Antioxidants in dermatology

Abstract

The skin cells continuously produce, through cellular respiration, metabolic processes or under external aggressions, highly reactive molecules oxidation products, generally called free radicals. These molecules are immediately neutralized by enzymatic and non-enzymatic systems in a physiological and dynamic balance. In situations where this balance is broken, various cellular structures, such as the cell membrane, nuclear or mitochondrial DNA may suffer structural modifications, triggering or worsening skin diseases. several substances with alleged antioxidant effects has been offered for topical or oral use, but little is known about their safety, possible associations and especially their mechanism of action. The management of topical and oral antioxidants can help dermatologist to intervene in the oxidative processes safely and effectively, since they know the mechanisms, limitations and potential risks of using these molecules as well as the potential benefits of available associations.

Full text

356
An Bras Dermatol. 2017;92(3):356-62.
review
Antioxidants in dermatology*
FlaviaAlvimSant´annaAddor1
s
Received on 15.02.2016
ApprovedbytheAdvisoryBoardandacceptedforpublicationon03.05.2016
* Studyconductedatprivateclinic–SãoPaulo(SP),Brazil.
Financial support: none.
 Conictofinterest:none.
1 Privateclinic–SãoPaulo(SP),Brazil.
 ©2017byAnaisBrasileirosdeDermatologia
INTRODUCTION
Skin and mucous membranes have a contact and defense
barrier role against chemical, physical and biological aggressions
continuously.1
Maintenanceof cellularintegrity,aswellasofallimmune
mechanisms,whetherinborn (cutaneous lipidsandplasma mem-
branes,forexample)orspecic(cytokinesynthesis,enzymesorcell
proliferation),involvesaseriesofchemicalreactionsthatgenerate
reactive oxygen species - highly reactive molecules that can rapidly
altermoleculesfundamentaltocutaneoushomeostasis,suchaspro-
teins,lipids,orDNA.2 Endogenous or exogenous antioxidant mech-
anismsactbyneutralizingthesereactivemolecules.Theimbalance
ofthisneutralization has multiple consequences:freeradicals are
implicatedintheetiopathogenesis of variousdermatoses,as well
as in the aging process and in the onset of cutaneous neoplasias.3
Proper use of antioxidants should be considered in these sit-
uationswhereevidencesoftheirbenetshavebeenaccumulatingin
the last decades.
OXIDATIVE MECHANISMS AND SKIN PHYSIOLOGY
Themainreactiveoxygen species (ROS)arethe hydroxyl
radicals(HO•)andsuperoxide(O2•-),peroxylandalkoxylradicals
(RO2•andRO•),thesingletoxygen(1O2)3-5,aswellashydrogenper-
oxide (H2O2)and organicperoxides(ROOH).4 In addition to direct
damagetomoleculessuch as lipids, aminoacidsand DNA, ROS
canactivateenzymaticandnon-enzymaticcellularresponses,with
the potential to modify other processes that end up interfering with
gene expression. 5
Antioxidantsare substancesthat combineto neutralizere-
active oxygen species preventing oxidative damage to cells and tis-
sues.6 Thecutaneousantioxidantsystemconsistsofenzymatic and
non-enzymaticsubstances.Among enzymatic antioxidants, gluta-
thioneperoxidase(GPx),catalase(CAT)andsuperoxidedismutase
(SOD)canbehighlighted. 7
Non-enzymaticor lowmolecular weightantioxidantsalso
contribute to the maintenance of cellular redox balance. Here some
hormonesaregroupedsuchasestradioland,melatonin,aswellas
somevitamins,suchasEandC.8
Figure1 summarizesthe mainoxidative sourcesandtheir
antioxidant systems; participating.9
THE PARADOX OF ANTIOXIDANTS EXCESS
GenerationofROSinphysiologicalconditions,suchasres-
pirationorevenphysicalexercise,isimportantinthemaintenance
of cellular functional integrity. These molecules generally induce
intracellular enzymatic processes via transcription factors (FoxO)
thatinducethe expressionof antioxidant enzymes,suchas SOD.9
Increased levels of FoxO reduce cell proliferation and induce apop-
tosis.Thesefactorsareinvolvedincellgrowth,proliferation,differ-
entiation and longevity.10
Balance of antioxidant systems and the endogenous genera-
tion of ROS is dynamic and tenuous.
