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206 Pol J Cosmetol 2016, 19(3): 206-213
β-carotene in skin care
β-Karoten w pielęgnacji skóry
J A, M M
Academy of Cosmetics and Health Care, Warsaw, Poland
β-carotene is a potent antioxidant: it possesses a high antiradical activity
and the ability to neutralize singlet oxygen. Due to these, it can slow
down skin ageing processes and prevent sun damage. In living tissues
it is partly oxidized to retinal, thus constituting a source of vitamin A.
Due to the mechanisms that limit its transformation, β-carotene intake
does not pose any danger, even at high doses.
The most important function of β-carotene is the protection against
oxidative stress, as the compound constitutes a signiﬁcant part of
non-enzymatic protective mechanisms of the body. It protects the
immune system from the damaging activity of the UVA radiation and
reduces the risk of developing skin cancer. Additionally, it stimulates
the melanogenesis process, at the same time reducing the risks of sun-
induced irritations, while additionally having anti-ageing properties. In
vitro studies have revealed that β-carotene protects liquid crystal lipid
structures from UV radiation, lowers the lipid oxidation level and inhibits
proline oxidation in collagen, induced by UV radiation. Applied topically,
β-carotene protects lipids in the intercellular matrix from oxidation.
Cosmetic applications of β-carotene offer multiple benefits, as
approximately 16% of this ingredient permeates the skin. However, its
use is limited due to a well-established common belief that this pigment
permanently changes skin tone when applied topically.
Key words: karotene, antioxidants, antiradical, vitamin A,
UVradiation, singlet oxygen
Adres do korespondencji / Address for correspondence
Wyższa Szkoła Zawodowa Kosmetyki i Pielęgnacji Zdrowia
ul. Podwale 13, 00-252 Warszawa
tel. 604 770 855, e-mail: firstname.lastname@example.org
© Polish Journal of Cosmetology 2016, 19(3): 206-213
Zakwaliﬁkowano do druku: 05.09.2016
β-karoten jest silnym antyoksydantem, wykazuje wysoką aktywność
przeciwrodnikową i zdolność do neutralizowania tlenu singletowego.
Dzięki temu spowalnia procesy starzeniowe w skórze i zapobiega
uszkodzeniom posłonecznym. W żywej tkance jest przekształcany
w retinal, stanowiąc źródło witaminy A. Dzięki mechanizmom
ograniczającym ten proces, nie stanowi zagrożenia dla zdrowia nawet
przy dużych dawkach.
Najważniejszą funkcją β-karotenu jest ochrona przed stresem
oksydacyjnym, stanowi on ważny element systemu nieenzymatycznej
obrony organizmu przed wolnymi rodnikami. β-karoten chroni system
immunologiczny przed niszczącym działaniem promieniowania UV-A
i obniża ryzyko rozwoju nowotworów skóry. Dodatkowo stymuluje
melanogenezę obniżając ryzyko podrażnień słonecznych. Badania
in vitro wykazały że β-karoten chroni ciekłokrystaliczne struktury
cementu międzykomórkowego w stratum corneum, hamuje utlenianie
lipidów i proliny w kolagenie powodowane przez promieniowanie UV.
Zastosowany zewnętrznie zapobiega utlenianiu składników matrix
międzykomórkowego w skórze właściwej.
β-karoten oferuje wiele cennych aplikacji skórze, jednak jego szersze
stosowanie jest ograniczone powszechnym przekonaniem o zdolności
tego związku do zmiany barwy obszarów na które został nałożony.
Słowa kluczowe: karoten, antyutleniacze, przeciwrodnikowe,
witamina A, promieniowanie UV, tlen singletowy
Along with the tanning eﬀect, exposure to the
UV radiation may adversely aﬀect the skin and the
whole body in various ways. The eﬀects of excessive
irradiation include among others the loss of skin
ﬁrmness and the development of wrinkles, as well as
the increased risks of developing various forms of skin
cancer, in addition to phototoxic and photoallergic
reactions. It is therefore crucial to prevent photoageing
and to mitigate the results of exogeneous oxidative
factors using e.g. the inhibitors of radical reactions.
One of the active ingredients with proven very
good antioxidative properties is β-carotene, an orange
pigment that is converted to vitamin A in living tissues,
and is widely used in cosmetics and diet supplements.
It has been established that this compound is very
eﬀective in preventing skin damage and irritation
caused by electromagnetic radiation in the range
Fig. 1. β-karotene
207Arct J, Mieloch M. β-carotene in skin care
The compound inhibits radical reactions without
any damage to the cells and tissues. Most probably, its
activity is connected with the change in the direction
of the energy of radiation through cis-to-trans
isomerisation of the carotenoid. A number of studies
testify to the fact that no other antioxidants neutralize
singlet oxygen to such a degree as β-carotene does.
