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Skin protection against UV light by dietary

antioxidants
Cite this: DOI: 10.1039/c4fo00280f
Elisabet Fernández-Garcı́a*

There is considerable interest in the concept of additional endogenous photoprotection by dietary

Received 1st April 2014
Accepted 17th May 2014
DOI: 10.1039/c4fo00280f
www.rsc.org/foodfunction
antioxidants. A number of efficient micronutrients are capable of contributing to the prevention of UV
damage in humans. These compounds protect molecular targets by scavenging reactive oxygen species,
including excited singlet oxygen and triplet state molecules, and also modulate stress-dependent signaling
and/or suppress cellular and tissue responses like inflammation. Micronutrients present in the diet such as
carotenoids, vitamins E and C, and polyphenols contribute to antioxidant defense and may also contribute
to endogenous photoprotection. This review summarizes the literature concerning the use of dietary
antioxidants as systemic photoprotective agents towards skin damage induced by UVA and UVB.
Intervention studies in humans with carotenoid-rich diets have shown photoprotection. Interestingly, rather
long treatment periods (a minimum of 10 weeks) were required to achieve this effect. Likewise, dietary
carotenoids exert their protective antioxidant function in several in vitro and in vivo studies when present at
sufficiently high concentration. A combination of vitamins E and C protects the skin against UV damage. It
is suggested that daily consumption of dietary polyphenols may provide efficient protection against the
harmful effects of solar UV radiation in humans. Furthermore, the use of these micronutrients in
combination may provide an effective strategy for protecting human skin from damage by UV exposure.

noxious substances, invasion by microorganisms, and radia-

1. Introduction
Human skin acts as a barrier between the internal and external
environments, protecting the body from mechanical damage,
Institute of Biochemistry and Molecular Biology I, Faculty of Medicine,
Heinrich-Heine-University Düsseldorf, PO Box 101007, D-40001 Düsseldorf,
Germany. E-mail: efernandez@cica.es; Fax: +49 211 13029; Tel: +49 211 8110526
Dr Fernández-Garcı́a is a Post-
doctoral Researcher at Andalu-
sian Center for Molecular Biology
and Regenerative Medicine, in
Seville, Spain. She studied
chemistry at the University of
Seville. From 2004 to 2011 she
worked in Food Biotechnology
Department, Instituto de la
Grasa (CSIC), Seville, Spain and
received her PhD. In 2012 she
joined the Institute of Biochem-
istry and Molecular Biology I in
Heinrich Heine-University Düsseldorf (Germany) supported by a
fellowship from the Postdoctoral Fellowship Program (Alfonso
Martin Escudero Foundation, Spain). Dr Fernández-Garcı́a has over
10 years of experience in the eld of dietary antioxidants.
tion. The skin plays an important role in regulating body
homeostasis by keeping water loss to a minimum and by
regulating body temperature. In recent years it has become clear
that the skin is an essential part of the immune system. The
skin condition and functioning are affected by environmental
factors, such as ultraviolet (UV) radiation, free radicals, toxic
and allergic compounds, and mechanical damage, and by
endogenous factors, such as genetic predisposition, immune
and hormone status, and stress. Consequently, the skin
undergoes alterations resulting in photoaging, inammation,
reduced immune function, imbalanced epidermal homeostasis
and other skin disorders.1
Upon exposure to UV radiation from sunlight, photo-oxida-
tive reactions are initiated which cause damage to biomolecules
and affect the integrity of skin cells and damage skin. Such
photo-oxidative damage plays a role in pathological processes
and is involved in the development of many disorders affecting
the skin.2 Based on wavelength, the UV radiation spectrum is
divided into three regions: UVA (400–320 nm), UVB (320–290
nm), and UVC (290–200 nm).