Thereisevidencethatsituationsofmildstress,suchasca-
loricrestrictionorphysicalactivity,canmodulatetheagingprocess,
DOI: http://dx.doi.org/10.1590/abd1806-4841.20175697
Abstract: Theskincellscontinuouslyproduce,throughcellularrespiration,metabolicprocessesorunderexternalaggres-
sions,highlyreactivemoleculesoxidationproducts,generallycalledfreeradicals.Thesemoleculesareimmediatelyneu-
tralizedbyenzymaticandnon-enzymaticsystemsinaphysiologicalanddynamicbalance.Insituationswherethisbalance
isbroken,variouscellularstructures,such as the cell membrane, nuclear or mitochondrialDNAmay suffer structural
modications,triggeringorworseningskindiseases.severalsubstanceswithallegedantioxidanteffectshasbeenoffered
fortopicalororaluse,butlittleisknownabouttheirsafety,possibleassociationsandespeciallytheirmechanismofaction.
The management of topical and oral antioxidants can help dermatologist to intervene in the oxidative processes safely and
effectively,sincetheyknowthemechanisms,limitationsandpotentialrisksofusingthesemoleculesaswellasthepotential
benetsofavailableassociations.
Keywords: Antioxidants;Carotenoids;Dermatitis;DNAdamage;Freeradicals;Polypodium;Skinaging

Antioxidants in dermatology 357
An Bras Dermatol. 2017;92(3):356-62.
sincetheyincreasemitochondrialactivity,alsoincreasingthegener-
ationofROS–whichwouldprovokeanadaptiveresponse,withim-
provementofdefensemechanismsandconsequentbetterresponse
and resistance to stress.11
Althoughthisquestionisnotyetstudiedforskinphysiolo-
gyandpathology,itmaybevalid,especiallyforchronologicalaging
in healthy individuals.
Therefore,theingestionorapplicationofantioxidantmole-
cules is indicated in situations in which there is an inability to neu-
tralize,bothbytheROS excessandby thedeclineofendogenous
systems,asoccursinagingandinsomediseases.
However,not all moleculesofantioxidantpotential, from
thephysiologicalpointofview,actlinearlyincutaneousoxidative
stress; an important example of this is the oral use of beta-carotene.
A randomized, controlled trial to determine whether the
impactofthe useofbeta-carotene supplementation,associatedor
notto sunscreens,coulddelaythesignsofphotoagingwas devel-
opedbetween1992and 1996; no signicanteffectof 30 mg daily
supplementationofbeta-carotenewasidentied.12 Likewise,anoth-
ercarotenoid,lycopene, does not presentaphotoprotective effect
wheningestedorally,bothinnaturaandinsupplementation.13
However,there is evidence that these molecules can also
lead to deleterious effects when used indiscriminately. The risk of
hypervitaminosisin olderpatients,inwhomrenalexcretoryfunc-
tionisreduced,isanexample.14
Most emblematic, however, is the issue of vitamin E: to-
copherol and its esters are some of the most documented antiox-
idants and they are commonly used for their proven action on
induced ultraviolet damage. Its indiscriminate use, however, can
inhibitglutathione-S-transferase,responsiblefortheremovalofcy-
totoxic compounds related to tumorigenesis in the skin.15,16
Resveratrolitself,with its recognizedantioxidantandan-
ti-inammatoryactivities, hasconictingdataregardingitsdoses:
recent data demonstrate its bioactivity in nanometric doses when
derived from phytochemicals in food – and this demonstrates how
itcanbedifculttoevaluatethesynergy,orevenantagonism,ofthe
association between dietary components.17
Theadministrationofantioxidantsinsmaller doses,butin
combination,hasbeenassertingasthesafestalternativeforitsuse.