Due to this, the compound is often termed as an
“extra sunscreen”. The highest SPF of a preparation
that contains β-carotene is no higher than 2, yet in
combination with typical UVA and UVB ﬁlters it can
contribute to a very high overall protection against
The consequences of the exposure to stress factors
can be prevented not only through using cosmetics
with antioxidants, but also thanks to appropriate
oral supplementation. It has been established that
β-carotene administered orally has the ability to
accumulate in the epidermis and has a signiﬁcant
impact on skin condition, both due to its anti-ageing
activity and the capability to reduce skin irritations. It
has been proved that the best results are obtained when
topical application of this compound is combined with
its oral ingestion .
β-carotene antioxidative properties
Ultraviolet radiation (UVA (320-400nm), UVB
(290-320nm) and UVC (200-290nm) is the primary
environmental factor that seriously aﬀects human
skin. Its eﬀects are both positive, such as the vitamin D
synthesis, and negative. The major consequences of the
exposure to the UV radiation include mutations and
the formation of neoplasms, sun-induced irritations,
chronic inﬂammations, and the deterioration in skin
Due to the action of the UV radiation, DNA in
skin cells might be damaged, most often as a result of
thymine-to-cytosine transition or the formation of
thymine dimers. Accumulated mutations may activate
proto-oncogenes or inactivate anti-oncogenes, thus
leading to the development of cancer .
Ultraviolet radiation initiates photo-oxidation
reactions in the body, harmful for the biologically
signiﬁcant molecules, such as DNA, proteins, enzymes
and lipids. It aﬀects the integrity and stability of
subcellular structures, and induces such reactions,
as inflammatory processes in the skin, epidermal
hyperproliferation, the acceleration of cross-linking
of collagen ﬁbres, as well as morphological changes
in keratynocytes and other skin cells. The ﬁrst visible
reaction to UVB irradiation is an erythema developing
several hours after the exposure .
Oxidative stress is considered a pathobiochemical
factor inducing a number of pathological changes,
including certain types of skin cancer, premature
ageing and chronic skin inﬂammations. UV radiation
catalyses the development of Reactive Oxygen Species
(ROS), including 1O2. Singlet oxygen may, however,
aﬀect the level of expression of many genes, including
those associated with photoageing, and induce the
production of metalloproteinases (MMP-1,MMP-3
and MMP-10) , involved in the degradation of
the extracellular matrix during skin ageing processes;
hemoxygenase-1, oxidative stress marker, and pro-
inﬂammatory interleukins (IL-1, IL-6).
Produced in the body reactive oxygen species,
including singlet oxygen (1O2), superoxide anion
and hydroxyl radicals, possess unpaired electrons in
their outer shell, which enable them to react quickly
and violently with nearly all encountered structures,
changing their molecular structure, and therefore their
function. ROS transfer their energy to living cells,
consequently damaging them.
Hydroxyl radicals initiate lipid peroxidation in
cell membranes, forming lipid peroxides, responsible
for premature skin ageing. There are numerous
strategies that prevent the body from the results
of solar irradiation of the skin. Natural preventive
mechanisms, such as UV radiation capturing,
absorption and dispersion do not provide adequate
protection, and hence it is indispensable to use
preparations that prevent adverse effects of the
Both protective cosmetics and diet supplements
can inhibit the formation and counteract the activity
of radical oxygen have to be absorbed in a non-
modiﬁed form in order to eﬀectively neutralize the
adverse eﬀects of ROS activity. The majority of them,
therefore, cannot be taken orally or applied topically.
For example, enzymes with high molecular weight,
such as superoxide dismutase, which catalyses the
Fig. 2. Biological changes evoked by reactive oxygen species
Electron Transport Chain
Nitrosylation and nitration
Tissue function disorders, cellular damage,
destruction of peptides, lipids, carbohydrates, DNA
NO − nitric oxide, ONNO− − peroxynitrite, O
− superoxide anion, OH
− hydroxyl radical
H2O2 − hydrogen peroxide, HOCl − hy pochlorous acid, SOD − superoxide dismutase
MPO − myeloperoxidase, GSSG − glutathione disulﬁde
O + O
GSSG + 2H
208 Pol J Cosmetol 2016, 19(3): 206-213
dismutation of superoxide anion, as well as reductase
and glutathione peroxidase do not permeate the
epidermal barrier, and are broken down by skin
enzymes, whereas those taken orally are broken
down by stomach enzymes. A solution might be Low
Molecular Weight Antioxidants (LMWA), which
LMWA may prevent oxidative damage reacting
directly or indirectly with ROS. The indirect
mechanism involves chelating transitional metals
and inhibiting the Haber-Weiss reaction catalysed by
Fe3+ + O2
–• →Fe2+ + O2
Fe2+ + H2O2 →Fe3+ + OH– + •OH
β-carotene reveals strong antioxidative properties
that enable it to effectively neutralize two most
reactive oxygen species: molecular singlet oxygen
(1O2) and superoxide radicals. As far as its 1O2
scavenging properties are concerned, β-carotene is
nearly 50 times more eﬀective than α-tocopherol .