UVA (400–320 nm) radiation, which contributes to up to 95%
of the total UV exposure, is not absorbed by DNA but it is a
strong oxidant and considered the most important source of
oxidative stress in human skin.3 UVA plays a major role in
photoaging. This radiation can penetrate into the deeper
dermis and induces the generation of reactive oxygen species

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Food & Function
(ROS), which can induce mutations in the mitochondrial DNA,
thus leading to the loss of enzymes involved in oxidative
phosphorylation and deciencies in energy metabolism.4
UVB (320–290 nm) is mainly absorbed by keratinocytes in the
epidermis. By direct interaction with the DNA, it causes muta-
tions and skin cancer. UVB also leads to sunburn, which is an
erythema resulting from an inammatory response to the
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photodamage to the skin.4 A frequently used measure of UV
irradiation-induced erythema is determination of the minimal
erythema dose (MED), which is dened as the minimal amount
of energy required to induce a uniform, clearly demarcated
redness 16–24 h aer exposure to UV radiation. Although nature
anticipates these conditions by increasing epidermal thickness,
stimulating melanogenesis, and providing natural antioxidants
in the supercial skin layers, supplementation with nutrients
may support these processes and thereby serve as an additional
protective measure against the harmful effects of UV light.1
2. Endogenous photoprotection by
dietary antioxidants
The concept of additional endogenous protection was proposed
about 30 years ago.5,6 In order to increase the barrier for UV
light, the compound should absorb UV light over a broad range
of wavelengths with high efficacy. Antioxidants protect molec-
ular targets by scavenging ROS, including excited singlet oxygen
and triplet state molecules. Compounds that modulate stress-
dependent signaling and/or suppress cellular and tissue
responses like inammation are suitable for this purpose. A
number of efficient micronutrients are capable of directly
scavenging lipophilic and hydrophilic prooxidants or serving as
constituents of antioxidant enzymes. Carotenoids, polyphenols,
vitamin E as well as vitamin C contribute to antioxidant defense
and may also contribute to endogenous photoprotection.7,8
The concept of endogenous photoprotection implies that the
active compound is available in sufficient amounts at the target
site.9 Thus, structural features are important, and inuence
pharmacokinetic parameters like absorption, distribution, and
metabolism that may affect the level of the compound in
skin.10,11
In this paper, photoprotective effects of dietary carotenoids,
vitamins E and C, and polyphenols towards skin damage
induced by UV light are reviewed in the available literature,
underlying human intervention studies are discussed, and in
vitro or in vivo assays are summarized.
3. Carotenoids
Carotenoids are a family of compounds of over 600 fat-soluble
plant pigments. Fruits and vegetables are major sources of
carotenoids.12 Carotenoids exhibit a variety of biological prop-
erties. These include their role in light harvesting and photo-
protection or provitamin and antioxidant functions in humans
and animals. Carotenoids present a long central chain of
conjugated double bonds carrying acyclic or cyclic substituents.
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Xanthophylls, also called oxocarotenoids, contain functional
oxygen groups7 (see Fig. 1).
Because of their structure and physicochemical properties,
carotenoids could be involved in several ways to protect skin
from sunlight damage, namely by increasing the optical
density, quenching the singlet oxygen (1O2) or, for provitamin A
carotenoids, via formation of retinoic acid. The role of 1O2 in
UVA-induced oxidative stress is well established and has been
reviewed extensively.13 Carotenoids can also scavenge other
reactive oxygen species, such as superoxide anions, hydroxyl
radicals or hydrogen peroxide. Under certain conditions,
however, i.e. higher oxygen partial pressure, carotenoids may
act as pro-oxidants.4
The most abundant carotenoids in the human organism are
b-carotene, a-carotene, and lycopene, as well as the xantho-
phylls lutein, zeaxanthin, and a- and b-cryptoxanthin.14,15
Carotenoids are transported to the skin and accumulate
mainly in the epidermal layers. The amount of these pigments
deposited in skin correlates with dietary intake and bioavail-
ability from the food source. Aer absorption, carotenoids are
transported in the bloodstream via lipoproteins to various target
tissues.16,17 Recently, cholesterol transporters such as scavenger
receptor class B member 1 (SR-B1) and cluster of differentiation
36 (CD 36) were shown to mediate a facilitated absorption of
carotenoids in the gut.18,19 It is likely that carotenoids are taken
up by these transporters also in epidermis, which is an active site
of cholesterol accumulation for the maintenance of permeability
barrier function. SR-B1 is expressed in human epidermis,20
predominantly in the basal layers.3
The levels of these compounds in skin vary with respect to
the skin area and skin layer. High levels of carotenoids are
found in the skin of the forehead, the palm of the hand, and in
dorsal skin; low levels are found in skin of the arm and the back
of the hand (see Table 1 with data from ref. 8).
