Oxidative stress and antioxidant strategies in

dermatology
Jinok Baek 1, Min-Geol Lee 2
1
Department of Dermatology, Gachon University of Medicine and Science, Incheon, Korea, 2Department of
Dermatology, Yonsei University, College of Medicine, Seoul, Korea

f
Oxidative stress results from a prooxidant-antioxidant imbalance, leading to cellular damage. It is mediated
by free radicals, such as reactive oxygen species or reactive nitrogen species, that are generated during

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physiological aerobic metabolism and pathological inflammatory processes. Skin serves as a protective
organ that plays an important role in defending both external and internal toxic stimuli and maintaining
homeostasis. It is becoming increasingly evident that oxidative stress is involved in numerous skin
diseases and that antioxidative strategies can serve as effective and easy methods for improving these
conditions. Herein, we review dysregulated antioxidant systems and antioxidative therapeutic strategies in
dermatology.
Keywords: Oxidative stress, Antioxidant, Dermatology, Skin

Introduction
Reactive oxygen species (ROS) include superoxide
dP
lycopene, curcumin, green tea, Coffea arabica, sily-
marin, polypodium leucotomos, resveratrol, grape
anion (O2 ○− ), peroxides, hydroxyl radical (OH°, and seed extract, pomegranate, pycnogenol, soy isofla-
singlet oxygen (1 O2 ).1 These molecules activate prolif- vones, propolis, and squalene.4 In skin, the epidermis
erative and cell survival signaling and can damage contains higher concentrations of antioxidants than
cte
DNA (DNA base damage, DNA single-strand and the dermis. These antioxidants generally are distribu-
double-strand breaks, DNA and protein crosslinks, ted in a gradient fashion with increasing concen-
DNA and chromosomal aberration), lipid mem- trations noted toward the deeper layer of the stratum
branes, collagen structures, and mitochondrial func- corneum.5
tion. ROS are produced by keratinocytes and Skin is the largest organ in body that is subjected to
virtually all types of skin cells in response to signals oxidative stress, and this stress is known to influence
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from cytokines, growth factors, airborne pollutants, numerous cutaneous diseases. In this review, we sum-
UV radiation, food additives/preservatives, cosmetics, marize current knowledge regarding oxidative stress
drugs, and physiologic stimuli. Antioxidants are gener- and antioxidant strategies in several cutaneous
ally classified as endogenous and exogenous. The skin diseases.
has a vast antioxidant system, including enzymatic
co

antioxidants, such as glutathione peroxidase (GPX), Contact dermatitis

glutathione S-transferase, glutathione reductase, Irritant contact dermatitis (ICD) and allergic contact
superoxide dismutase (SOD) and catalase, as well as dermatitis (ACD) exhibit similar clinical, histological,
non-enzymatic antioxidants, including ascorbic acid and molecular features; however, these conditions
(vitamin C), glutathione (GSH), ubiquinol, uric acid, exhibit different forms of pathogenesis. ICD is a
Un

vitamin A, melanin, alpha-tocopherol (vitamin E), non-immunologic inflammatory reaction in response

carotenoids (beta-carotene, lutein, zeaxanthin, and to toxic materials, whereas ACD is an antigen-specific,
alpha-carotene) and sulfhydryls.2,3 Flavonoids, coen- memory T-cell-mediated delayed-type hypersensitivity
zyme Q10, alpha-lipoic acid, selenium, pyruvate, and reaction. ROS play a central role in the development of
bilirubin are other examples of endogenous non-enzy- both forms of contact dermatitis.6 The response to
matic antioxidants. We can also obtain antioxidants irritants or allergens involves the synthesis and
exogenously via food intake. Examples of this class release of proinflammatory cytokines as well as the
of antioxidants, or foods that contain them, are generation of signals to attract leukocytes, upregulate
surface costimulatory molecules, activate matrix
Correspondence to: Min-Geol Lee, Department of Dermatology, Yonsei
metalloproteinases (MMPs) and carbonylate proteins.
University, College of Medicine, Seoul, Korea. Email: mglee@yuhs.ac ROS also directly activate or provide costimulatory