VitaminE acts in synergy withvitaminC,which regenerates the
radicaltocopheryl,aproductofalpha-tocopheroloxidation. 18
Supplementation with beta-carotene, this time associated
with lycopene and a probiotic, promoted the preventionof poly-
morphiclighteruptioninastudyalsorandomized.19Similarly,an-
otherrandomizedstudy,conductedwithanassociationofvitamins
A,C,E,selenium,pomegranateextract,quercetin,greentea, coen-
zymeq10andcarotenoids,suchaslutein,lycopeneandzeaxanthin,
led to an improvement in the erythematous dose and absorption
levels of free radicals after 4 weeks of use.20
Thesendingssuggestthattheuseofcombinationsofmul-
tiple antioxidant molecules allows not only to amplify the antioxi-
dantactionin severalsitesbut alsotoobtain anampliedaction,
comparableto amonotherapy inhigh doses.For thisreason, each
association should be ideally evaluated for its clinical effects.21
MAIN INDICATIONS IN DERMATOLOGY
Photodamage
Currently,there isenough evidencetoassert thatallsolar
spectrum favors the generation of free radicals; this generation pos-
siblyfavors,toagreaterorlesserextent,photoaging,photoimunio-
suppression and photocarcinogenesis. 22
Ultraviolet (UV) radiation, in its UVB range (290-320 nm),
isresponsiblefor theimmediatedamages of solarradiation,acting
mainlyonkeratinocytes;UVAband(320-400nm),whichinducescel-
lularchanges,particularlycompromisesmelanocytesandbroblasts.
Inadditiontoconsumingantioxidantsystems,UVdamage
leadstoinammation,andneutrophilinltrateactivatesNAD(P)H
oxidase,generatingROSthatalter theproductionofkeratinocytic
cytokines.23,24
Use of antioxidants in the prevention and repair of ultravio-
letphotodamageiswidelystudied,beingthemostknownandused
indication.Association ofantioxidant molecules,fromvitamins to
phytoextracts, in photoprotectors and moisturizers with appeal
againstaging,isfrequent. 25-27
Astudywiththeobjectiveofprovingtheefcacyofanas-
sociation of antioxidants with trace elements and glycosaminogly-
cansinarandomizedcontrolstudyshowedclinicalimprovementof
signs of photoaging after 3 months of use. 28
Oral use of antioxidants does not dispense the use of sun-
screensandisthereforeasecondlineofprotectionagainstUVpho-
todamageevenwhentheyreducetheappearanceofsolarerythema,
such as Polypodium leucotomos. 29
Antioxidantaction ofthisphytoextractnotonlyoccursby
theneutralizingeffectofROS,blockinglipidperoxidation,butalso
by activating natural antioxidant systems.
AlthoughtheindicationofPolypodium leucotomos in our sce-
narioisforpolymorphiclighteruption,thereisconsistentevidence
of its use in other dermatoses as well as in photoaging.30
The combination of oral antioxidants at physiological doses
recommendeddailyintake(RDI)isalsoableto increaseminimum
erythemaldoselevels(MED).31
Regardingvisiblelight(400-720nm),itproducesabout50%
Cell damage
Cell death
Change in proliferative response
Change in immune response
Mitochondria
Peroxisomes
Cycle/ lipoxygenases
NAPDHoxidase
Nitric oxide synthase
Etc.
Sunlight(UV,Visible,IR)
Ionizingradiation
Pollutants
Xenobiotics
Etc.
Enzymaticsystems:SOD,CAT,etc.
Non-enzymaticsystems:glutathione,
vitamins,elatonin,etc.
