CUTANEOUS PHOTOCHEMOPROTECTION ASSOCIATED WITH APOPTOSIS AND PROLIFERATION INDUCED BY ULTRAVIOLET-B RADIATION IN THE HAIRLESS MICE

Previous studies have indicated that solar ultraviolet (UV) radiation is the major etiological agent in skin cancer development. The first step in skin carcinogenesis by UV radiation involves the induction of DNA damage, which then leads to a cascade of events including cell cycle arrest, DNA repair, mutation, and transformation.We examined the effects of ultraviolet (UV) radiationon the time course for induction of expression of proteins known to be associated with growth arrest and apoptosis in SKHhr1 mouse skin. Sixty female mice SKH-1 randomly divided in six groups of 10 animals each were formed. Two extracts (Caluna vulgaris and a grape seed extract) were applied 30 minutes before the UVB (240 mJ/cm2) irradiation and exposures were made 10 consecutive days. Skin tissues were analyzed at various times after irradiation (1 hour, 24 hours and 10 days) for the presence of apoptotic cells (caspase 3) and expression of p53, bcl-2, bax, and proliferating cell nuclear antigen. Our results indicated that p53 expression was induced early in the epidermis, reaching maximum levels 24 hours after irradiation. UV radiation induced high levels of bax at 24 hours after irradiation with a concomitant decrease in bcl-2 expression. Apoptotic cells reached a maximum at 24 hours after irradiation. Proliferating cell nuclear antigen expression, initially confined to the basal layer, became dispersed throughout the basal and suprabasal layers of the skin at 10 days and paralleled marked hyperplasia. Thus UV irradiation induces apoptosis mediated by the p53/ bax/bcl-2 pathway and dead cells are replaced by hyperproliferative cells (epidermal hyperplasia) and the Burgund and Caluna vulgaris extracts reduces the negative effects of UV radiations.