3.1. Human intervention studies
Intervention studies in humans with carotenoid-rich diets have
shown photoprotection of the skin as measured by decreased
sensitivity to UV radiation-induced erythema (see Table 2).27–34
Stahl et al., 2001 (ref. 31) found that ingestion of tomato paste
(40 g per day, equivalent to 16 mg lycopene per day) over a
period of 10 weeks led to a 40% reduction in skin erythema
development induced by exposure to solar-simulating UV radi-
ation. Erythema was induced by a solar light simulator at 1.25
MED, and reddening of the skin was evaluated before and 24
hours aer irradiation by chromametry. Erythema intensity was
lower aer the treatment. No signicant protection was found
at week 4, but aer 10 weeks, erythema formation was signi-
cantly lower in the group consuming the tomato paste than in
the controls. In another study, protection against UV-induced
erythema can be achieved aer ingestion of 24 mg of b-carotene
(from the alga Dunaliella salina) for a period of 12 weeks.
Erythema intensity was signicantly diminished from 8 weeks.
However erythema suppression was more pronounced when a
combination of carotenoids and vitamin E was supplied.29
Similar results have been found in other studies shown in
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Review
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Fig. 1 Examples of dietary antioxidants that protect against damage by UV radiation.
Table 2. Also listed are several intervention studies where no
protection was observed. It is interesting to note that protection
was only determined in studies where the intervention was for
more than 10 weeks. Apparently a sufficiently long interval of
treatment is needed to provide optimal protection of the skin
against UV-induced erythema.
3.2. Photoprotection in vitro and in vivo
Several studies have used cultured human or other skin bro-
blasts to examine the protective effects of carotenoids on UV-
induced lipid peroxidation.3 A variety of experimental studies
investigated the antioxidant function of beta-carotene in the
skin in vivo and in vitro. In rodents, beta-carotene was found to
reduce lipid peroxidation.35 It has also been demonstrated that
this compound quenches singlet oxygen-mediated photo-
chemical reactions in rodent skin.36
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In cultured skin cells, a few in vitro studies have investigated
the antioxidant potential of b-carotene. This compound
decreased the photoinactivation of the enzymes catalase and
superoxide dismutase as well as protein cross-linking.37 In rat
kidney broblasts, b-carotene diminished UVA-induced cata-
lase deactivation and lipid peroxidation.38
Lycopene, b-carotene and lutein, applied in liposomes as
vehicles, decreased the UVB-induced formation of thio-
barbituric acid-reactive substances (TBARS) at 1 hour to levels
40–50% of those of controls free of carotenoids.14 The amounts
of carotenoid needed for optimal protection were 0.05, 0.40 and
0.30 nmol mg 1 protein for lycopene, b-carotene and lutein,
respectively. A further increase of carotenoid content in cells
beyond the optimum levels led to pro-oxidant effects. In another
study, the depletion of catalase and superoxide dismutase by
UVA was restored, and TBARS was reduced by culturing rat
kidney broblasts with b-carotene or lutein (1 mM each), or with
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Table 1 Carotenoids, a-tocopherol and ascorbic acid levels in human of oxidative stress in cells.3 Carotenoids could be expected to
skin. Adapted from ref. 8 suppress the UVA induced HO-1 gene activation in human cells.
