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Photosensitizing properties of melanin upon excitation with
visible light
ABSTRACT
When the subject is sun protection it seems that
several of the basic rules of photochemistry are
not being considered. If one wants to avoid a
photochemical-induced reaction, the first question
should be if there are and what are the absorbing
molecules. This simple consideration would make
clear that visible light should be considered in
photo-protection strategies, since there are several
photoactive molecules that are present in our skin
and hair and that absorb in this wavelength region.
This review will focus on the antagonist roles of
melanin, which is a fundamental molecule that
protect against UV-B exposure, but as any
photoactive molecule, generates reactive agents,
including singlet oxygen (1O2), upon photoexcitation.
We aim to provide a generic overview of the
reactivity of 1O2 against different types of
biomolecules and a critical evaluation of the
recent literature dealing with the photochemistry
of melanin, with emphasis on the generation
of 1O2 and its consequences to the health of skin
and hair.
KEYWORDS: melanin, sun protection, visible
light, UV-A, ROS, triplets, singlet oxygen, skin,
hair, photoaging
INTRODUCTION
A myriad of intrinsic and extrinsic factors affect
the health of skin and hair [1]. Without doubt,
one of the major extrinsic factors is sun exposure
[2, 3]. It is becoming increasingly evident that
in order to improve human health, both the excess
and the lack of sun exposure should be avoided [4,
5]. Aiming to have a comprehensive understanding
of the effects of light, it is fundamental to pay
attention to the chemical reactions that are
induced by the excited states of specific biological
compounds that absorb light [6]. Herein, we will
give special emphasis to the effect of visible light,
touching also the effects of ultraviolet (UV) to
give a sense of comprehensiveness to the review.
Although there is a naïve belief that only UV-B
and UV-A light damage hair and skin, several
literature reports show unequivocally that visible
light can also damage both tissues [6-9]. Therefore,
it no longer makes sense to talk about innovation
in terms of sun care, without considering visible
light.
The damaging mechanisms induced by UV-A and
visible light are mainly due to photosensitization,
a process by which molecules transform energy of
light into chemical reactivity (see further information
on photosensitization below) [6, 7, 8, 10]. By
definition, an excited state is more reactive than
its respective ground state, being capable of
engaging in both electron and energy transfer
reactions [10]. Hence, the key questions that
should be asked to understand whether a
determined light source has the potential to affect
a specific tissue are: 1. Is there a chromophore
light absorption in this wavelength region? and
2. Is this molecule known to participate in
1Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil;
2Centro Universitário do Espírito Santo - UNESC, Brazil.
Orlando Chiarelli-Neto1,2 and Maurício S. Baptista1,*
*Corresponding author: baptista@iq.usp.br
Trends in
Photochemistry
&
Photobiology
Vol. 17, 2016
photochemical reactions? The second question is
not as important as the first, because most of the
excited states will engage in some sort of
photochemical event [10]. Unfortunately, these
questions are hardly ever being asked and almost
never being answered [11]. Thus, humans still
have to cope with the crude separation of
ultraviolet (UV) being considered dangerous and
visible light good, which is based on the way our
eye photoreceptor responds. In other words, what
we see should be fine, what we do not see is
probably harmful!
During the evolution of Homo sapiens from our
primate ancestor, several changes occurred in our
skin, including loss of most of the fur protection,
and also induction of melanin production, which
is a biopolymer selected during this transformation
to protect our skin against UV-B. However, melanin
also produces reactive oxygen species (ROS)
under exposure to UV and visible radiation [7, 8,
9, 12]. Publications of our group [7, 8] definitely
showed that under UV-A and visible light
excitation, melanin produces singlet oxygen (1O2),
which adds to the double bonds of biomolecules
and can damage hair and skin [7, 8, 10, 12]. We
will start this article by reviewing the photochemistry
of melanin, with emphasis on the generation of
58 Orlando Chiarelli-Neto & Maurício S. Baptista
1O2. We will also review the reactivity of 1O2
against different types of biomolecules and the
consequences of these reactions to the health of
skin and hair.
Melanocytes and melanins
The skin is the largest organ in the body and is
sub-divided into three layers: epidermis, dermis
and hypodermis. These layers have specific cells
and extracellular structures that are important for
aesthetics and for the body defense against
microorganisms and sunlight [1, 2]. Melanocytes
are located in the epidermal layer and its main
function is the production of melanin, which is
exported to keratinocytes and to hair fibers
growing from the follicles (Figure 1). Melanin has
been known to prevent human skin cancer in
epidemiological and experimental studies and also
for being an efficient protectant against UV
exposure. Yet, its role in photoprotection continues
to be controversial [13].
