Participação de enzimas de reparo por excisão de bases na restauração de lesões induzidas pela associação da radiação ultravioleta A e cloreto estanoso em Escherichia coli

Abstract

Stannous chloride (SnCl2) and ultraviolet radiation A (UVA) are able to induce lesions in different cellular structures, including DNA, manly through ROS generation. The aim of this work was to study the mutagenesis and repair of lesions induced by the association of UVA (pre treatment) with SnCl2. It was evaluated the action of base excision repair (BER) enzymes in Escherichia coli (E. coli) by alkaline gel electrophoresis and bacterial survival. It was also evaluated the SoxRS system induction by chromotest and mutagenesis through the Ames test. According to the results: i) UVA induced DNA strand breaks in all strains and fpg-nfo and fpg mutants showed greater delay in the repair of lesions; ii) SnCl2 induced more breaks than UVA and nfo and fpg mutants showed more difficult to repair the damage; iii) UVA + SnCl2 caused more breaks than the SnCl2 and nfo and fpg mutants also showed a slowest repair of injuries; iv) UVA did not inactivate any bacterial strains tested; v) nfo and fpg strains were more sensitive to SnCl2; vi) UVA + SnCl2 caused higher mortality in all strains tested, when compared to SnCl2, and, again, nfo and fpg mutants were the most sensitives to the treatment with both agents; vii) the transformation of nfo mutant with the plasmid pBW21 (nfo+) and fpg mutants with plasmid pFPG (fpg+) increased the survival of the strains to SnCl2 and UVA + SnCl2 treatments; viii) SnCl2 was able to induce SoxRS system; ix) SnCl2, UVA + SnCl2 and UVA did not induce mutagenesis; x) damage repair seems to be preferentially performed by Fpg and Nfo proteins.