Unexpectedly, two studies with skin broblasts in vitro found an
Skin level
Micronutrient (skin layer) (pmol mg 1
wet wt) Reference opposite effect. The rst study applied b-carotene in cyclodex-
trins at levels of 0.5 and 5 mM.41 A signicant pro-oxidative effect
Carotenoids (epidermis and dermis) and enhancement of UVA-induced HO-1 expression were
b-Carotene 0.05  0.04 21 observed. In the second study, b-carotene or lycopene (0.5–
a-Carotene 0.02  0.01
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Lycopene 0.13  0.10

1.0 mM) were prepared in nanoparticle formulations. As in the
Phytoene 0.12  0.04 study above, either b-carotene or lycopene led to a further 1.5-
Phytouene 0.03  0.02 fold rise in the UVA-induced HO-1 mRNA levels.42 It should be
b-Carotene 0.11  0.01 22 pointed out that the protective properties of carotenoids are
a-Carotene 0.01  0.01 probably at least two-fold, consisting of (1) their potent anti-
Lycopene 0.22  0.01
Lutein 0.03  0.01
oxidant activity and (2) their ability to induce cellular protective
response. Thus, dietary carotenoids and their metabolites
a-Tocopherol induce phase 2 cytoprotective enzymes and share with all other
Epidermis 24.8  9.6 23 classes of phase 2 inducers a common chemical property, the
Dermis 16.2  1.1 24 ability to react with sulydryl groups.43
Stratum corneum 33.0  4.0 25
Overall, these in vitro and in vivo studies show that caroten-
Ascorbic acid oids can exert their protective antioxidant function when
Epidermis from forearm 363.7  24.8 26 present at sufficiently high concentration in the skin cells.
Dermis from forearm 162.4  18.6
Epidermis from upper-inner arm 354.7  23.5
Dermis from upper-inner arm 152.0  19.0 4. Vitamins E and C
Vitamin E refers to a family of eight nutrients of which
a-tocopherol is the most abundant and biologically active form
astaxanthin, which was reported to give superior protective in the human body (Fig. 1). This essential lipophilic nutrient is
activity at concentrations as low as 10 nM.38 Lyons et al.39 well known for its role as a chain-breaking antioxidant during
examined the ability of an algal extract to protect against UVA- lipid peroxidation and it protects polyunsaturated fatty acids in
induced DNA alterations in human skin broblasts (1BR-3), cell membranes from oxidation.14 Food sources include vege-
human melanocytes (HEMAc) and human intestinal CaCo-2 tables, vegetable oils, cereals and nuts.44 a-Tocopherol concen-
cells. DNA damage was assessed using single cell gel electro- trations in skin can be increased with oral or topical delivery
phoresis or comet assay. The algal extract displayed protection and are decreased with UV exposure. Vitamin E is the most
against UVA-induced DNA damage when 10 mM astaxanthin was abundant lipophilic antioxidant found in human skin (see
added to all three cell types. However, at lower concentrations Table 1). In humans, levels of vitamin E in the epidermis are
(10 and 100 nM) no signicant protection was evident. In 1BR-3 higher than the dermis. Vitamin E and carotenoids are absor-
cells, preincubation (18 h) with 10 mM of either the synthetic bed by the same pathway.14
astaxanthin or the algal extract prevented UVA-induced alter- Vitamin C is an effective antioxidant and an essential
ations in cellular superoxide dismutase activity and cellular cofactor in numerous enzymatic reactions. The major source for
glutathione content. vitamin C in the diet are fruits, especially citrus fruits, kiwifruit,
Studies in mouse models also conrm the prevention of cherries and melons, and vegetables such as tomatoes, leafy
oxidative stress induction in skin, caused by UV irradiation, by greens, broccoli, cauliower, Brussels sprouts, and cabbage.45
carotenoids.40 Vitamin C comprises two major forms: L-ascorbic acid, the
Heme-oxygenase 1 (HO-1) gene is strongly activated within reduced form, and L-dehydroascorbic acid, the oxidized form
the rst few hours that follow UVA irradiation of normal human (Fig.1). Vitamin C uptake and distribution into tissues are
dermal broblasts and this response is being used as a marker mediated by an active transport mechanism. Levels of vitamin C

Table 2 Antioxidant mixtures with photoprotective effects. Adapted from ref. 34

Carotenoid supplement and dose Duration (week) Result Reference

b-Carotene 180 mg per day 10 MED increased 27

b-Carotene 30 mg per day 12 Erythema less pronounced 28
b-Carotene 24 mg per day 12 Erythema less pronounced 29
Mixed carotenoids (24 mg per day) (b-carotene, lycopene, lutein, 8 mg each) 12 Erythema less pronounced 30
Lycopene 16 mg per day 10 Erythema less pronounced 31
b-Carotene 60 mg per day + canthaxanthin 90 mg per day 4 No effect 32
b-Carotene 90 mg per day 3 No effect 33

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Review
in the epidermis are higher than the dermis (see Table 1).
