Reid T M, Loeb L A
Joseph Gottstein Memorial Cancer Research Laboratory, Department of Pathology, University of Washington School of Medicine, Seattle 98195.
Mutat Res. 1993 Oct;289(2):181-6. doi: 10.1016/0027-5107(93)90068-q.
Cytosine to thymine transitions are among the most common types of mutations produced by oxygen damage to DNA. One possible mechanism for these transitions is deamination of cytosine to uracil. Using both a forward mutation assay as well as a reversion assay specific for damage to cytosines we show that direct deamination to uracil does not play a significant role in mutagenesis induced by reactive oxygen free radicals. In contrast, lesions sensitive to repair by E. coli endonuclease III play a major role in oxidative mutagenesis as evidenced by the ability of endonuclease III to modulate the extent of mutagenesis that results from exposure of DNA to oxygen free radicals.
胞嘧啶向胸腺嘧啶的转变是DNA受氧损伤产生的最常见突变类型之一。这些转变的一种可能机制是胞嘧啶脱氨基形成尿嘧啶。我们使用正向突变试验以及针对胞嘧啶损伤的回复突变试验表明，直接脱氨基形成尿嘧啶在活性氧自由基诱导的诱变中不起重要作用。相比之下，对大肠杆菌内切酶III修复敏感的损伤在氧化诱变中起主要作用，这一点可由内切酶III调节DNA暴露于氧自由基所导致的诱变程度的能力来证明。
