Verna L K, Chen D, Schluter G, Williams G M
American Health Foundation, Valhalla, New York, USA.
Cell Biol Toxicol. 1998 Jun;14(3):237-42. doi: 10.1023/a:1007474912498.
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.
通过测量洛美沙星和紫外线A（UVA）照射的培养肝源细胞中的氧化性DNA损伤，研究了喹诺酮类抗生素的光遗传毒性机制。洛美沙星与UVA照射相结合，导致细胞DNA中7,8-二氢-8-氧代-2'-脱氧鸟苷（8-氧代-dG）呈剂量依赖性增加。通过与叠氮化钠（NaN3）或2,2,6,6-四甲基-4-哌啶酮（TMP）共同孵育，这种DNA损伤得到了显著抑制，这两种化学物质可特异性淬灭单线态氧。N-叔丁基-α-苯基硝酮（TBP）或α-生育酚主要清除羟基自由基，它们对8-氧代-dG的形成没有显著降低作用。我们得出结论，喹诺酮类药物光动力产生8-氧代-dG至少部分是由单线态氧介导的。