Vitamin C distribution within the skin has also been
determined.26
4.1. Human intervention studies
One study showed that subjects treated with 400 IU per day a-
tocopherol for 8 weeks had reduced skin malondialdehyde aer
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UV exposure but this intervention provided no protection from
erythema.46 Werninghaus et al.47 showed no photoprotective
effect aer 6 months of daily dietary supplementation of a-
tocopherol acetate (400 IU) in 12 subjects with skin types II–IV.
In both studies, a clinical measure of the minimum dose of UV
necessary to induce erythema in a subject and a histologic
measure of sunburn cells were compared. No difference was
seen in skin a-tocopherol concentrations between treatment
and placebo groups. Plasma a-tocopherol concentrations
increased by 65% in the treatment group and by 18% in the
placebo group, so there was no question of bioavailability.
Other dietary studies have shown vitamin E as a photo-
protectant when combined with other antioxidants (Table 3).48
Fuchs et al.55 reported no protection when vitamin C (3 g) and a-
tocopherol (2 g or 3000 IU) were supplemented individually, but
in combination these nutrients provided protection as assessed
by increased MED aer 50 days of daily supplementation.
Eberlein-König et al.51 also observed increased MED in subjects
supplemented daily with a combination of vitamin C (2 g) and
a-tocopherol (1000 IU) aer only 8 days. Placzek et al.56
demonstrated a photoprotective effect aer 3 months of daily
dietary supplementation with vitamin C (1 g) and a-tocopherol
(500 IU). Participants showed increased resistance to UVB-
induced sunburn and protection from UVA damage. This study
provides evidence of long-term photoprotection of lower doses
than had been previously tested.
Table 3 Antioxidant mixtures with photoprotective effects. Adapted from ref. 48
Antioxidant mixtures
Vitamin C and E, lycopene, b-carotene, the
rosemary polyphenol and carnosic acid
a-Tocopherol and ascorbate
Oral vitamin E and b-carotene supplementation
Carotenoids and tocopherols
Quercetin, hesperetin and naringenin
Combination of vitamins E and C
Lycopene, b-carotene, a-tocopherol and
selenium
b-Carotene, lycopene, a-tocopherol and ascorbic
acid
Carotenoids (b-carotene and lycopene), vitamins
C and E, selenium, and proanthocyanidins
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These studies suggest that vitamin C regenerates tocopherol
from the tocopheroxyl radical and transfers the radical load to
the aqueous compartment where it is nally eliminated by
antioxidant enzymes.