© W. S. Maney & Son Ltd 2015

DOI 10.1179/1351000215Y.0000000015 Redox Report 2015 VOL. 0 NO. 0 1
Baek and Lee Oxidative stress and antioxidant strategies in dermatology

signals for nuclear factor kappa B (NF-κB), thereby Seborrheic dermatitis

resulting in the regulation of the prostaglandin Serum total antioxidant status (TAS) values were sig-
pathway and the expression of COX-2.7 Thioredoxin nificantly reduced in seborrheic dermatitis patients.
is induced by ROS and functions as a chemoattractant However, patients exhibited significantly increased
for polymorphonuclear leukocytes, monocytes, and T- serum total oxidative status (TOS) and OSI values.22
lymphocytes in inflammatory tissues.8 ROS initially SOD and catalase activities and MDA levels were sig-
mediate extracellular matrix changes that facilitate nificantly higher in in scraping samples of patients’
ACD. Contact sensitizer-induced, hyaluronidase- scalp.23
mediated hyaluronic acid degradation and sensitiz-
ation is completely prevented by antioxidants or pre- Lichen planus
treatment with the hyaluronidase inhibitor, aristo- In oral lichen planus, 8-oxo-7,8-dihydro-2′ -deoxygua-
lochic acid.9 Th1 and Th2 response patterns in nosine (an indicator of oxidative DNA damage) and
antigen-presenting cells are modulated by GSH.10 8-nitroguanine (a marker of nitrative DNA damage)

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N-Acetylcysteine inhibits IL-1-induced mRNA in oral epithelium were increased.24 Anthocyanin
therapy of oral lichen planus was equal to or better

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upregulation and expression of E-selectin and vascular
cell adhesion molecule 1 (VCAM-1) in endothelial than clobetasol propionate/neomycin/nystatin
cells and reduces NF-κB binding to the NF-κB cream, especially for erosive forms.25
binding site of the VCAM-1 gene.11 N-
Scleroderma
Acetylcysteine, resveratrol, and tea polyphenols
Oxidative stress is hypothesized to play an important
inhibit ROS-regulated expression of MMPs.12
role in disease development. Serum 8-isoprostane (a
Although N-acetylcysteine, alpha-tocopherol and
marker of oxidative stress) was increased in sclero-
ascorbate inhibit the expression and functional activity
of cutaneous lymphocyte-associated antigen (CLA) in
isolated human T-lymphocytes,13 these antioxidants
do not inhibit contact dermatitis when administered
dP
derma patients.26 Similarly, serum TOS and OSI
levels indicative of systemic sclerosis were increased
and TAC was reduced. Furthermore, TAC may serve
as a marker that predicts the risk of lung and gastroin-
in topical form.14 In keratinocytes, cell-permeable
testinal tract involvements.27
SOD suppresses TNF-induced MMP-9; thus, SOD is
Recently, N-acetylcysteine was shown to attenuate
thought to be an immunomodulatory agent in inflam-
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skin fibrosis in a bleomycin-induced mouse model of
matory skin diseases.15
scleroderma; this antioxidant significantly reduced
A topical PPAR-alpha activator induces antioxi-
the MDA and protein carbonyl content in the skin
dant enzymes and reduces inflammation in irritant
of mice.28
and ACD models.16
Pemphigus vulgaris and pemphigus foliaceus
Alopecia areata
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Serum GPX, catalase and GSH in erythrocyte and