Moreover, it is an effective deactivactor of
sensitisers involved in the formation of free radicals
and singlet oxygen. β-carotene present in blood
plasma and human tissues is the main representative
of a group of very active 1O2 neutralizers.
Speciﬁc properties of this lipophylic carotenoid
account for its important role in the protection of
cellular membranes and lipoproteins against oxidative
damage. Reactive oxygen species neutralization stops
a chain of reactions that would otherwise eventually
damage lipophilic compartments. Singlet oxygen (1O2)
is the oxygen in an excited state with a half-life of
about 10–5 s, generated through light energy transfer
via appropriate photosensitisers to molecular oxygen.
Singlet oxygen reacts with biomolecules through the
excitation energy transfer or oxidation reactions.
Neutralization of 1O2 seems to be one of the basic
biological skin protection mechanisms. It can take
two pathways. Physical quenching of this reactive
oxygen species is a predominant mechanism and it
involves the transfer of excitation energy from 1O2 to
carotenoids, due to which oxygen relaxes to its ground
state (3O2) and carotenoid reaches excited triplet state
1O2 + CAR →3O2 + 3CAR
β-carotene and the carotenoids with a similar
structure have triplet energy levels matching energy
levels of singlet oxygen, which enables energy transfer
in this case. The carotenoid does not undergo any
further chemical transformations, but returns to
the ground state. Its energy is then dispersed by
rotational oscillations between excited carotenoid and
its environment. In this process carotenoid returns to
the ground state and releases its energy as heat.
3CAR → CAR + heat
In the process of physical quenching carotenoid is
not damaged and can undergo further singlet oxygen
neutralization cycles. Reaction rate constants for
carotenoid reactions with singlet oxygen are within
the range 108 -109 M –1 s–1. The reaction rate constant
depends on the number of double conjugated bonds
in a molecule. β-carotene and lycopene reveal the
highest values of reaction rate constants (2.3-2.5 x109
M–1s–1), whereas the lowest value has been established
for lutein (1.1 x108 M –1 s–1) .
As mentioned before, those divergences might
arise from the diﬀerences in carotenoid structures and
their impact on the properties of the lipid membrane.
It is also argued that aggregate formation by polar
carotenoids might have an inﬂuence on their ability
to neutralize singlet oxygen. There is an empirical
correlation between the excitation energy π, π* and
carotenoid structure. The capacity of carotenoids for
physical quenching is connected with the number
of double conjugated bonds present in a molecule,
determining their lowest triplet energy level. In this
process, carotenoid isomerization might occur.
An alternative pathway is the chemical mechanism
to neutralize reactive oxygen species. It has been
proved that the products of respective reactions are
stable mono- and di-endoperoxides, such as β-carotene
5,8-endoperoxide. Their formation might explain
an intriguing pro-oxidative and cytotoxic activity of
carotenoids [10,11]. Non-regenerated pro-oxidative
carotenoid derivatives might undergo auto-oxidation,
forming potentially toxic apocarotenols, apocarotenals
or epoxides, which might be particularly harmful for
cell functions . However, contrary to physical
neutralization of singlet oxygen, chemical reactions
between singlet oxygen and carotenoid constitute less
than 0.05% of the total quenching process.
Intense research is being conducted on the methods
that would enable the regeneration of carotenoids after
their reaction with singlet oxygen, thus preventing
their transformation into potentially pro-oxidative
compounds. There has been a hypothesis that they
might be retrieved in the presence of vitaminC and
Oxidized vitamin C is regenerated through
the action of a skin enzyme, NADH-dependent
Fig. 3. Oxidized carotenoid regeneration by ascorbate and
209Arct J, Mieloch M. β-carotene in skin care
semidehydroascorbate reductase. Since β-carotene
is a hydrophobic carotenoid, its interaction with
ROS occurs in a lipophilic environment, such as cell
membranes and lipoprotein structures. Depending on
their structures, carotenoids in cells and tissues are
selectively absorbed by membranes, with membrane
properties playing the crucial role in this process.
Those properties define the effectiveness of
incorporation and the ability to adjust carotenoids to
lipid bilayers. Speciﬁc interactions with membranes
may occur in the presence of both non-polar
carotenoids, such as β-carotene and lycopene, as well as
more polar ones, such as lutein and zeaxanthin. It has
been established that antioxidant abilities of these two
classes of compounds are dependent on their diﬀerent
location in phospholipid bilayers.
Carotenoids can be regenerated in skin
phospholipid bilayer, and due to that, they can
participate in the neutralization of skin phospholipid
bilayer in the area of high ROS prevalence, while at
the same time they are being regenerated in another
area through the reduction of ascorbic acid from the
side of the cell membrane cytosol, where the level of
ROS is low . The hypothesis that radicals can be
neutralized by carotenoids acting as transmembrane
radical channels in the area of phospholipid bilayer is
tempting, yet requires further research.