Source: Pastore et al, 2010.9
ROS:reactiveoxygenspecies(oxygen-freespecies);RNS:reactivenitrogenspecies(nitro-
gen-freespecies);SOD:superoxidedismutase;CAT:catalase
ROS
RNS
FIgure 1: Diagram of the redox balance in the skin

358 Addor FAS
An Bras Dermatol. 2017;92(3):356-62.
of the total oxidative stress caused by sunlight. Reactive species
such as O2- * and * * OH CHR are generated by visible light.32
Althoughthereisevidenceofcutaneouscarotenedepletion
inducedbyvisiblelight,useoftopicalororalantioxidants,toreduce
freeradicalsgeneratedbythisrange,hasnotyetbeenelucidated. 33
Lutein,acarotenoidalreadyusedinophthalmologyin the
treatmentofmaculardegeneration,hasbeenassociatedwithapro-
tectiveeffectofoxidativedamagefromsunlight,particularlybyvis-
iblelight,byabsorbingbluelight.34
A double blind, placebo-controlled study compared the
efcacyoforal supplementationwithtopical applicationof lutein
combinedwithzeaxanthintoveparameters:epidermallipids,hy-
dration,photoprotectiveactivity,skinelasticityandlipidperoxida-
tionunderUVradiation.After12weeks,bothtreatmentsimproved
thesemeasures,andoraladministrationwassuperior,butthecom-
bination(oralandtopical)providedthegreatestprotection.35
Morerecently,studieshaveshownthatthermogenicinfra-
red radiation is also capable of generating free radicals in human
skin;its ambiguouseffect,sinceitisalsoused therapeutically,de-
pends on two distinct mechanisms: the NF-kB signaling pathway is
responsibleforthetherapeuticeffects,whereastheAP-1pathwayis
responsible for the pathological effects.29AP-1isresponsibleforthe
productionofmetalloproteinases thatpromotecollagen breakage,
clinically inducing wrinkles.36,37
The ability of infrared radiation to deeply penetrate favors
thegenerationoffreeradicals,asitcancausemutationinmitochon-
drialDNA.38
Some studies have been conducted with the objective of
investigatingwhichantioxidants would bethemost adequate for
inhibitingtheeffectofthisradiation,usingcombinationsoftopical
use of known molecules; a topical combination of vitamins C, E,
ubiquinoneandgrapeextractshowedpositiveresultsinacompar-
ative study. 39
Aging
Concomitant with solar radiation and other environmental
factorsresponsibleforoxidativephenomena,skinaging,aswellas
ofallorgans,isaccompaniedbythedeclineoftheendogenousan-
tioxidant mechanisms.
Clinically,thendingsofphotoagingarethepredominant,
anditisdifcult–andoftenunnecessaryinpractice–todistinguish
theimpactofexogenousfactorsonthechronologicalprocess,butit
isknownthatthemainndingofintrinsicagingiscutaneousatro-
phy,bythereductionofepidermis,but,mainly,bythe decreasein
the collagen content and other dermal elements.40
Intheintrinsicagingprocess,progressivedamagetomito-
chondrialDNAoccurs,withincreasedROSproduction,whichcaus-
es cell aging and impairs protein proliferation.41
The theory of aging from free radicals was developed in the
1950s;later,it wasobserved thatthe cellularorganelleresponsible
forthecellularmetabolism,themitochondria,wasthemaingener-
ator of free radicals due to the cellular respiration that occurs in it.42
Initsreducedform,ubiquinol(coenzymeQ10)preventsthis
oxidativeactivityandalsoregeneratesalpha-tocopherol.Coenzyme
Q10 is the only soluble lipid antioxidant that animal cells can syn-
thesizeandforwhichthereisanappropriateenzymaticmechanism
to regenerate it – which also declines over time.43 Finally,coenzyme
Q10hasbeenshowntoinuence(bymechanismofgeneinduction)
the synthesis of key cutaneous proteins and to inhibit the expression
ofsomemetalloproteinases,suchascollagenase,bypreservingthe
collagen content of the skin.44
Inskinaging,there isaprogressiveaccumulation ofpro-
teins,DNAandmodiedlipids,reinforcingtheassociationbetween
ROS and intrinsic aging.45
Amongthemultipleantioxidantmechanisms,SODplaysa
centralrolein the variety ofreactivemolecules it neutralizes.Al-
though there is still no direct correlation, animal models suggest
that the lack of SOD leads to degenerative changes with reduced
