[Photocarcinogenesis].

Abstract

Sunlight-induced skin cancer is the most frequent cancer. Ultraviolet-B (UVB) (290-315 mm) and UVA (320-400 mm) radiation can induce DNA damage with resulting epithelial squamous cell carcinoma and melanoma by causing mutations and immunosuppressive effects that presumably contribute to photocarcinogenesis. The efficacy of photo- and photochemotherapeutic modalities is thought to result, at least in part, from the induction of immunomodulatory effects. In particular, UV radiation has been shown to affect (i) the production of soluble mediators, (ii) the expression of cell-surface receptors and (iii) to induce apoptosis in pathogenetically relevant cells. UVB radiation-induced immunomodulatory effects are limited to the epidermis, whereas UVA radiation-affects both epidermal and dermal cell populations. UVB and UVA radiation can exert essentially identical immunomodulatory effects, which result, however, from different photobiological mechanisms. UVB radiation-induced cyclobutane pyrimidine dimers within the DNA of epidermal cells are detrimental to human health. Photolyase-induced dimer repair completely prevented these UVB radiation-induced immunosuppressive effects as well as erythema and sunburn-cell formation. The Xeroderma pigmentosum (XP) is a rare syndrome of sensitivity to UV due to an inherited defect in nucleotide excision repair or daughter strand repair. Ionising radiation sensitivity is not part of the recognised syndrome. Extreme caution is advised before treating XP patients with radiotherapy. Determining the complementation group and radiosensitivity prior to treatment is recommended.