Diet supplementation with preparations
containing β-carotene and other carotenoids has
become very popular in recent years . It is
recommended especially in the summer, when
the body is exposed to damaging eﬀects of the UV
light. Oral supplementation with carotenoids gives
particularly interesting eﬀects due to their ability to
accumulate in the skin .
The effect of appropriate supplementation is
the noticeable inhibition of oxidative processes
that undergo in lipid, protein and carbohydrate
skin structural elements. According to the majority
of research findings reported so far, carotenoid
supplementation brings undisputedly advantageous
results, especially in the area of the protection against
UV radiation, free radicals and reactive oxygen
The limitations imposed on high carotenoid
concentration in diet supplements arises from
their potential pro-oxidative activity. This issue is
being thoroughly researched, yet the ﬁndings are
not conclusive yet. Due to this, supplements with
β-carotene are not recommended for cigarette
smokers, people who abuse alcohol and are exposed
to toxic substances in their place of work .
The baseline level of β-carotene in the skin
is usually rather low, and it has been estimated
as 0.03 to 0.4 nmol/g of tissue . Recurring
exposition to sunlight reduces the concentration of
this compound in the skin. Adopting a diet rich in
carotenoids or using oral supplementation may raise
the level of β-carotene content in the skin 17-fold in
comparison with the baseline level. This may lead
to the hypothesis that raising the level of β-carotene
through supplementation before the exposition to
sunlight may create a deposit that reduces the risk of
photodamage in the circumastances of acute radical
The scope of the conducted research varies as far
as dosage and supplementation period are concerned
. The degree of obtained protection largely
depends on the duration of supplementation period.
Noticeable protective activity has been observed in
the studies with β-carotene given to subjects for at
least 10 weeks[12,19]. In the studies with a shorter
supplementation period , i.e. 3-4 weeks, this eﬀect
has not been observed.
After the application of 24 mg or 30 mg β-carotene
daily for the period of 10 or 12 weeks, skin susceptibility
to sunlight, measured in terms of erythema intensity,
lowers considerably . Stahl et al  proved that
oral supplementation with carotenoids harnessed from
sea algae Dunaliella salina (94% β-carotene and a little
amount of cryptoxanthin, zeaxanthin and lutein)
protects human skin against erythema induced by UV
Supplementing the diet with a carotenoid mixture,
including three major carotenoids: β-carotene,
lutein and lycopene in the dose 24 mg/24h (8 mg of
each/24h) also provides protection from irritations
induced by the exposure to the UV radiation. The
eﬀect was comparable with β-carotene used in the
same dosage (24 mg/24 h) . In both groups
erythema intensity reduced in comparison with
the control. Simultaneously, a synergistic eﬀect was
obtained through the application of topical sunscreens.
With the β-carotene supplementation in the amount
24mg/24 h erythema underwent visible reduction
only after 8 weeks. The eﬀect was even more visible
after 12 weeks. Similar results were obtained in natural
conditions with UV lamps substituted with sunlight
. Protective activity of β-carotene has been pointed
out in other studies as well [23-25]. There have also
been negative results reported in literature [26,27],
with even relatively high doses of β-carotene not giving
It has been observed that in patients with
dysplastic nervous syndrome (approximately 6%
of the population) the number of nevi grows in the
period of adolescence and after the exposition to UV
210 Pol J Cosmetol 2016, 19(3): 206-213
light. Research ﬁndings show that β-carotene applied
both orally and topically reduces the frequency of
solar-induced melanocytic nevi. Since melanocytic
lesions very frequently turn into skin cancer, including
melanoma, preventing their occurrence reduces the
risk of developing this kind of condition .
β-carotene has also turned to be partially eﬀective
in the treatment of photosensitivity disorders, such as
erythropoietic protoporphyria (EPP), where singlet
oxygen acts as a crucial mediator. In patients suﬀering
from EPP high-dosage β-carotene supplementation
(180 mg/24 h) alleviated the symptoms without side-
eﬀects . The signiﬁcance of anti-oxidative action
of carotenoids that alleviate UV-induced erythema
in healthy people is not yet fully understood, yet
the majority of studies conducted so far confirm
the effectiveness of β-carotene used both as a diet
supplement and topically. The eﬀectiveness of protection
is not comparable with UV ﬁlters with high SPF’s, yet
β-carotene in a diet may contribute to higher levels of
basic protection, and hence, increase the protection
against skin damage induced by UV radiation.
In literature, there are relatively few studies
devoted to dermal bioavailability of carotenoids and
their accumulation in the skin. It was observed that
prolonged oral intake of high doses of β-carotene
resulted in skin adopting a visibly yellow hue .