collagen.Possibly,vitaminCwouldhaveapositiveimpactonSOD
reduction states preventing atrophy due to collagen degradation.46
The most physiological protective effect against oxidative
stress seems to be the support to the endogenous system, using
antioxidantsnormallypresent intheskin. This strategy,however,
should not be confused with the permanent use of high non-physio-
logicaldosesofisolatedantioxidants,norconsideredasasubstitute
foradequatefood.47
Melasma
InducedUV melanogenesisthatoccursinmelasmaisam-
plied by increasing the oxidation of dopaquinone; antioxidants
suchasvitaminC,whichreducedopaquinone(DOPA),preventthe
formation of free radicals.48
TheinducedUV inammatory processalsofavors thein-
crease of melanogenesis.49
AclinicalAclinicaltrialtostudytheendogenoustheendog-
enous antioxidant systems in patients with melasma demonstrat-
inga signicantconsumption ofsuperoxidedismutase(SOD)and
glutathione peroxidase. This result demonstrates the rupture of the
redoxequilibrium.50
Oxidationisaprocessthatmayfavormelasma,buttheex-
clusive use of antioxidants in its treatment does not seem to have a
relevanteffect.Antioxidant moleculesemployedthathaveproven
utility also have whitening action by inhibition of tyrosinase (for
example,ascorbicacid and ellagicacid)or anti-inammatory (for
example,pycnogenol).51-53
Non-melanoma skin cancer
GenerationofUVinducedfreeradicalsintheskindevelops
oxidative stress when it exceeds the ability of natural defense: the
onlyskinprotectionsystemsareantioxidantenzymesandmelanin,
therstlineofdefenseagainstDNAdamage.54
DNAabsorbsultravioletlight,whoseenergycanbreakits
molecular bonds; most of these breaks are repaired by enzymes
presentinthenucleusitself,howevertheremainingdamagesgen-
erate mutations that lead to neoplasia.55
The two main actions of defenses that antioxidants can pro-
vide are in relation to preventing the formation of free radicals or
neutralizingtheradicalsalreadygenerated.56
Epidermal antioxidant capacity is much higher than the
dermal:catalase,glutathioneperoxidaseandglutathionereductase
systems were higher in the epidermis than in the dermis – both the
lipophilicantioxidants(tocopherol,ubiquinol9,etc.)andthehydro-
philicones(ascorbicacid and glutathione). Thestratumcorneum

Antioxidants in dermatology 359
An Bras Dermatol. 2017;92(3):356-62.
containsbothhydrophilic andlipophilicantioxidants. VitaminsC
andE,aswellasglutathione(GSH)anduricacid,werefound.Sur-
prisingly,theyarenotevenlydistributed,butingradientform,with
lower concentrations in the outer layers and higher concentrations
toward the deeper layers of the stratum corneum. 57
Itisalsoconrmedthattheacute exposureofhumanskin
to solar radiation leading to oxidation can be prevented by previous
treatmentswithantioxidants,reducingtheriskofcarcinogenesis.58
In contrast, there is evidence that treatment with topical
antioxidantsafterUVdamage can interfere with thecellcycleor
apoptosisofdamagedcells,notbringingbenetorevenpotentiat-
ing the damage.59
Therefore, endogenous photoprotection with antioxidants
iscomplementaryto photoprotectionwith sunscreens,andis cur-
rentlythe mostadequateformofphotocarcinogenesisprevention,
in addition to, of course, the photoprotection behavior (seeking
shadows,avoidinghoursofgreatersunshine,etc.). 60
Psoriasis
There are consistent systemic signs of oxidative stress in
patients with active psoriasis: plasma levels of malonyldialdehyde
(MDA)aresignicantlyelevated,suggestingthedepletionofnatu-
ralenzymaticandnon-enzymatic antioxidant systemsandconse-
quentlytheprevalenceofperoxidationprocessesincellmembranes
and plasma lipid processes of circulating cells.61Similarly,SOD is
reduced in erythrocytes of psoriatic patients.62
Theinammatoryprocessitselfinthelesionareasinduces
the formation of reactive oxygen and nitrogen species.63
Ontheotherhand,classictreatmentssuchasphototherapy
or methotrexate are also capable of generating ROS and RNS.