The life cycle of melanocytes is composed of
several stages, including differentiation, migration,
proliferation of melanoblasts and conversion
to melanocytes [14]. The maturation involves
the activation of melanogenic enzymes, proper
Figure 1. Schematic representation of melanocytes producing melanin: Melanin is produced by
melanosomes of mature melanocytes (Melanin granules) and exported to keratinocytes in the
epidermis (Servier Medical Art - adapted) [14].
Photosensitizing properties of melanin upon light excitation 59
Melanin is a polymer derived from several sequential
reactions of oxidation and polymerization of L-
amino acid tyrosine, and it is usually divided in
two types: eumelanin and pheomelanin [7, 8, 9,
14, 23-25]. Eumelanin has no sulfur in its structure
and has coloration ranging from dark brown to
black. Pheomelanin has sulfur in its structure and
has red color (Figure 2). There is controversy in
the literature regarding the control mechanisms in
the synthesis of eumelanin and pheomelanin. The
most accepted hypothesis considers that in the
presence of cysteine the ratio of pheomelanin is
larger than that of eumelanin, and when the
reservoir of cysteine is depleted, eumelanin is
synthesized. Subsequently, the formation of melanin
granules begins by pheomelanin synthesis followed
by a wrapping of eumelanin [24] (Figure 3). Both
melanins are rich in conjugated double bonds and
thus absorb light in the UV and in visible regions,
serving as the main blockers of light, protecting
against the excess of sun exposure, especially
against the effects of UV-B [13, 25].
Sunlight
Solar radiation has a continuous spectrum of
electromagnetic radiation, which is usually divided
into ultraviolet (200 to 400 nm), visible (400 to
700 nm) and infrared (IR). IR extends from the
edge of the visible red spectrum at 700 nanometers
(nm) to 1 mm (Figure 4) [11, 26].
UV radiation is sub-divided into three regions:
UV-C (100-290 nm), UV-B (290-320 nm) and
structuration of melanosomes, efficient melanin
synthesis and transport to keratinocytes and/or to
hair shafts [15].
The synthesis of melanin occurs in specific
organelles called melanosomes, which are present
in melanocytes in four different maturation stages
(I, II, III, IV) in accordance with the structure,
quality, quantity and arrangement of melanin
production [16, 17]. Melanosomes in stage I are
spherical and do not have enzymatic activity for
melanin production. In stage II there is already
small tyrosinase activity [17]. In stage III melanin
is arranged evenly and in stage IV melanin
granules are formed and exported in large
quantities to the keratinocytes of the skin and to
growing hair fibers [14].
The biochemical pathways of pigment formation
in epidermal melanosomes and follicles are
similar, although epidermal melanocytes are long-
lived, whereas the hair melanocytes die at the end
of the hair cycle [18]. Consequently, melanocytes
of hair follicles are more sensitive to aging,
resulting in gray hair [19, 20]. The melanin
granules from skin migrate with the keratinocytes
that are differentiating into corneocytes [14]. In
hair, melanogenesis occurs only during the anagen
(growth phase), and pigment formation is not
present at the catagen (regression) and telogen
(resting) phases [18, 21, 22]. Melanin granules
accumulate in the cortex of the hair shaft, which is
the intermediate layer between the cuticle and the
medulla [11-13].
Figure 2. Schematic representation of melanins: Structures of eumelanin and pheomelanin.
Adapted from Ito and Wakamatsu [24].
Figure 4. Spectra of solar radiation on earth. Intensity of solar radiation as a function of wavelength before and after
passage through the earth’s atmosphere. (www.who.int/uv/publications/UVEHeffects.pdf, with modifications).
photochemical reactions induce the formation of
pyrimidine dimers and 6-4 photoproduct, as well
as of other DNA adducts that usually but not
always can be detected and repaired by the DNA
repair systems [28]. Damages in DNA are frequently
recognized by p53 that can trigger several events
including senescence or apoptosis [28-30]. The
worst case comes from chronic exposure to UV-B
that allows for the accumulation of mutations
(thymine to cytosine transversion) in repair genes
(e.g., p53), with consequent malignant transformation
[31]. It is worth mentioning that UV-B is also
fundamental for vitamin D metabolism; in fact, it
is not a good health habit to totally avoid exposing
bare skin to the sun [4, 5, 32].