As mentioned above, it was also established that with
β-carotene supplementation in doses (10-20 mg daily)
throughout 4-12 weeks, its concentration in the skin
was increased. This did not lead to carotenodermia,
though. Simultaneously, it was established that the
intake of 30 mg of β-carotene daily for the period
longer than 4 weeks leads to its 5 times higher
concentration in the stratum corneum, which may
lead to a reversible yellowing of the skin, disappearing
after the cessation of supplementation.
Cosmetic applications of β-carotene
After the topical application of carotenoids, their
distribution in the skin remains heterogeneous and
is characterised by a considerable gradient, with the
maximum concentration near the skin surface (4-8 µm
deep). β-carotene is accumulated in the skin, and the
majority of studies testify to its higher concentration
in the epidermis than in the dermis.
Until recently, carotenoids, especially β-carotene,
a dominant precursor of vitamin A in people, were
believed to be converted to vitamin A only in the liver
This could mean that topical application of
carotenoids does not raise the concentration of vitamin
A in the skin. Consequently, further experiments were
conducted in order to explain the bioconversion of
topical β-carotene to pure vitamin A. The experiments
have been conducted ex vivo on human skin and in vivo
on mice. Twenty-four hours after a single application
on human skin, the β-carotene content increased by
160 times in comparison with the 17-fold increase of
the concentration of this carotenoid in the skin after
12 weeks of everyday supplementation. The research
also pointed out to a good ability of β-carotene
to permeate the stratum corneum, leading to the
10-fold raise of retinyl esters in the human epidermis.
β-carotene applied topically effectively penetrates
human and mouse epidermis , and that it induces
a 10- and 3-fold raise in the level of epidermal retinyl
esters in humans and mice, respectively. The results
implicate that β-carotene applied topically undergoes
a conversion into retinyl esters at an early stage,
namely in the epidermis. Ex vivo studies revealed
that β-carotene in the human epidermis is converted
to retinal, which, in turn, is reduced to produce
retinol. Then, retinol is estriﬁed by fatty acids. The
end products of the β-carotene bioconversion into
retinoids by the human skin are, therefore, retinyl
esters . Parallel results were obtained in the studies
conducted on hairless mice. The enzyme responsible
for the conversion of β-carotene into vitamin A in the
epidermis is β-carotene-15,15’-dioxygenase[32,33].
As mentioned above, in the group of subjects
whose diet had been enriched with β-carotene
supplementation for 10 weeks considerably fewer
cases of solar-induced irritations were noted than
in the control group . Similar effects can be
achieved using topical preparations with pro-vitamin
A. It is by about 50% that applying 5% β-carotene
solution 15 minutes prior to the exposure to the UV
radiation reduces the formation of thiobarbituric
acid reactive substances (TBARS) in the skin (such
as malondialdehyde and other compounds that form
thiobarbituric acid coloured derivatives), considered
lipid peroxidation markers. The presence of rotenoid
indispensable for the optimal protection was 0.40
nmol/mg protein .
It was also observed that introducing a higher
amount of carotenoids into cells has pro-oxidative
effects. This finding is confirmed by a number of
other studies that prove the photoprotective activity
of β-carotene and witamin A, resultant from the
diminished amount of lipid peroxide radicals in the
mouse skin . The in vivo studies of β-carotene
applied topically to mice and guinea pigs revealed its
protective properties against UVA radiation [33,34].
In the study with microencapsulated β-carotene
emulsion it was observed that the compound has
avery wide range of cosmetic applications. In addition
to the protection against damage induced by free
radical activity, including that of singlet oxygen, it
211Arct J, Mieloch M. β-carotene in skin care
was observed that skin roughness was reduced by
30% (replica analysis test). Additionally, uneven skin
surface also visibly smoothened. Corneometer testing
revealed that the β-carotene emulsion raised the
stratum corneum moisture level by about 20%.
Introducing β-carotene into washing agents and
hand care creams prevents irritations, itching and skin
thinning. Thanks to pro-vitamin A roughness is also
reduced, which has a positive eﬀect on skin appearance
As a natural colorant, β-carotene has wide
application in colour cosmetics. Recently, natural
dyes and pigments have become increasingly popular.
β-carotene is treated similarly to other colorants,
including anthocyanins, chlorophyll and indigo, and
can be used in all cosmetic products. As the majority
of natural dyes and pigments that are non-soluble in
water, β-carotene is used in such cosmetics as face
powders, moisturizers, bath liquids and capsules,
cleansing products (lotions, liquids), face and neck
care preparations, lipstics, soaps, blushes, bronzers, self-
tanning products, body and hand care preparations,
eye makeup preparations, eyebrow pencils, skin
protection products, sunbathing oils, toners, and
preparations for hair care and protection.
