Ito K, Kawanishi S
Department of Public Health, Graduate School of Medicine, Kyoto University, Japan.
Biol Chem. 1997 Nov;378(11):1307-12.
This paper summarizes our recent findings on the sequence-specific DNA damage induced by UVA radiation in the presence of various endogenous molecules. The Type I (electron transfer) mechanism can induce hydroxylation specifically at C-8 of guanine located 5' to guanine in double-stranded DNA. In contrast, the major Type II (singlet oxygen) mechanism can damage most guanines without sequence specificity. With the minor Type II (superoxide anion radical) mechanism, DNA damage could be induced via metal-mediated reactions. Active species generated in the presence of Cu(II) were shown to induce piperidine-labile lesions frequently at thymine. We discuss the sequence-specific DNA damage in relation to UVA carcinogenesis.
本文总结了我们最近关于在各种内源性分子存在下,紫外线A辐射诱导的序列特异性DNA损伤的研究结果。I型(电子转移)机制可在双链DNA中位于鸟嘌呤5'端的鸟嘌呤的C-8位特异性诱导羟基化。相比之下,主要的II型(单线态氧)机制可无序列特异性地损伤大多数鸟嘌呤。对于次要的II型(超氧阴离子自由基)机制,DNA损伤可通过金属介导的反应诱导。已表明在铜(II)存在下产生的活性物质可在胸腺嘧啶处频繁诱导哌啶不稳定损伤。我们讨论了与紫外线A致癌作用相关的序列特异性DNA损伤。