UV-A (320-400 nm) [26]. UV-C is the most
harmful, because it induces photochemical
reactions in a wider range of biomolecules.
Practically, all organic molecules absorb radiation
in the UV-C region and react without a defined
specificity. However, thanks mainly to the ozone
layer, photons on this range are absorbed before
reaching the surface of the earth.
UV-B radiation is absorbed by melanin, and by
several compounds having conjugated double
bonds such as ketones and carboxylic acids,
nucleic acids (260 nm) and proteins (280 nm)
[27]. Pyramidine bases (cytosine and thymine) are
the main sites of UV-B absorption in the DNA.
After electronic excitation, direct and specific
60 Orlando Chiarelli-Neto & Maurício S. Baptista
Figure 3. Scheme showing a typical melanin granule containing pheomelanin in
the inside and eumelanin externally. Adapted from Ito and Wakamatsu [24].
Photosensitizing properties of melanin upon light excitation 61
transfer reactions, which are called type I and type
II reactions, respectively (Figure 5). Type I occurs
via direct electron transfer reaction with biological
targets, producing radicals that can interact with
molecular oxygen, which produce oxygenated
products such as superoxide anion radicals (O2
-.),
peroxyl radical (HOO•) and hydroxyl radical
(HO.); type II reactions involve an energy transfer
to molecular oxygen (3O2) forming singlet oxygen
(1O2), which is highly reactive and electrophilic
(Figure 5B) [38, 39]. These reactions lead to the
formation of reactive species, frequently with the
return of the photosensitizer to the ground state,
allowing it to perform a new cycle of light
absorption (Figure 5A).
It is important to emphasize that photosentization
reactions are the rule and not the exception after
an excited state is formed [34]. That is to say, it is
actually difficult to find a chromophore that will
not induce any amounts of triplets. Some may
form in small amounts, but frequently that is
enough to be of significance. This is symbolized
by the reaction centers of photosynthetic organisms.
Although these organisms survive from the direct
absorption and transformation of energy from
light, they also generate fair amounts of triplets
and of 1O2 when excited by light [40]. In fact,
plants use a reasonable amount of energy to cope
with the damage in the photosynthetic apparatus
caused by 1O2 [41].
1O2 reacts efficiently with proteins, lipids and
nucleic acids. The major chemical modification in
nucleic acids induced by 1O2 is the generation
of 8-Oxo-2'-deoxyguanosine (8-oxo-dG), which
normally causes G:C to T:A transversion [42, 43].
In relation to protein oxidation, several amino
acids are sensitive to oxidation by 1O2, including
cysteine, histidine, methionine, tryptophan and
tyrosine. The oxidation of an amino acid in a
protein will alter its structure and activity [44-47].
In the case of biological membranes, lipid
oxidation by 1O2 causes the formation of
hydroperoxides, which is the initial step in the
formation of peroxidation chain reactions that can
cause membrane destruction [48].
Skin and hair have several molecules that absorb
UV-A and produce 1O2 [6, 37, 49, 50] Therefore,
1O2 is mainly responsible for photoinduced skin
damage by UV-A [6, 7, 49]. It is interesting that
Unlike UV-B, which is directly absorbed by DNA,
UV-A radiation is absorbed by natural chromophores
and essentially act by photosensitization (see
next section for a deeper explanation of the
photosensitizing processes) and generates triplet
species, 1O2 and subsequently, other radical
species [6, 12, 33]. In addition, UV-A penetrates
deeper into the dermis, compared to UV-B.
Consequently, UVA is responsible for tumors that
develop in the deeper layers of the skin [3, 34]
and for the premature aging of the skin, which is
also called photoaging [2, 3, 28, 34].
The paradigm that melanin had only a protective
role against sun radiation, started to be broken
when it was shown that UV-A light generates
reactive species by the excitation of melanin in
melanoma cells [35]. High melanin content on
B16-F10 melanoma cells accumulated twice as
much 8-hydroxy-dGuanosina after UV irradiation,
compared to cells with low melanin content [35].