For many years there have been attempts to modify
the appearance of preparations that contain natural
pigments with the addition of substances that improve
their compatibility, hydrophilicity, stability, and other
cosmetic properties. One of the methods to improve
β-carotene solubility in water is to use cyclodextrins
that form inclusion complexes with hydrophobic
compounds . The most characteristic property of
the altered pigments is their increased hydrophilicity
and higher stability in O/W and Si/W emulsions. Due
to these, the colour of preparations does not change
once applied to the skin .
In self-tanners β-carotene is an additive that
modiﬁes the colour obtained in the Maillard reaction
(dihydroxyacetone) with the amino groups of
amino acids and peptides of corneocytes. β-carotene
application probably activates the melanogenesis
process, thus helping to obtain a permanent tan,
simultaneously reducing the risk of solar-induced
irritations and having anti-ageing properties.
Findings concerning the inﬂuence of his compound
on the synthesis of melanin in the skin are not
conclusive, though. In the case of pigmentation
disorders, such as discolorations, vitiligo, melasma,
or post-acne discolorations, it has been observed that
β-carotene may not only prevent the formation of
those lesions, but also to accelerate the process of their
removal. Research conducted on pigment-producing
cells in people and mice shows that β-carotene may
inhibit the synthesis of melanin.
It has been established that β-carotene inhibits
the synthesis of melanin through such mechanisms as
blocking the activity of tyrosynase, a superior enzyme
responsible for the induction of melanin biosynthesis.
These ﬁndings lead to the formation of a new thesis,
namely, that β-carotene additionally has whitening
properties. This may seem rather controversial, as
it is widely known as a tan-accelarating substance
that increases the duration of suntan. Whitening
properties of β-carotene have been conﬁrmed by the
ﬁndings of research conducted on a group of people
Thirty-one people with acquired discolorations
were treated topically with a preparation containing
β-carotene enclosed in vesicles with UVA/UVB ﬁlters.
The cosmetic was applied throughout 8 weeks to 21
people and 24 weeks to 9 people. Adverse effects
were observed in 4 patients with a slight erythema
and limited skin irritation. In those patients the
experiment was discontinued.
After 8 weeks lesions disappeared in people
with stage one melasma and in one person with
stage two involvement. In 10 people regression from
stage two lesions to the stage one involvement was
observed, whereas in 12 people stage three melasma
lightened to stage two, in one person melasma stage
two was reduced to melasma stage one and in one
person no changes were observed . The results
of the experiment show that β-carotene has positive
inﬂuence on melasma, as regression occurred in the
majority of cases. The ﬁndings also testify to the high
bioavailability of this compound .
Anticarcinogenic properties of β-carotene
β-carotene acts as an immunostimulant by
increasing the cytotoxicity of macrophages against
cancer cells. It also raises the number and activity of
T and B lymphocyte cells. It can aﬀect the process
of cancerogenesis by stimulating immune response.
Additionally, it can modulate cancerogenic process by
reducing lipid peroxidation in the human skin both as
a free radical scavenger and as a speciﬁc lipoxygenase
The substrates for lipoxygenase are polyunsaturated
fatty acids, particularly n-6 acids (linoleic acid,
arachidonic acid and others). In the reaction
leukotrienes, lipoxins and physiologically active
oxidized fatty acids are produced. Linoleic acid is one
of the major constituents of phospolipid membranes
of living cells which are damaged by reactive oxygen
species, which leads to the pathological conditions of
the body and to the ageing processes.
Excessive exposure to UV radiation induces
not only skin ageing but also increases the risk of
212 Pol J Cosmetol 2016, 19(3): 206-213
Piśmiennictwo / References
1. Draelos ZD. Cosmetic dermatology. Wiley & Sons, 2015.
2. Karr HK. Eﬃcacy of β-carotene topical application in mela-
sma: An open trial. Indian J Dermatol Venereol Leprol 2003,
3. Morganti P. The photoprotective activity of nutraceuticals.
Part II. Nutraceuticals 2009, 27:166-74.
4. Rona C, Berardesca E. Aging skin and food supplements: the
myth and the truth. Clinics in Dermatology 2008, 26:641-7.
5. Harry RG, Rosen M. Harry’s cosmeticology. Chemical
Publishing Company, Los Angeles 2015.
6. Wertz K, Seifert N, Hunziker PB, Riss G, Wyss A, LankinC,
Goralczyk R. β-carotene inhibits UVA-induced matrix metal-
loprotease 1 and 10 expression in keratinocytes by asinglet
oxygen-dependent mechanism. Free Radical Biol Med 2004,
7. Stahl W, Sies H. Bioactivity and protective eﬀects of natural
carotenoids. Carotenoids Dietary Lipids 2005, 1740: 101-7.
8. Rutkowski R, Pancewicz SA, Rutkowski K, Rutkowska J.
Znaczenie reaktywnych form tlenu i azotu w patomechani-
zmie procesu zapalnego. Pol Merkur Lek 2007, 23: 131-6.
