Skin’s Intrinsic Photoprotection
Sunlight has many positive effects on the body: It increases our vitality and well-being, promotes circulation and metabolic processes and activates vitamin D production. Just a small dose of sunlight is enough to achieve this “feeling of well-being”.
Through its own protective mechanisms the skin is able to protect itself from the negative effects of UV radiation. These mechanisms include:
- Pigmentation
- Thickening of the horny layer
- DNA repair mechanisms
- Formation of the body’s own UV filtering substances, such as urocanic acid
- Activation of the body’s own antioxidants
It takes about 2 to 4 weeks at a low UV dosage level for the skin to produce the pigmentation and thickening of the horny layer necessary for its own photoprotection.
Protective mechanisms
Pigment formation (melanin synthesis)
Tanning results from the synthesis of melanin in pigment- forming cells (melanocytes) of the epidermis. Pigment formation is induced by UV radiation.
In the epidermis, melanin pigments form a natural protection from the sun by reducing the radiation energy through dispersion and absorption. Formation of new melanin is stimulated (indirect pigmentation).
Direct or immediate pigmentation is triggered mainly by UVA radiation: Weakly coloured melanin precursors are darkened by 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 via the 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 with the epidermal cells.
A feedback mechanism triggered by the increased activity of the enzyme tyrosinase needed for melanin formation possibly also slows cell renewal, causing a thickening in the horny layer of the skin.
Pigmentation types:
An individual's sensitivity to UV radiation and proneness to sunburn are determined by the thickness of the skin's horny layer and its pigment content. Europeans are classified into 4 different pigmentation types:
Stratum corneum thickening
Exposure to sunlight stimulates physiological photoprotection, leading not only to melanin formation but also a considerable thickening of the horny layer (hyperkeratosis). Together with melanin this thickening forms an effective shield against UV radiation.
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 excision repair (dark repair), damaged DNA segments are recognised and removed by enzymes. The damaged DNA segments are replaced by intact segments produced by enzymatic synthesis.
In photoreactivation, damaged DNA segments are repaired by an energy-dependent enzyme in two steps. The enzyme obtains the energy required for this 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 inadequate, and the DNA repair mechanisms will be overburdened. The cells either die from too much radiation damage or they mutate and pass on false genetic information. The result is chronic light-induced damage with solar elastosis, precancerous lesions and squamous cell carcinomas. Unlike acute light-induced damage (sunburn), these chronic manifestations of light-induced damage are irreversible.
Urocanic acid
Urocanic acid is formed from the amino acid histidine in the keratinocytes of the stratum corneum and found only in sweat. After exposure to UVB radiation the trans isomer of urocanic acid is converted to the higher energy cis isomer, thus protecting the skin by absorbing and dissipating the harmful radiation energy.
Radical scavengers (antioxidants)
The cells of the skin are equipped with enzymes (such as superoxide dismutase and peroxidases) for protection against the cell-damaging effects of free radicals. Among the most effective radical scavengers are tocopherol, ascorbic acid and ß-carotene, all of which are assimilated with food. Melanin formed by the melanocytes also acts as a radical scavenger.