Since melanin absorbs light both in the UV and in
the visible regions of the solar spectrum, it is
expected that the photosensitizing properties of
melanin could extend to visible region. In fact,
visible light is known to induce pigmentation in
individuals with skin types IV and V [9, 36]. As it
will be clarified with more detail below, melanin
is photoactivated by visible light [7, 8, 37].
Nevertheless, before going there, it is important to
review the backgrounds of the photosensitization
reactions.
Photosensitization processes
Just after the absorption of a photon by a molecule
in the ground state, an excited state is formed,
which is a lot more reactive than its respective
ground state [10, 38]. Usually, the first singlet
excited state (1PS*) reaches a condition of pre-
equilibration and starts to decay back to the
ground state by releasing heat into the surroundings,
or by emitting light (fluorescence). Excited states
can also have a spin inversion, which is called
inter-system crossing (CIS), forming triplet excited
states (3PS*). Because triplets are reactive and
remain in the excited state for longer periods, they
are the main species responsible for the photo-
oxidation reactions. Depending on its intrinsic
properties as well as on its surroundings, triplets
can engage either in electron transfer, or in energy
62 Orlando Chiarelli-Neto & Maurício S. Baptista
in the equator and tropics, and fair-skinned
populations in higher latitude places. This is the
reason why fair-skinned individuals are more
prone to several types of skin cancer, particularly
in regions with high UV-B incidence. On the
other hand, dark-skinned individuals, especially
those living in high latitude places are at greatest
risk of disease caused by insufficient levels of
vitamin D [13, 53, 54]. As a consequence, health
problems that originate from the lack of sun
exposure are a lot more costly to the health system
of the United States of America, than those caused
by the excess of sun exposure [55].
It is clear, therefore, that melanin acts as a sun
blocker, absorbing broadband UV and visible
light [13, 53]. The primary biological function of
melanin is to protect nuclear DNA against direct
attack of UV-B and, consequently, the absorption
in the UV-B is the strongest factor that favors its
selection [56]. Melanin also acts as an anti-oxidant
and protects mitochondrial DNA by preventing
several of these compounds that are known to
absorb light in the UV-A region also absorb
visible light [6]. As it will become clear in this
section, the same type of photosensitization reactions
are also induced by visible light.
Photosensitization of melanin and the effects of
visible light on skin and hair
Melanin negatively affects the development of
two very important reactions that are induced by
light in the same wavelength region (UV-B), and
in the same part of the human body (skin): i) the
photochemical reactions after direct DNA excitation,
which trigger the formation of several types of
pre-mutagenic photoproducts and ii) the activation
of vitamin D, which is a hormone involved in
several processes that are vital for humans [4, 5,
51, 52]. The direct participation of UV-B light
and the role of melanin in these two reactions
have contributed as factors of human evolution,
favoring the selection of dark-skinned populations
Figure 5. (A) Schematic representation of type I and type II photosensitization mechanisms: Photosensitizers (PS)
are brought to the singlet excited state (1PS*) and return to the ground state by emitting light (fluorescence, hυ’) or
go to a state excited triplet (3PS*) by intersystem crossing (ICS). Triplet states can react by electron transfer with
biomolecules (biological targets) (Type I reaction). Triplet states can also transfer energy to molecular oxygen (3O2)
forming singlet oxygen (1O2) (type II reaction). (B) shows the layout of the 1O2 detection equipment that consists of
a laser (365 nm and 532 nm), detector (NIR PMT), and monochromator that transmits signal through the spectrum
of NIR to detect 1270 nm (see the internal spectrum in Figure B). Spin Multiplicity of molecular oxygen (3O2) and
singlet oxygen (1O2) are also shown.
Photosensitizing properties of melanin upon light excitation 63
cause an expressive increase in the level of 1O2
production [7, 8].
Pheomelanin generates larger amounts of 1O2 than
eumelanin (Figure 6B). Pheomelin is less bleached
than eumelanin during photolysis (Figure 6C).
Note that during 1 hour of irradiation with visible
light, the absorption of eumelanin decreases by
30% compared to a 7% decrease in the absorption
of pheomelanin (Figure 6C). These data indicate
that pheomelanin is a better 1O2 photosensitizer
than eumelanin [7]. The amount of 1O2 generated
is larger after excitation in the UV-A compared
with excitation in the visible light, as a consequence
of a stronger absorption in the UV-A and also
because of a higher efficiency production, which
depends on the type of melanin [7, 8, 59].
