-text available
Purpose To report Multicolour® imaging (MCI) findings in commotio retinae (CR) involving macula and correlate topographically with outer retinal layers on optical coherence tomography (OCT). Methods This retrospective study included participants with CR involving macula without any other type of traumatic maculopathy and imaged with OCT and MCI. Results The study included 16 eyes of 16 patients (14 males). Age of presentation ranged from 7 to 56 years and presenting vision ranged from 6/6 to 6/24. On OCT, increased reflectivity and obliteration of hyporeflective ellipsoid zone (EZ) and interdigitation zone (IZ) at CR region were seen. Fovea and other retinal layers were spared. On MCI, white areas due to hyperreflectance corresponding to CR were noted on individual colour reflectance channels and on composite multicolour image. In all cases, foveal reflectance pattern was unaffected. The affection of the EZ and IZ at the CR on OCT was associated with increased reflectance on individual wavelength colour channels on MCI. Foveal sparing on MCI correlated with photoreceptor layer sparing at the fovea on OCT. In 6 (38%) cases with follow-up details, normal reflectivity of EZ and IZ was noted in the region of previous CR as early as 1-week post-presentation. White coloration on multicolour image showed resolution. Conclusion Foveal sparing was common and rod-dominated areas were affected in CR. Corresponding changes on MCI showed hyperreflectance areas on individual wavelength colour channels. Studies combined with photoreceptor-specific electrophysiological tests, adaptive optics imaging and histological evidences would be required in future.
... There may be a minimum L&Z requirement for visual development, beyond which only minimal benefit is seen unless very high doses are supplemented. The physiological effects and relative importance of L&Z intake are likely to differ across the life span, as antioxidant stores including lutein and zeaxanthin accumulate and subsequently deplete in adult life, increasing the risk of macular disfunction and degeneration [54]. ...
Full-text available
(1) Background: Lutein and zeaxanthin (L&Z) are essential dietary nutrients that are a crucial component of the human macula, contributing to visual functioning. They easily cross the placental barrier, so that retinal deposition commences during foetal development. This study aims to assess associations between maternal L&Z intake during pregnancy and offspring visual function at 11–12 years. (2) Methods: Using the Spanish INfancia y Medio Ambiente project (INMA) Sabadell birth cohort, 431 mother–child pairs were analysed. L&Z data were obtained from food frequency questionnaires (FFQ) at week 12 and 32 of pregnancy, alongside other nutritional and sociodemographic covariates. Contrast vision (CS) and visual acuity (VA) were assessed using the automated Freiburg Acuity and Contrast Testing (FRACT) battery. Low CS and VA were defined as being below the 20th cohort centile. Associations were explored using multiple logistic regression. (3) Results: After controlling for potential confounders, L&Z intake during the 1st and 3rd trimester did not reveal any statistically significant association with either CS or VA in offspring at age 11/12 years. (4) Conclusions: No evidence of a long-term association between L&Z intake during pregnancy and visual function in offspring was found. Further larger long-term studies including blood L&Z levels are required to confirm this result.
... Therefore, the protective efficacy of the two well-known eye-specific natural antioxidants, lutein and astaxanthin, has been here investigated. Lutein is a carotenoid with a chemical structure that gives the molecule the ability to absorb blue-violet light somewhat more efficiently than astaxanthin [52]. It has been demonstrated both in vitro and in vivo that lutein can protect the retina not only from photo-oxidative damage but also from inflammation by reducing cytokine expression levels and oxidative stress-induced apoptosis in photoreceptors [53][54][55]. ...
Full-text available
The aim of this study was to compare in vitro the protective and antioxidant properties of lutein and astaxanthin on human primary corneal epithelial cells (HCE-F). To this purpose, HCE-F cells were irradiated with a blue-violet light lamp (415–420 nm) at different energies (20 to 80 J/cm2). Lutein and astaxanthin (50 to 250 μM) were added to HCE-F right before blue-violet light irradiation at 50 J/cm2. Viability was evaluated by the CKK-8 assay while the production of reactive oxygen species (ROS) by the H2DCF-DA assay. Results have shown that the viability of HCE-F cells decreased at light energies from 20 J/cm2 to 80 J/cm2, while ROS production increased at 50 and 80 J/cm2. The presence of lutein or astaxanthin protected the cells from phototoxicity, with lutein slightly more efficient than astaxanthin also on the blunting of ROS, prevention of apoptotic cell death and modulation of the Nrf-2 pathway. The association of lutein and astaxanthin did not give a significant advantage over the use of lutein alone. Taken together, these results suggest that the association of lutein and astaxanthin might be useful to protect cells of the ocular surface from short (lutein) and longer (astaxanthin) wavelengths, as these are the most damaging radiations hitting the eye from many different LED screens and solar light.
... Yellow carotenoid, lutein is another important product of microalgae involved in the making of drugs and cosmetics. They protect the photoinduced damage to the lens and retina of eyes [88]. The strains known to produce lutein are Chlorella protothecoides, C. zofingiensis, Muriellopsis sp., Chlorococcum citriforme, Neospongiococcus gelatinosum, and S. almeriensis. ...