Plasma beta-carotene, vitamin E, selenium GPX plasma, plasma β-carotene, vitamin E, and vitamin
activity and GSH in plasma and erythrocytes, levels A are decreased, whereas MDA in erythrocyte and
are decreased, whereas thiobarbituric acid reactive plasma is increased, in pemphigus vulgaris (PV)
substance (TBARS, a marker of lipid peroxidation) patients.29 Serum TOC and lipid hydroperoxide
in plasma and erythrocytes is increased in alopecia (LOOH) are increased in PV patients.30 Plasma uric
co

areata (AA) patients.17 GPX and SOD in scalp acid is reduced, whereas GPX, vitamin C, selenium,
tissue are increased.18 Given that oxidative stress is and bilirubin levels did not differ in PV patients com-
associated with cell apoptosis, hair follicle cell apopto- pared with controls.31
sis may be related to oxidative stress in AA. Oxidative MDA, conjugated dienes, catalase, and SOD activi-
stress index (OSI) and total oxidant capacity (TOC)
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ties are increased, whereas protein thiol levels are

were increased, whereas total antioxidant capacity decreased, in the skin of pemphigus foliaceus (PF)
(TAC) was decreased in AA patients.19 patients.32

Atopic dermatitis Vitiligo

SOD, catalase, GPX, GSH, and vitamins A, C, and E Various conflicting results have been reported with
are decreased in blood of atopic dermatitis patients.20 regard to oxidative stress in vitiligo. These differences
Urinary 8-hydroxy-2′ -deoxyguanosine (a marker of may be attributed to variations in the innate levels in
oxidative DNA damage), acrolein-lysine adducts (a different tissue samples, disease duration, or disease
marker of lipid peroxidation), and bilirubin oxidative activity.33
metabolites (a marker of antioxidant activity of biliru- Among ROS, hydrogen peroxide (H2O2) plays a
bin under oxidative stress) were higher in acute exacer- pivotal role in the onset and progression of vitiligo.34
bated atopic dermatitis.21 Nuclear transcription factor Nrf2 is thought to

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 Baek and Lee Oxidative stress and antioxidant strategies in dermatology

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mainly regulate heme oxygenase-1 expression, which is
involved in protecting human melanocytes against
H2O2-induced oxidative stress.35 Nrf2 regulates the
dP
carotenoids, D-alpha-tocopherol acetate, chromium,
selenium and vitamin E, as well as lactoferrin.43
On the other hand, oral isotretinoin treatment for
expression of various antioxidant enzymes, including severe acne increases erythrocyte lipid peroxidation,
catalase, GPX and SOD, via the use of GSH as a sub- GSH, and GPX and decreases serum paraoxonase-1
strate. The nuclear factor erythroid 2-related factor activity by increasing oxidative stress. This action
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2/antioxidant response element (Nrf2-ARE) pathway was suggested to be a pathomechanism of the side
is important in protection against oxidative stress- effects of isotretinoin.44
induced cellular injury, and its dysfunction can lead
to oxidative stress and melanocyte injury.36 It was Rosacea
recently demonstrated that narrowband ultraviolet Inflammation is suggested to be associated with ROS
(UV) B phototherapy, the well-known treatment of produced by inflammatory cells, such as neutrophils
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vitiligo, reduces erythrocyte MDA levels and increases in rosacea.45 Serum peroxide and cutaneous ferritin
GPX levels in patients with vitiligo.37 levels are increased, whereas serum total antioxidative
potential levels are decreased, in patients with
rosacea.46 Effective therapeutic agents for rosacea,
Acne including metronidazole, tetracyclines, azelaic acid
SOD and GPX activities are decreased in leukocytes, and azithromycin, exhibit antioxidant activity.47 Oral
co

