Skin's Own Photo Protection

Through its own protective mechanisms, the skin had the ability to protect itself against the negative effects of UV radiation.  These protective mechanisms include:

• Pigmentation & Thickening of the Horny Layer
• DNA Repair Mechanisms
• Formation of the body’s own UV filtering substances, such as urocanic acid
• 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.
• Activation of the body’s own antioxidants

Pigmentation & Thickening of the Horny Layer

Tanning results from the synthesis of melanin pigment-forming cells (melanocytes) in the epidermis. The formation of pigment is induced by UV radiation.  An individual's sensitivity to UV radiation and the formation of a sun burn is determined by the thickness of the skin's horny layer and its pigment content.  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: lightly colored melanin precursors become darkened through oxidation. This immediate tanning of the skin offers inadequate sun protection.  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.  Melanin formation slows down cell regeneration which causes the horny layer of the skin to thicken.

DNA Repair Mechanisms

The skin has DNA repair mechanisms (excision repair and photoreactivation) that can somewhat reduce the amount of cell-damage caused by light.

In 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 photoreactivation, damaged DNA-segments are repaired by an energy-dependent enzyme in two steps.

If the skin is exposed for too long and left in the sun unprotected, 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. This damage is irreversible. 

Radical Scavengers (Antioxidants)
The cells of the skin are equipped with enzymes to protect against the cell-damaging effects of free radicals. The most effective radical scavengers are tocopherol, ascorbic acid and carotene, all of which come from food. Melanin, formed by the melanocytes also acts as a radical scavenger.