The chemical reaction responsible for the
photobleaching of eumelanin (Figure 6B) is the
addition of 1O2 to a reactive double bond and the
consequent formation of a hydroperoxide in the
C3 position of the indol group [8]. This type of
photoproduct was detected from the photolysis
of eumelanin and not from the photolysis of
pheomelanin. Recent data from Ito’s group in
Japan indicated that 1O2 is also responsible for
UV-A-induced degradative oxidation of a melanin
intermediate 5,6-dihydroxyindole-2-carboxylic acid
(DHICA) [61].
We have shown that 1O2 reactions are the main
cause of photobleaching in hair by visible light
[8]. 1O2 generated inside hair shafts suspended in
different solvents shows lifetimes a lot smaller
than expected, indicating that 1O2 is generated and
suppressed inside hair structure. A model was
proposed to explain the formation and suppression
of 1O2 in hair by photosensitization of melanin
with visible light [8, 37].
Cells that produce higher levels of melanin suffer
greater damage by visible light [7]. Phototoxicity
observed in M+ melanocytic cells, which produce
large amount of melanin (Figure 7A), were
correlated to the absorption of visible light and the
production of 1O2 [7]. Control cells and pigmented
M+ cells were excited with visible light (532 nm)
and 1O2 emission spectra were recorded. Note that
only M+ cells showed measurable amounts of 1O2
(Figure 7A). In order to confirm direct oxidation
of DNA by melanin photosensitized oxidation,
superoxide generation by UV irradiation [57].
However, as any other chromophore, after melanin
excitation there is the formation of excited states
and photosensitization reactions are prone to
occur. In fact, Nofsinger and colleagues observed
the formation of ROS from eumelanin irradiated
by UV-A. They also found that melanin granules
form aggregates that produce 10 times less radical
superoxide anion (O2•-) than oligomers not aggregated
[58], suggesting that intermediate molecules of
melanin generate reactive oxygen species [35].
There seems to be differences in the phototoxicity
of the main types of melanin, i.e., eumelanin and
pheomelanin; however this issue remains largely
controversial [7, 24, 59]. There is evidence that
redhead people have a higher prevalence of skin
cancer, but this is not necessarily correlated with
photo-induced reactions [60].
An interesting result, in terms of the photo-
damaging role of melanin, came out in the
literature in 2010, from Mahmoud and co-workers
[9]. Studies performed with human subjects with
different skin types exposed to visible light
showed darkening in people with skin types IV
and V, but not in individuals with type II skin.
They showed that darkening depended on the
melanin content present in the skin before
irradiation, suggesting a direct role of melanin in
inducing tanning after exposure to visible light.
Seeking to prove the role of photosensitizing
reactions of melanin induced by visible light, we
began to characterize the excited-state reactions of
melanin. A possible explanation for the damage
induced by visible-light excitation of melanin was
the formation of 1O2, which we and others have
proven to occur in several experimental models
[7, 8, 59].
The definitive way to prove the generation of 1O2
is through its emissive properties in the near
infrared, especially its characteristic spectra peaking
at 1270 nm (Figure 6A). In fact, both eumelanin
and pheomelanin generate 1O2 after excitation in
the visible (532 nm) and in the UV-A (355 nm)
(Figure 6A). The amount of 1O2 generated by
melanin was shown to be highly dependent on the
granular structure of the pigment. Agents (heat,
pH, urea, oxidation) that induce opening of the
biopolymer granular structure and the consequent
exposure of the internal parts of the pigment,
64 Orlando Chiarelli-Neto & Maurício S. Baptista
Figure 7
Figure 6
Photosensitizing properties of melanin upon light excitation 65
were in use at that time and until few years ago,
did not protect the skin against UV-A. This
information, which was available for scientists,
was not well propagated to the general public.
Consequently, people were encouraged to expose
themselves to the sun using sunscreens that only
protected them against UV-B. After using UV-B
sunscreens, people could stay for longer periods
under the sun, because they did not feel the acute
inflammatory processes characteristic of UV-B
(skin erythema, for example). However, their skin
was being harmed by light in other wavelength
regions. In fact, we know today that most of the
skin cancers that are deeper in the skin are
originated from injuries caused by oxidative-type
lesions, characteristic of UV-A exposure [3, 28, 34].
We and others have recently shown that visible
light also induces production of reactive oxygen
species, including 1O2, by melanin photosensitization,
causing oxidative DNA damage [7]. This finding
indicates that protection against visible light
should not be ignored, but rather be seriously
considered by health professionals as well as by
general population. Continuous exposure to visible
light without proper protection can promote
molecular damage that cumulates in the skin [40].
