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Differential Effect of UV-B and UV-C on DNA Damage in L-132 Cells

机译:UV-B和UV-C对L-132细胞DNA损伤的差异作用

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Ultraviolet radiation is known to induce skin cancer. The induction of DNA damage caused by UV-B and UV-C was investigated using cultured L-132 cells. DNA strand breaks assayed by the alkaline elution procedure occurred in a dose-dependent manner, the extent of the strand breaks were inversely well correlated with the number of viable L-132 cells after 24 h incubation. About a 10-fold dose of UV-B irradiation was required to induce a similar degree of strand breaking to that induced by UV-C. Similarly about a 10-fold dose of UV-B was required to produce a similar amount of pyrimidine dimers, such as cyclobutane-type dimers and pyrimidine-(6-4)-pyrimidone photoproducts, which were determined by EL1SA using the specific monoclonal antibody, to that produced by UV-C. Strand breaks induced by UV-B, however, were not fully repaired in viable cells remaining after incubation of cells for a longer period of time, although UV-C-induced strand breaks were repaired in a time-dependent manner. Furthermore, an experiment with a cell-free system, where the induction of strand breaks by repair enzymes did not take place, indicated that UV-B caused significantly more direct DNA strand breaks than that caused by one-tenth the dose of UV-C. The data shown here suggest that UV-B-induced DNA damage is mediated, at least in part, via a different mechanism from the UV-C induced one.
机译:已知紫外线辐射会诱发皮肤癌。使用培养的L-132细胞研究了由UV-B和UV-C引起的DNA损伤的诱导。通过碱性洗脱程序测定的DNA链断裂以剂量依赖性方式发生,在24小时温育后,链断裂的程度与存活的L-132细胞的数量成反比。需要大约10倍剂量的UV-B辐射来诱导与UV-C诱导的相似程度的链断裂。同样,需要约10倍剂量的UV-B才能产生类似量的嘧啶二聚体,例如环丁烷型二聚体和嘧啶-(6-4)-嘧啶酮光产物,这是由EL1SA使用特异性单克隆抗体测定的,由UV-C产生。然而,尽管紫外线-C诱导的链断裂以时间依赖性方式修复,但是在长时间孵育后剩余的存活细胞中,UV-B诱导的链断裂并未得到完全修复。此外,在无细胞系统的实验中,未发生修复酶诱导的链断裂,这表明,UV-B引起的直接DNA链断裂比由十分之一的UV-C剂量引起的直接断裂要明显得多。 。此处显示的数据表明,UV-B诱导的DNA损伤至少部分是通过与UV-C诱导的DNA损伤机制不同的机制介导的。

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