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Solar radiation produces a series of positive
effects in the organism: It raises the levels of vitality, induces
a feeling of well-being, promotes circulatory and metabolic processes,
and stimulates the formation of vitamin D. Only low dose of sunlight
is necessary for this feeling of well-being to be achieved.
The
skin, through its own protective mechanisms, has the ability to protect
itself from the negative effects of the UV radiation. Among these
are:
 pigmentation
thickening of the
horny layer of the skin
DNA repair mechanisms
formation of the
body's own UV-filtering substances such as urocanic
acid
activation of the
body's own antioxidants
The skin's photoprotective mechanisms of pigment formation and thickening
of the stratum corneum require a period of about 2 to 4 weeks to develop
at low UV dosage levels.
Pigment formation (melanin synthesis)
Tanning results from the synthesis of melanin pigment-forming cells
(melanocytes) in the epidermis. The formation of pigment is induced
by UV radiation.
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Urocanic acid is formed by UVB radiation from
the amino acid histidine, in the keratin of the stratum corneum,
and only found in sweat. Urocanic acid protects from UVB radiation,
in that under its influence the trans form of urocanic acid is converted
into the high energy cis form. In this way, energy from radiation
is absorbed and dispersed.
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Pigmentation types: An individual's
sensitivity to UV radiation and the formation of a sun erythema is
determined by the thickness of the skin's horny layer and its pigment
content. Europeans are classified into 4 groups of pigmentation types:
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Epidermal melanin forms
a natural protection from the sun, by which the pigments reduce the
radiant energy by dispersion and absorption. The formation of more
melanin is then stimulated (indirect pigmentation).
Direct or immediate pigmentation is triggered mainly by UVA radiation:
Weakly coloured melanin precursors become darkened through oxidation.
However, this immediate tanning of the skin is transitory, and offers
only inadequate protection from the sun.
Melanosomes are transferred from the melanocytes to the keratinocytes
by means of so-called pigment units (one melanocyte per 36 keratinocytes).
The released melanin protects the DNA by surrounding the cell nuclei.
The pigment subsequently migrates to the skin surface along with the
epidermal cells.
Possibly a feedback mechanism is triggered by increased activity of
the enzyme tyrosinase needed for melanin formation leading to slowing
of the cell regeneration, thus causing a thickening in the horny layer
of the skin. |
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Stratum corneum thickening
Exposure to the sun stimulates the physiological light defences, leading
not only to melanin formation but also a considerable thickening of
the horny layer of the skin (hyperkeratosis). Along with melanin,
this forms an effective protection against UV radiation. |
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DNA
repair mechanisms
UVB irradiation can cause dose-dependent DNA-damage to the epidermal
cells. The skin has DNA repair mechanisms (excision repair and photoreactivation)
that can somewhat reduce the amount of cell-damage caused by the action
of light.
In the case of excision
repair (dark repair), damaged DNA-sections are recognised and removed
by enzymes. Through enzymatic synthesis, this DNA is replaced by intact
DNA segments.
In the case of photoreactivation,
damaged DNA-segments are repaired by an energy-dependent enzyme in
two steps. The enzyme obtains the energy required by absorbing UVA
radiation in the region of 340 to 430 nm.
However, if the skin is exposed for too long and left in the sun unprotected,
such as when on holiday, the skin's photoprotection is insufficient,
and the DNA repair mechanisms will be overburdened. The cells either
die from too much radiation damage, or deteriorate and transmit false
genetic information. The result is light-induced damage, along with
solar elastosis, precancerous lesions
and squamous cell carcinomas. These chronic
manifestations of light damage are irreversible, unlike acute light
damage (sun erythema).
Radical scavengers (antioxidants)
The cells of the skin are equipped with enzymes (such as superoxide
dismutase, peroxidase or glutathione) for protection against the cell-damaging
effects of free radicals. The most effective radical scavengers are
tocopherol, ascorbic acid and carotene, all of which are assimilated
with food. Melanin, formed by the melanocytes also acts as a radical
scavenger.
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Solar elastosis:
Damage to the connective tissue and atrophy of the skin cells through
chronic high-dosage UV radiation.
Squamous cell carcinoma: Skin carcinoma as a consequence of excessive,
cumulative UV exposure. |
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