Remember also that exposure to visible light
changes color of hair by photobleaching of melanin,
as many perceive during summer holidays.
Good sunscreens available today allow photons
in the visible range to freely penetrate the skin,
causing deleterious effects similar to those caused
M+ cells were irradiated with visible light in a
lower dose regime (6 J/cm2), which is a light dose
that does not induce any decrease in survival even
in M+ cells. After treating these cells with
endonuclease FPG and Endo III, which recognize
specific oxidative lesions and cleave DNA, we
observed a 5-fold increase in the comet tail by
comet essay (gel electrophoresis for measuring
DNA strand break in eukaryotic cell) (Figure 7B)
[7]. These FPG and EndoIII-sensitive DNA
lesions are pre-mutagenic alterations in DNA.
These experiments showed that visible light causes
the formation of pre-mutagenic DNA lesions as it
has been observed for UV-A light. Additional
experiments are needed to confirm the possible
involvement of visible light in the induction of
tumorigenesis.
The fact that melanin is able to generate 1O2 by
light could, in principle, be used as a tool by some
pathogenic organisms to cause biological harm in
others. In fact, Beltran-Garcia and co-workers
have shown that melanin contributes to virulence
of pathogenic fungi Mycosphaerella fijiensis,
allowing tissue invasion and inactivation of the
plant defense system [62].
Considerations on the effect of visible light on
the skin and hair
Thirty years ago, photobiologists knew that UV-A
radiation was able to cause oxidative damage in
molecules, to cause cell death and to affect cell
proliferation [63]. However, the sunscreens that
Legend to Figure 6. Singlet oxygen generation after melanin excitation. (A) Transient emission after exciting
samples of eumelanin with UV-A light (355 nm) and visible (532 nm). The inset shows the emission spectra upon
excitation in the UV-A and visible in the presence of sodium azide, the compound that suppresses singlet oxygen.
(B) Pheomelanin and eumelanin before and after irradiation with visible light. (C) Photodegradation of melanin as a
function of irradiation time in the visible. Data originally published in the article: Photosensitization and the Effect
of Visible Light on Epithelial Cells. PLoS One, 2014, 9(11), e113266. doi:10.1371/journal.pone.0113266 [7].
Legend to Figure 7. Intracellular production of singlet oxygen by photosensitization of melanin and oxidative
damage induced in DNA: (A) correlation between the amount of intracellular melanin and the level of singlet
oxygen generation. Cells with increased production of melanin (M+) present the characteristic spectrum of singlet
oxygen (black line). The basal production of melanin (CT) in the cell indicated by the black arrow is correlated with
no NIR emission. B16-F10 control cells (CT) and B16-F10 pigment cells (M+) are represented besides the graph.
(B) Simplified scheme of the damage that photosensitization of melanin cause in cells. Two main targets of damage
were identified: membranes and nucleic acids. Pre-mutagenic lesions were identified by the recognition of FPG and
EndoIII enzymes. Data were originally published in the article: Photosensitization and the Effect of Visible Light on
Epithelial Cells. PLoS One, 2014, 9(11), e113266. doi:10.1371/journal.pone.0113266 [7].
by UV-A. Therefore, the habit of using sunscreen
and staying under the sun for long periods of time
can cause irreparable damages to the health of the
skin, including photo-aging and possibly the
formation of tumors. The ideal routine for an
individual that does not have skin sensitivity is the
old recipe of exposing to the sun for a short time
without external protection. In doing so one gets
the benefits of the sun, for example, activation of
vitamin D, without suffering the risk that
prolonged exposure offers, even with the use of
current sunscreens. Those who have had previous
hypersensitivity problems in the skin should avoid
contact with sun light by physical means such as
clothing, because the use of sunscreen only will
not be enough. For those that also mind about the
beauty of hair, excess of sun exposure should be
avoided for the same reasons above-mentioned.
The recently-developed hair products that have
sunscreen included in its formulation will not help
much, because hair bleaching is mainly caused by
visible light [8]. We hope this review will help
companies to develop new sunscreens that operate
in a wider spectral range (including visible light),
so that people can get a better protection of skin
and hair.
CONFLICT OF INTEREST STATEMENT
There are no conflicts of interest.
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