9. Cantrell A, McGarvey DJ, George Truscott T, Rancan F,
BöhmF. Singlet oxygen quenching by dietary carotenoids
in a model membrane environment. Arch Biochem Biophys
2003, 412: 47-54.
10. Fiedor J, Fiedor L, Haeßner R, Scheer H. Cyclic endope-
roxides of β-carotene, potential pro-oxidants, as products
of chemical quenching of singlet oxygen. Biochim Biophys
Acta – Bioenergetics 2005, 1709: 1-4.
developing skin cancer. During ex vivo studies on
skin samples obtained from women aged 18-25 it
was observed that β-carotene noticeably reduces
the number of arachidonic acid and linoleic acid
metabolites formed during lipoxygenase. In 1980,
β-carotene was acknowledged as an anticancer agent.
However, further research did not provide any ﬁndings
that would testify that this compound protects against
It was established that oral intake of β-carotene at
a daily dose of 30 mg for 4 years does not reduce the
risk of developing basal-cell carcinoma and squamous-
cell carcinoma, as does using solar ﬁlters . The
incidence of non-melanoma skin cancers reveals
inverse correlation with the appearance of β-carotene
in blood plasma, and earlier research points to the
protective activity of this carotenoid in UV-induced
However, the role of β-carotene as an anticancer
agent was questioned by the ﬁndings of the randomized
trial, where β-carotene supplementation did not
contribute to the reduction of the incidence of non-
melanoma skin cancer in people. What is more, there
are controversies over prolonged intake of high doses
of β-carotene due to the potential harmful eﬀects of its
high-dose supplementation for human skin (over 15
mg daily). Two studies testing β-carotene supplied in
the dose of 20-30 mg daily revealed the increased risk
of carcinogenesis in the oncological risk groups.
Two other studies did not confirm the increased
risks of cancer development. The long-term safety of
high-dose oral supplementation with β-carotene still
remains a controversial issue [28, 40].
Literature review on β-carotene activity in
biological systems points to the fact that this compound
is one of the most valuable active ingredients used
in cosmetics. β-carotene reveals potent antiradical
properties, conﬁrmed both in in vitro and in vivo
studies. It is one of the few agents that eﬀectively
neutralize the singlet form of oxygen. It seems to well
penetrate stratum corneum and to a certain extent it
accumulates in cell membranes of corneocytes.
In living layers of the epidermis β-carotene is
transformed into retinol and its esters. It is very well
tolerated by the skin, and the cytotoxicity of the
side products of β-carotene reaction with singlet
oxygen, established during in vitro research, has not
been conﬁrmed by in vivo studies. The mentioned
properties qualify this compound as a particularly
valuable active ingredient in protective and anti-
An additional advantageous characteristic of
β-carotene is its cosmetic eﬃcacy accompanying oral
supplementation with this compound. For cosmetic
applications it is not insigniﬁcant that β-carotene has
colouring eﬀects. On the one hand, they limit its use in
cosmetic preparations; whereas on the other hand, they
account for its usability in colour cosmetics and self-
tanners. The inﬂuence of β-carotene on the processes
of melanogenesis is an interesting issue. Literature
provides rather contradictory data, which accounts
for further research into this area. Similarly, dermal
bioavailability of β-carotene requires further studies.
As far as this issue is concerned, unpublished ﬁndings
obtained by the authors of this publication point to the
fact that the composition and the form of a cosmetic
product might play a crucial role in this respect.
213Arct J, Mieloch M. β-carotene in skin care
11. Bando N, Hayashi H, Wakamatsu S, Inakuma T, Miyoshi M,
Nagao A, Yamauchi R, et al. Participation of singlet oxygen in
ultraviolet-a-induced lipid peroxidation in mouse skin and
its inhibition by dietary β-carotene: an ex vivo study. Free
Radical Biol Med 2004, 37: 1854-63.
12. Stahl W, Sies H. Antioxidant activity of carotenoids. Fat
Soluble Vitamins: Old Molecules with Novel Properties
2003, 24: 345-51.
13. Johnson J. Do carotenoids serve as transmembrane radical
channels? Free Radical Biol Med 2009, 47: 321-3.
14. Tapiero H, Townsend DM, Tew KD. The role of carotenoids in
the prevention of human pathologies. Biomed Pharmacother
2004, 58: 100-10.
15. Woodside J, McGrath A, Lyner N, McKinley M. Carotenoids
and health in older people. Maturitas 2015, 80: 63-8.
16. Coetzee V, Di Perrett. Eﬀect of beta-carotene supplementa-
tion on African skin. J Biomed Opt 2014, 19: 25004.
17. Gruber BM, Anuszewska EL. Czy uzasadniona jest suple-
mentacja diety β-karotenem? Prz Lek 2002, 7: 42-7.
18. Stahl W, Krutmann J. Systemische Photoprotektion durch
Karotinoide. Hautarzt 2006, 57: 281-5.
