Inhibition by singlet oxygen quenchers of oxidative damage to DNA produced in cultured cells by exposure to a quinolone antibiotic and ultraviolet A irradiation.

The photogenotoxicity mechanism of quinolone antibiotics was investigated by measuring oxidative DNA damage in lomefloxacin- and UVA-exposed cultured liver-derived cells. The combination of lomefloxacin and UVA irradiation produced a dose-dependent increase in 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxo-dG) in cell DNA. This DNA damage was substantially inhibited by co-incubation with sodium azide (NaN3) or 2,2,6,6-tetramethyl-4-piperadone (TMP), chemicals that specifically quench singlet oxygen. No significant reduction of 8-oxo-dG formation was produced by N-t-butyl-alpha-phenylnitrone (TBP) or alpha-tocopherol, which primarily scavenge hydroxyl radicals. We conclude that the photodynamic generation of 8-oxo-dG by quinolones is mediated, at least in part, by singlet oxygen.