4.2. Photoprotection in vitro and in vivo
Kondo et al.57 suggested that DL-alpha-tocopherol protects
human skin broblasts against the cytotoxic effect of UVB, and
its mechanism seems to be related to the inhibition of UV-
induced lipid peroxidation or to the antioxidation effect of DL-
alpha-tocopherol. The lipid hydroperoxide concentration
(determined by HPLC) in the ultraviolet radiation irradiated
skin of a-tocopherol supplemented mice (diet containing
10.000 IU kg 1, fed over 30 days) was about one third of that
seen in unsupplemented mice.58 Several mechanisms of action
for a-tocopherol reducing the detrimental effects of ultraviolet
radiation are possible. Besides scavenging reactive oxidants a-
tocopherol may act as a cellular response modier or as a
sunscreen. a-Tocopherol modulates the arachidonic acid
cascade59 and modies the membrane uidity.60
Preincubation of mouse keratinocytes with vitamin C resul-
ted in a signicant reduction in UVB-induced oxidative
damage.61 Tebbe et al.62 investigated the antioxidative effect of L-
ascorbic acid on lipid peroxidation and on secretion and mRNA
expression of interleukin (IL)-1 alpha and IL-6 aer UVA irra-
diation (20 J cm 2) in cultured human keratinocytes. L-Ascorbic
acid was able to downregulate the IL-1 alpha mRNA expression
in both UVA-irradiated and nonirradiated cells; however, IL-6
mRNA expression remained unaffected. These ndings indicate
a major cell-protective effect of L-ascorbic acid on UVA-induced
lipid peroxidation and the secretion of pro-inammatory cyto-
kines by UVA-irradiated human keratinocytes.
Outcome of the study Reference
Vitamin C, vitamin E, and carnosic acid showed 42
photoprotective potential human dermal
broblasts exposed to UVA
MED increased markedly aer intake of the 48
combination of these micronutrients
UV radiation-induced oxidative stress in human 49
skin
Scavenging ROS generated during 29
photooxidative stress
Protective agents in certain skin diseases 50
caused, initiated, or exacerbated by sunlight
irradiation
Mean MED increased in the group received 51
vitamins compared with baseline
Many parameters of the epidermal defense 52
against UV-induced damage were signicantly
improved
Signicant increase of melanin concentrations 53
in skin was detected
A selective protection of the skin against 54
irradiation was conrmed
Food Funct.

Food & Function
5. Polyphenols
Polyphenols are a large family of naturally occurring plant
products that are widely distributed in plant foods, including
fruits, vegetables, nuts and seeds. Important dietary sources of
polyphenols are onions (avonols); cacao, grape seeds (proan-
thocyanidins); tea, apples, and red wine (avonols and cate-
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chins); citrus fruits (avanones); berries and cherries
(anthocyanidins); and soy (isoavones)63 (Fig. 1). These poly-
phenols contribute to the benecial health effects of vegetables
and fruits. Most of the natural polyphenols are pigments, typi-
cally yellow, red or purple, and can absorb UV radiation. The
radiation that polyphenols can absorb includes the entire UVB
spectrum of wavelengths and part of the UVA spectra.
The bioavailability and metabolism of polyphenols may
inuence their effectiveness. The considerable structural
diversity among the polyphenols can inuence the bioavail-
ability of the individual components. Small molecules, like
catechin monomers, can be easily absorbed through the gut
barrier, whereas the large molecular weight polyphenols, such
as proanthocyanidins and even ( )-epigallocatechin-3-gallate
(EGCG), are poorly absorbed. Once absorbed, polyphenols are
conjugated to glucuronide, sulphate and methyl groups in the
gut mucosa and inner tissues. Non-conjugated polyphenols are
virtually absent in plasma. During digestion in the gut, the large
polyphenolic molecules break into multiple small molecules or
metabolites and these may systemically induce benecial
effects in the body.64
5.1. Human intervention studies
EGCG from green tea (Camellia sinensis) is the most extensively
studied polyphenol in terms of protection against UV radiation-
induced photodamage. In a pharmacokinetic and safety study
of green tea polyphenols, groups of eight healthy human
subjects received one of the ve following treatments for a
period of four weeks: 800 mg EGCG once a day, 400 mg EGCG
twice a day, 800 mg EGCG within a dened decaffeinated green
tea polyphenol mixture (polyphenol E) once a day, 400 mg EGCG
as polyphenol E twice a day, or a placebo once a day.65 Skin
erythema was evaluated, and the dose of UV radiation causing
just perceptible erythema was determined at baseline and aer
four weeks of green tea polyphenol intake. No change in MED in
response to solar-simulating UV radiation was observed, but,
interestingly, subjects reported that they experienced less-
intensive sunburn reactions aer receiving the green tea poly-
phenol treatment. It is thus possible that there were subtle
changes in skin photosensitivity without an impact on the MED.