19. Stahl W, Sies H. Carotenoids and protection against solar
UV radiation. Skin Pharmacol Appl Skin Physiol 2002, 15:
20. Klotz LO, Holbrook NJ, Sies H. UVA and singlet oxygen as
inducers of cutaneous signaling events. Curr Probl Dermatol
2001, 29: 95-113.
21. Heinrich U, Gartner C, Wiebusch M, Eichler O, Sies H,
Tronnier H, Stahl W. Supplementation with beta-carotene
or a similar amount of mixed carotenoids protects humans
from UV-induced erythema. J Nutr 2003, 133: 98-101.
22. Stahl W, Heinrich U, Jungmann H, Sies H, Tronnier H.
Carotenoids and carotenoids plus vitamin E protect against
ultraviolet light-induced erythema in humans. Am J Clin
Nutr 2000, 71: 795-8.
23. Young A, Sheehan J. UV-induced pigmentation in human
skin. [in:] Comprehensive series in photosciences sun pro-
tection in man. Giacomoni PU (ed). Elsevier 2001.
24. Urbach F. Clinical effects of solar radiation. The nega-
tive effects of solar radiation: a clinical overview. [in:]
Comprehensive series in photosciences sun protection in
man. Giacomoni PU (ed). Elsevier 2001.
25. Heenen M, Giacomoni PU, van Kranen HJ. Erythema, a link
between UV-induced DNA damage. Cell death and clinical
eﬀects? [in:] Comprehensive series in photosciences sun
protection in man. Giacomoni PU (ed). Elsevier 2001.
26. Garmyn M, Ribaya-Mercado JD, Russel RM, Bhawan J,
Gilchrest BA. Eﬀect of beta-carotene supplementation on the
human sunburn reaction. Exp Dermatol 1995, 4: 104-11.
27. Wolf C, Steiner A, Honigsmann H. Do oral carotenoids
protect human skin against ultraviolet erythema, psoralen
phototoxicity, and ultraviolet-induced DNA damage?
JInvest Dermatol 1988, 90: 55-7.
28. Bayerl C. Beta-carotene in dermatology: Does it help? Acta
Dermatovenerol Alp Pannonica Adriat 2008, 17: 160-2,
29. Stahl W. Carotinoide. [in:] Vitamine, Spurenelemente
und Mineralstoffe: Prävention und Therapie mit
Mikronährstoﬀen. Biesalski AO, Köhrle HK, Klaus JS (ed).
Thieme, Stuttgart 2002.
30. Freitas JV, Praça F, Bentley M, Gaspar LR. Trans-resveratrol
and beta-carotene from sunscreens penetrate viable skin
layers and reduce cutaneous penetration of UV-ﬁlters. Int J
Pharmaceutics 2015, 484: 131-7.
31. Antille C, Tran C, Sorg O, Saurat JH. Topical beta-carotene is
converted to retinyl esters in human skin ex vivo and mouse
skin in vivo. Exp Dermatol 2004, 13: 558-5621.
32. Eichler O, Sies H, Stahl W. Divergent optimum levels of
lycopene, beta-carotene and lutein protecting against UVB
irradiation in human ﬁbroblastst. Photochem Photobiol
2002, 75: 503-6.
33. Lindqvist A, Andersson S. Cell type-specific expression
of β-carotene-15,15’-mono-oxygenase in human tissues.
JHistochem Cytochem 2004, 52: 491-9.
34. Kopcke W, Krutmann J. Protection from sunburn with beta-
Carotene-a meta-analysis. Photochem Photobiol 2008, 84:
35. Morganti P. The protective action of a β-carotene emulsion
against dehydratation phenomena. [in:] Proceeings of IFSCC
Conference 1986: 893.
36. Gottschalck T, McEwen G. International cosmetic ingredient
dictionary and handbook. Cosmetic Toiletry Fragrance
Association, Washington DC 2005.
37. Gomboeva SB, Gessler NN, Shumaev KB, Khomich TI,
Moiseenok AG, Bykhovskii VY. Some natural and synthetic
antioxidants as stabilizers of beta-carotene conversion into
vitamin A. Biochemistry 1998, 63: 185-90.
38. Wertz K, Hunziker PB, Seifert N, Riss G, Neeb M, Steiner G,
Hunziker W, et al. Beta-carotene interferes with ultraviolet
light A-induced gene expression by multiple pathways.
JInvest Dermatol 2005, 124: 428-34.
39. Evelson P, Ordóñez C, Llesuy S, Boveris A. Oxidative stress
and in vivo chemiluminescence in mouse skin exposed to
UVA radiation. J Photochem Photobiol B: Biology 1997, 38:
40. Black HS. The role of nutritional lipids and antioxidants in
UV-induced skin cancer. Front Biosci (Schol Ed) 2015, 7: