Abstract
8-Methoxypsoralen (8-MOP) is used for photochemotherapy of psoriasis and vitiligo. In therapy, called PUVA therapy, the affected skin of a patient who has previously been prescribed 8-MOP is irradiated with UV-A (> 320 nm). As a result of the photochemical reaction, 8-MOP forms a covalent bond with the pyrimidine bases of DNA and forms both monofunctional and bifunctional adducts. The latter cause 8-MOP-mediated cytotoxicity, leading to the death of psoriatic cells. However, in surviving cells, these same adducts can cause 8-MOP genotoxicity. For a comparative study of the cytotoxicity and genotoxicity of 8-MOP, the E. coli MG1655 lux biosensor (pColD-lux), carrying a recombinant plasmid with a lux operon controlled by the colD gene promoter, was first used. The colD gene (cda) is part of the E. coli SOS-regulon, which provides DNA repair and cell resistance to DNA damage. The death of bacteria was taken into account as an indicator of the cytotoxicity of 8-MOP+UV-A, and the death of bacteria was taken into account by the change in the luminescence intensity of the biosensor. Induction of 8-MOP-mediated SOS-response in bacteria depends on the dose of UV-A, and on the concentration of 8-MOP. At high UV-A doses, a 25-fold decrease in the survival of bacterial cells was detected (from 2 × 108 to 8 × 106 CFU), and in viable cells, an increase in the intensity of the SOS response by 675 times in terms of 106 cells. Thus, it was shown that in the bacterial test system, the genotoxic effect of 8-MOP is several times higher than its cytotoxicity. Key words: 8-methoxypsoralen, lux biosensor, E. coli, colD gene promoter, SOS response, UV radiation, adducts.