Increase in atmospheric concentrations of CO2 and other greenhouse gases (GHGs), after the advent of the industrial revolution, have become a matter of global concern, calling for immediate climate action and adoption of approaches to mitigate the global climate change. The available carbon capture and storage (CCS) methods are cumbersome and cost intensive. Biosequestration, on the other hand, has come up as a promising approach of CO2 recycling into biomass and biomaterials via photosynthesis. Microalgae, which do not compete for arable lands and can also be grown in wastewaters, have been found promising candidates for CO2 sequestration from the ambient air as well as large industrial point sources using the CO2 concentrating mechanisms mediated by various enzymes. The advantage of using microalgae is that the good lipid content in their cell biomass can be usefully converted to biofuels such as biogas, bioalcohols, biohydrogen, biodiesel, and several value-added biomaterials. Biodiesel [mixture of fatty acid methyl ester (FAME)] is the product of transesterification reaction of oils and is one of the most valued biofuels derived from microalgae. The chapter critically assesses the merits, prospects, and challenges of using microalgae as biological systems for sequestration of CO2 from air or flue gas that can be converted to useful energy resources and valuable biological compounds, along with role of biosequestration as a GHG mitigation tool.
Diatoms are among the opaquest photosynthetic microorganism found in oceans, rivers, and freshwaters. They play a major role in reducing global warming as they fix more than 25% of atmospheric carbon di oxide (CO2). They are a reservoir of untapped potential with the multifaceted application including CO2 mitigation, play a vital role in the aquatic food web as primary producers, and wastewater remediation by quenching pollutants originating from diverse sources such as industries, agricultural, and human sources. Despite their abundance and diversity in nature, only a few species are currently used for biotechnological applications. Diatom biorefinery has gained importance in recent years as more and more algae are identified and explored as a source for lipids, pigments, and other biomolecules. In this chapter, the role of diatom biorefinery has been elaborated extensively displaying the potential of diatoms in carbon dioxide (CO2) mitigation, lipid production for biofuel, nutraceutical potential, and development of new-age drug molecules for therapeutic applications.
Full-text available
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.
The process of sight (photostasis) produces, as a by-product, a chromophore called 2-[2,6-dimethyl-8-(2,6,6-trimethyl-1-cyclohexen-1-yl)-1E,3E,5E,7E-octatetraenyl]-1- (2-hydroxyethyl)-4-[4-methyl-6-(2,6,6-trimethyl-1-cyclo-hexen-1-yl)-1E,3E,5E-hexatrienyl]-pyridinium (A2E), whose function in the eye has not been defined as yet. In youth and adulthood, A2E is removed from human retinal pigment epithelial (h-RPE) cells as it is made, and so it is present in very low concentrations, but with advanced age, it accumulates to concentrations reaching 20 muM. In the present study we have used photophysical techniques and in vitro cellular measurements to explore the role of A2E in h-RPE cells. We have found that A2E has both pro- and antioxidant properties. It generated singlet oxygen (Phi(80) = 0.004) much less efficiently than its precursor traps-retinal (Phi(80) = 0.24). It also quenched ringlet oxygen at a rate (10(8) M-1 s(-1)) equivalent to two other endogenous quenchers of reactive oxygen species in the eye: alpha-tocopherol (vitamin E) and ascorbic acid (vitamin C). The endogenous singlet oxygen quencher lutein, whose quenching rate is two orders of magnitude greater than that of A2E, completely prevented light damage in vitro, suggesting that singlet oxygen does indeed play a role in light-induced damage to aged human retinas. We have used multiphoton confocal microscopy and the comet assay to measure the toxic, phototoxic and protective capacity of A2E in h-RPE cells. At 1-5 muM, A2E protected these cells from UV-induced breaks in DNA; at 20 muM, A2E no longer exerted this protective effect. These results imply that the role of A2E is not simple and may change over the course of a lifetime. A2E itself may play a protective role in the young eye but a toxic role in older eyes.
The adverse effects of sunlight, from melanoma to cataracts, are well known and frequently reported (1). However, because humans evolved under sunlight, it is not surprising that there are many positive effects of light on human health. Light that reaches the human eye has two fundamental biological functions: regulation of the visual cycle and of circadian rhythm. We report here the most recent developments in both of these areas.
Photobiological effects upon the human retina, cornea and lens are highly dependent on the optical exposure geometry as well as spectral characteristics of the exposure. The organ of sight is exquisitely sensitive to light because it performs well in very low nighttime illumination levels and yet it also must adapt to extremely bright environments where light exposures are greater by many orders of magnitude. The eye has evolved to protect itself reasonably well against excessive exposure in bright environments. The retina is minimally exposed in extremely bright environments and the cornea and lens are surprisingly well protected in harsh environments. Although these protective mechanisms are good, they are not perfect and adverse changes from both acute and chronic exposures to sunlight still exist. The geometrical protective factors must be understood and appreciated whenever assessing potential adverse effects of environmental UV radiation and light on ocular structures. These natural ocular protective factors also work with the ever-changing spectrum of sunlight and the different spectral distribution of light and UV radiation across the eye's field of view. Spectral characteristics of the ocular media are also important. One can visualize a series of intra-ocular color filters that progressively filter shorter wavelengths and thereby aid in color vision, reduce the impact of chromatic aberrations and significantly reduce the optical radiation hazards to the lens and retina.
What is maculopathy?Management of maculopathyExudates close to the fovea (Figure 8.1)Severe retinopathy close to the macula (Figure 8.2)Widespread exudates (Figure 8.3)Large plaque exudates (Figure 8.4)Linear exudates close to the fovea (Figure 8.5)Plaque exudates near the fovea (Figure 8.6)Circinate exudates within the arcades (Figure 8.7)Widespread exudates with circinates (Figure 8.8)Coalescent exudates in the macular region (Figure 8.9)