whereas serum TBARS and MDA are increased, in supplementation of zinc sulfate demonstrated conflict-
patients with acne.38 SOD, catalase, GSH, MDA, ing results regarding the improvement of rosacea.48
and adenosine deaminase levels are increased in scrap-
ings of acne tissues.39 Plasma levels of vitamin A and Chronic venous ulcer
E are decreased in patients with acne.40 Levels of squa- Oxidative stress potentially results in disturbed wound
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lene peroxides, which diminish GSH, are increased, healing.49 Increases in the allantoin:uric acid percen-
whereas vitamin D levels are decreased, in the sebum tage ratio (AUR) and 8-isoprostane levels are reported
of acne. Plasma vitamin E, vitamin A, and zinc in chronic wounds.50 Selenium, zinc, and iron levels as
levels were significantly reduced in acne patients, and well as GPX activity are decreased, and ROS-elevated
a negative correlation between acne severity and iron deposition and superoxide are increased.51
vitamin E and zinc levels was noted.41 Increased activity of inducible cyclooxygenase-2
Among various antioxidants, the vitamin C precur- from macrophages and endothelial cells was noted.52
sor sodium ascorbyl phosphate, topical or oral zinc, Total iron levels in chronic exudates are also
and nicotinamide were proved effective for acne in increased,53 along with the proteolytic activity of
several studies.42 Other antioxidants that demon- MMPs and serine proteases.54 SOD, MDA, and NO
strated efficacy in acne include a multi-nutrient antiox- levels are upregulated in valve tissues, thereby indicat-
idant capsule consisting of zinc, vitamin C, ing increased oxidative stress.55

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Baek and Lee Oxidative stress and antioxidant strategies in dermatology

UV-associated skin cancer and skin photoaging numerous cutaneous diseases via various redox-sensi-
ROS can cause DNA damage, which results in muta- tive pathways, conflicting results have been reported
genesis and carcinogenesis. Phytochemicals from plant regarding the oxidant/antioxidant states in these dis-
compounds can prevent UV-induced carcinogenesis eases. This discordance can be explained by the follow-
via their antioxidant function. These compounds ing: (1) the innate levels in different tissue samples
also potentially modulate gene expression and signal differ; (2) ROS can affect different complex signaling
transduction pathways. Black and green tea, grape and biochemical pathways; and (3) oxidative stress
seed proanthocyanidins, resveratrol, quercetin, api- can be the result of inflammation, not the cause.
genin, silymarin, curcumin, genistein, ascorbic acid Conclusions supporting the efficacy of antioxidative
and garlic derivatives inhibit or reduce tumorigenesis treatments remain still elusive. But there have been
in murine models or cell lines. many reports about effective antioxidant treatment
UV induces the generation of ROS and lipid peroxi- for cutaneous disease, as well as conventional drugs
dation products (TBARS) and the depletion of that have antioxidant activity. Targeting oxidative

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endogenous antioxidants. UV depletes GPX, ascor- stress may be an effective strategy for various skin dis-

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bate, GSH, SOD, catalase, alpha-tocopherol, and ubi- eases; thus, further studies are required to establish a
quinol in the skin. Damage to antioxidant systems is framework for antioxidative therapeutic plans for
more prominent in the epidermis than the dermis.56 each disease.
It is important to prevent damage to the skin with anti- .
oxidants before UV exposure. Antioxidants, including
vitamin C, vitamin E, coenzyme Q10, lycopene, caro-
Acknowledgements
tenoids, tretinoin, GSH, zinc, resveratrol, genistein,
The authors wish to acknowledge the support of the
cocoa, selenium, and polypodium leucotomos, can
exert photoprotective effects. Other antioxidants exhi-
biting photoprotective properties include melatonin,
green tea, silymarin, soy isoflavones, lutein, and
dP
Gachon University, Graduate School of Medicine,
and the Gil Hospital Research Foundation.

zeaxanthin.57 Disclaimer statements

Contributors None.
Psoriasis
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Funding None.
The imiquimod-induced mouse model of psoriasis
exhibits an aberrant antioxidant system. Conflicts of interest No potential conflicts of interest
Myeloperoxidase (MPO) and GSH/GSH disulfide relevant to this article are reported.
(GSSG), one of oxidative stress marker levels are
Ethics approval None.
increased, and SOD activity and levels are decreased
in mouse skin.58 Cellular signaling pathways, such as
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