Mroczkowska M M, Kuśmierek J T
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warszawa.
Mutagenesis. 1991 Sep;6(5):385-90. doi: 10.1093/mutage/6.5.385.
The miscoding potential of N2,3-ethenoguanine (epsilon G), one of the carcinogen vinyl chloride adducts to DNA bases, has been evaluated in an Escherichia coli DNA-dependent RNA polymerase in vitro system. Epsilon G present in poly(C) templates causes incorporation of cytosine (C), uridine (U) and adenosine (A) under competitive and non-competitive conditions, and in the presence of either Mn2+ and Mg2+ cations, indicating that this modified base still retains the coding properties of unmodified G and can also act as A or U. The formation of hydrogen bonded pairs between different tautomeric forms of epsilon G and C, U and A is proposed. The possible role of epsilon G, along with a role of other vinyl chloride adducts in causing of GC----AT transitions, the most frequent mutation induced by a vinyl chloride metabolite, is discussed.
N2,3-乙烯基鸟嘌呤（εG）是致癌物氯乙烯与DNA碱基的加合物之一，其错编码潜力已在大肠杆菌DNA依赖性RNA聚合酶体外系统中进行了评估。聚（C）模板中的εG在竞争和非竞争条件下，以及在存在Mn2+和Mg2+阳离子的情况下，会导致胞嘧啶（C）、尿苷（U）和腺苷（A）的掺入，这表明这种修饰碱基仍保留未修饰G的编码特性，并且还可以充当A或U。有人提出εG的不同互变异构形式与C、U和A之间形成氢键对。本文讨论了εG以及其他氯乙烯加合物在导致GC→AT转换（氯乙烯代谢产物诱导的最常见突变）中可能发挥的作用。