Other reasons for the apparent lack of change in MED could be
that the local concentration of EGCG in skin aer oral intake
was insufficient to provide protection or that protection could
have been achieved by a longer duration of treatment.12
The effects of consumption of a avanol-rich cocoa beverage
were studied54 observing a decreased UV-induced erythema by
15% aer only six weeks. In another study, two groups of
women consumed either a high dose of avanol (326 mg per
day, containing 61 mg epicatechin and 20 mg catechin) or a low
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dose of avanol (27 mg per day, containing 6.6 mg epicatechin
and 1.2 mg catechin) cocoa powder dissolved in 100 mL water
for 12 weeks.66 There was no change in erythema development
in the group that consumed a low dose of avanol compared
with baseline, there was an improvement in the skin condition
and a signicant reduction in erythema in the group that
consumed a high dose of avanol, by 15% at 6 weeks and by
25% at 12 weeks of treatment.12
5.2. Photoprotection in vitro and in vivo
Mechanistic studies of photocarcinogenesis have revealed that
the oral administration of green tea polyphenols (through
addition to the drinking water) in SKH-1 hairless mice resulted
in signicant inhibition of erythema.67 In this study, it was
found that although administration of green tea polyphenols in
drinking water signicantly reduced the UVB-induced tumor
development in wild-type mice, this treatment had a nonsig-
nicant effect in IL-12-knockout mice. Green tea polyphenols
resulted in reduction in the levels of markers of inammation
(cyclooxygenase-2, prostaglandin E2, proliferating cell nuclear
antigen, and cyclin D1) and proinammatory cytokines (tumor
necrosis factor-a, IL-6 and IL-1b) in chronically UVB-exposed
skin and skin tumors of wild-type mice but less effective in IL-
12p40-KO mice. Prevention of photocarcinogenesis by green tea
polyphenols is mediated through IL-12-dependent DNA repair
and a subsequent reduction in skin inammation. Also dietary
intake of grape seed proanthocyanidins and/or silymarin
inhibited UVB radiation-induced erythema.64
Very recently it has been shown that exposure to green tea
polyphenols protected against UV radiation-mediated DNA
damage and apoptosis in human keratinocytes and human skin
equivalents.68 This protection correlated with induction of IL-12
secretion and was almost completely reversed by the addition of
an anti-IL-12 antibody, strongly implicating IL-12 as an impor-
tant mediator of the protective effects of green tea polyphenols.
Adult human skin broblasts and normal epidermal keratino-
cytes, cultured separately, had signicantly less DNA damage
from UVA irradiation when treated with EGCG.69 EGCG treat-
ment of human broblasts in culture blocked the UV-induced
increase in collagen secretion and collagenase mRNA levels,
and also inhibited the binding activities of the UV-induced
nuclear transcription factors nuclear factor-kappaB (NF-kB) and
activated protein AP-1.70 When HaCaT cells were treated with
( )-epicatechin-3-gallate (ECG) and exposed to UVB radiation, it
was observed that avonoid could act as a free-radical scavenger
when keratinocytes were photodamaged.71 The treatment of
HaCaT cells with ECG also demonstrated its free-radical scav-
enging effects, when cells were irradiated with UVA radiation.