However,the eventual use of antioxidants should aim to
recovertheredox balance,leadingtoan anti-inammatory effect,
possibly by the activation of antiproliferative and proapoptotic
pathways,bothinthelocalandintheinammatorycells.9
Alopecia
Thepossiblebenetoftheuseofantioxidantsintelogenef-
uviumwillbeaccordingtotheunderlyingcause,especiallywhen
linked to systemic inammatory processes, but there is no direct
evidence of any oxidative mechanism directly linked to this tricose.
In alopecia areata, there is evidence of increased plasma
SODactivityandintheaffectedtissue,howeverthestudiesarestill
controversial. 64
Other dermatoses
Many inammation conditions demonstrate redox imbal-
ance and signicant consumption of their antioxidant systems in
localcells,such as atopicdermatitisor burned skin,aswell as in
thescarringprocess,inwhichtheexcessofROShindersdermaland
epidermalrepair,especiallyinthemomentofacuteinammation.65
Observational studies of melanoma patients demonstrate a
correlation between the lower incidence of the disease and the daily
consumptionof carotenoidandvitaminC-richtea andvegetables,
aswellasthehigh consumption(atleast threeportions/week) of
darkgreenvegetablesrichinlutein;however,thereisnoelucidation
whether the antitumor mechanism involved would be antioxidant.66
Polypodium leucotomos extract has demonstrated a com-
plementaryeffecton the limitation of melanomacellgrowth,but
the impact of the antioxidant mechanism on this effect is unclear.67
There is also evidence of oxidative stress in dermatoses such as vit-
iligo,lichen planus,acne vulgaris,seborrheicdermatitisand pem-
phigusfoliaceus,buttherearenoclinicalstudiesdemonstratingthe
impactoftheuse of antioxidantsinthecontrol of thesediseases,
both oral and topically.68-72
PRACTICAL ASPECTS ON THE USE OF ANTIOXIDANTS
Use of oral or topical antioxidants in the treatment of derma-
tosesbasically seekstoneutralizeexcessfreeradicals,reducingor
preventingtheattackoncellularstructures.Asthepreservationor
reestablishmentoftheredoxbalanceisthegoalinthesesituations,
the use of antioxidants should always be in line with treatments or
otherpreventivemeasures,asinthecaseofphotoprotection.73
Inthiscontext,theuseofconcentrationsclosetothephysi-
ologicalonesispreferential,sincetheyadjustmoreeasilytothecel-
lularphysiology,inadditiontoreducingrisksoftoxicityorevenof
drug interaction with any drugs that the patient uses. Effects of an-
tioxidants can vary considerably depending on the concentrations.74
It is important to note that the use of oral or topical antioxi-
dantsdoesnotreplaceadietwithfruitandvegetableconsumption,
inwhichthecombinationoftheactiveelementsexpandsitseffects,
anddoesnotinvolveanyrisk.Lycopene,forexample,readilyfound
intomatopaste,ingested on theorderof 55 g/dayfor12weeks,
ledtoasignicantreductionofMMP-1expressioninarandomized
controlled study.75
Rich and varied diet should be encouraged in normal in-
dividuals;however,groupssuchaspatientsafterbariatricsurgery,
elderly,andpeoplewithdietary restrictionsmayhave vitaminde-
ciencies,in whichrepositioninphysiological doseswouldbein-
dicated.
