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A role for ultraviolet A in solar mutagenesis.

机译:紫外线A在太阳诱变中的作用。

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摘要

It is well established that exposure to solar UVB (290-320 nm) gives rise to mutations in oncogenes and tumor suppressor genes that initiate the molecular cascade toward skin cancer. Although UVA (320-400 nm) has also been implicated in multistage photocarcinogenesis, its potential contribution to sunlight mutagenesis remains poorly characterized. We have determined the DNA sequence specificity of mutations induced by UVB (lambda > 290 nm), and by UVA (lambda > 350 nm), at the adenine phosphoribosyltransferase locus of Chinese hamster ovary cells. This has been compared to results previously obtained for stimulated sunlight (lambda > or = 310 nm) and 254-nm UVC in the same gene. We demonstrate that T-->G transversions, a generally rare class of mutation, are induced at high frequency (up to 50%) in UVA-exposed cells. Furthermore, this event comprises a substantial proportion of the simulated sunlight-induced mutant collection (25%) but is significantly less frequent (P < 0.05) in cells irradiated with either UVB (9%) or UVC (5%). We conclude that the mutagenic specificity of broad-spectrum solar light in rodent cells is not determined entirely by the UVB component and that UVA also plays an important role.
机译:公认的是,暴露于日光UVB(290-320 nm)会引起致癌基因和抑癌基因的突变,从而引发针对皮肤癌的分子级联反应。尽管UVA(320-400 nm)也与多阶段光致癌作用有关,但其对日光诱变的潜在作用仍然很差。我们已经确定了在中国仓鼠卵巢细胞的腺嘌呤磷酸核糖基转移酶基因座上,由UVB(λ> 290 nm)和由UVA(λ> 350 nm)诱导的突变的DNA序列特异性。将该结果与先前在同一基因中对日光(λ>或= 310 nm)和254 nm UVC所获得的结果进行了比较。我们证明,在暴露于UVA的细胞中,高频率(高达50%)可以诱导T-> G转化,这是一种通常很少见的突变类型。此外,该事件在模拟的阳光诱导的突变体收集中占很大比例(25%),但在用UVB(9%)或UVC(5%)照射的细胞中发生的频率明显较低(P <0.05)。我们得出的结论是,啮齿动物细胞中广谱太阳光的诱变特异性并不完全由UVB组分决定,而且UVA也起着重要作用。

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