These observations indicate that EGCG could play an important
role in the attenuation of oxidative stress-mediated cellular
signaling responses, which are essential factors in various skin
diseases in humans.64
Resveratrol, a stilbene found in grapes, red wine, and nuts, is
also a potential polyphenolic antioxidant. Pretreatment of
human epidermal keratinocytes with resveratrol inhibited the
UVB-mediated activation of the NF-kB pathway.72 The treatment
This journal is © The Royal Society of Chemistry 2014

Review
of HaCaT cells with resveratrol before UVB irradiation resulted
in an increase in cell survival of UVB-irradiated cells which was
associated with the reduction in ROS production.73 Soybeans
are a rich source of the isoavones, genistein and daidzein, and
are photoprotective.74 Genistein has been shown to reduce UV
radiation-induced oxidative and photodynamic DNA damage.75
Treatment of the human keratinocyte cell line NCTC 2544 with
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genistein prevented the UV-induced enhancement of the DNA-
binding activity of the signal transducer and activator of tran-
scription-1 by acting as a tyrosine kinase inhibitor, thus,
limiting lipid peroxidation and increases in ROS generation.76
Based on the epidemiological evidence and laboratory
studies conducted using in vitro and in vivo systems, it is sug-
gested that routine consumption of these polyphenols may
provide efficient protection against the harmful effects of solar
UV radiation in humans.64
6. Endogenous photoprotection by
dietary antioxidant combinations
As mentioned before in this review, combinations of different
antioxidants applied simultaneously can provide a synergistic
effect. Several studies observed that dietary antioxidants are
most effective when used in combination (Table 3).48 Offord
et al.42 observed that b-carotene and lycopene must be delivered
together with vitamin E to prevent the formation of oxidative
derivatives, which may inuence the cellular and molecular
responses. According to Offord et al.,42 interactions between
structurally different compounds with variable antioxidant
activity may provide additional protection against increased
oxidative stress. Fernández-Garcı́a77 observed similar effects.
This study strengthens the hypothesis that the combination of
dietary antioxidants present in tomato (naringenin and lyco-
pene) other than lycopene alone could play a role in the health
effects of tomato as evidenced by epidemiological studies. Long-
term radical-initiated UV damage may be mitigated by a
balanced diet.78 Therefore, combinations of micronutrients may
be envisaged for effective photoprotection.
7. Conclusions
Upon exposure to UV radiation from sunlight, photo-oxidative
reactions are initiated which cause damage to skin. A diet rich
in antioxidants such as carotenoids, vitamins E and C, and
polyphenols can provide photoprotection against the harmful
effects of solar UV radiation in humans. The literature is replete
with intervention studies which nd that supplementation with
carotenoids, vitamins E and C, and polyphenols may protect
from several markers of UV damage including lipid perox-
idation, erythema, DNA damage, and apoptosis. Nevertheless,
photoprotection can only be achieved if these micronutrients
are available in sufficient amounts at the target site. More
investigation of optimal doses and mechanisms of protection is
needed to better target and prevent photodamage with diet.
However, endogenous protection associated with the diet must
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Food & Function
be considered complementary to the topical use of a sunscreen
with a high-sun protection factor.
The use of dietary antioxidants in combination may provide
an effective strategy for mitigating the effects of UV radiation
that will lead to the protection of the skin from various skin
diseases caused by excessive sun exposure.
Abbreviations
ECG ( )-Epicatechin-3-gallate
EGCG ( )-Epigallocatechin-3-gallate
HO-1 Heme-oxygenase 1
IL Interleukin
MED Minimal erythema dose
NF-kB Nuclear factor-kappaB
ROS Reactive oxygen species
1
O2 Singlet oxygen
TBARS Thiobarbituric acid-reactive substances
UV Ultraviolet
Acknowledgements
E.F.G. is supported by fellowships from the Postdoctoral
Fellowship Program (Alfonso Martı́n Escudero Foundation,
Spain), and the Junta de Andalucia (PII-CTS-7962 MO)/Euro-
pean Union (FEDER).
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