Use of antioxidants in long-term pharmacological concen-
trations should only be considered in situations where there is a di-
agnosed need under strict medical supervision.76,77
Association of antioxidants with complementary mecha-
nisms allows a broader neutralizing action, with adequate safety
of use during the period of oxidative stress – which can be from a
simple sun exposure to extensive and acute phase dermatosis.78,79
Useofsupplementswithoutindication,oringestedinhigh
doses, or even for a prolonged time can, in thesis, cause adverse
events precisely in the physiological antioxidative balance. Hence
the importance of medical monitoring.11
Itisimportanttohighlightthat,amongtheexogenousanti-
oxidantsavailableonthemarket,thescienticevidenceregarding
the actual effect on skin cell lines is varied.
Likewise, the proposed associations may have varied re-
sponses according to the concentrations and molecules involved.
The evaluation of clinical response should be made in order to better
understand the effects in relation to the proposed indication.
Anotherimportantpointisthattheinvitroeffectdoesnot
necessarilycorrespondtotheclinicaleffect,inuencedbyrouteof
administration,level ofconcentrationinadministrationandtarget
cell, level of degradation etc. Chart 1 lists the major antioxidants
with action on the skin by oral or topical administration and their
mechanisms of action.

CONCLUSION
Theskinisthesiteofmultipleoxidativereactions,neutral-
ized by exogenous or endogenous enzymatic and non-enzymatic
systems,inacomplexbutefcient,equilibrium.Interactionwiththe
environment(characteristicof theintegumentarysystem),as well
asthepeculiarities of itscells,especially epidermal cells(ofgreat
metabolicand proliferativeactivity), islargelyresponsiblefor this
generationof reactivespecies.Anychangeinthisbalancemayin-
duce or aggravate dermatoses and the use of antioxidants may be of
greatvalue,iftheyareadministered,orallyand/ortopically,ratio-
nally. Each molecule with antioxidant action has actions in certain
sitesand,therefore,theassociationof these molecules,insmaller
doses,seemstobemoreefcient.Inaddition,associationsallowad-
ministeringconcentrationsclosertothe physiologicalones,which
reduces toxicological risks and even of aggravation of imbalance of
the antioxidant systems. q
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*Informationonthemechanismofactionisrestrictedonlytotheantioxidanteffect,althoughmanyofthecitedmoleculeshaveothereffectsdescribed.
360 Addor FAS
An Bras Dermatol. 2017;92(3):356-62.
Molecule Mechanism of antioxidant action
VitaminE Neutralizationofsingletoxygeninthecellmembrane;involvementwithmembranestabilization,
preventinglipidperoxidation-oxidationofunsaturatedfattyacids,suchasarachidonicacid
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Polypodiumleucotomos InhibitionofUVinducedROSgeneration,includingsuperoxideanion30,83
Lycopene Carotenoidofgreaterbiologicalactionintheneutralizationofsingletoxygen84
Lutein CarotenoidthatprotectsthebroblastsfromUVA-inducedoxidativeaction,alsopreventingthe
decreaseoftheantioxidantenzymescatalaseandsuperoxidedismutase(SOD)85,86
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Epigallocatechingallate(greentea) Flavonoidwithbroadscavengingactionoffreeradicals,inhibitingtheproductionofROSand
lipidperoxidationproducts,inadditiontoprotectingtheendogenousantioxidativesystems89,90
Lipoicacid Repairofendogenousantioxidantsystems,freeradicalneutralizer91
Delphinidin Inhibitionoflipidperoxidationandformationof8-hydroxy-2’-deoxyguanosine(8-OHdG),mark-
erofoxidativestresstoDNAandcarcinogenesis92
CoenzymeQ10 ReductionoftheproductionoffreeradicalsandregenerationofvitaminE;reductionofkeratino-
cyteDNAdamageandUVA-inducedmetalloproteinaseproductioninthebroblasts;reduction
of mitochondrial oxidative damage43,93
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