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辐射诱导产生的长寿命自由基会导致突变和转化。

Radiation-induced long-lived radicals which cause mutation and transformation.

作者信息

Koyama S, Kodama S, Suzuki K, Matsumoto T, Miyazaki T, Watanabe M

机构信息

Laboratory of Radiation and Life Science, School of Pharmaceutical Sciences, Nagasaki University, 14-1 Bunkyo-machi, Nagasaki 852-8521, Japan.

出版信息

Mutat Res. 1998 Oct 12;421(1):45-54. doi: 10.1016/s0027-5107(98)00153-5.

Abstract

Using electronic spin resonance (ESR), we found a new type of radical with a long life-time in cells (T1/2>20 h) and which may play a more important role in the induction of mutation and transformation than either the active, short-lived, H, or OH radicals. When cells were treated with dimethyl sulfoxide (DMSO) and l-ascorbic acid (AsA) just before irradiation, the short-lived radicals were well-scavenged. On the other hand, if cells were treated with the scavengers 20 min after irradiation, then AsA scavenged the long-lived radicals, but DMSO did not. AsA treatment 20 min after the start of irradiation drastically reduced both the frequencies of mutation at the hypoxanthine guanine phosphoribosyl transferase (HGPRT) locus in human cells and morphological transformations in mouse m5S cells, but DMSO treatment did not. In addition, AsA treatment 20 h after irradiation also reduced the mutation frequency in human cells. These results suggested that mutations and morphological transformation are probably caused by the presence of long-lived radicals in the cells, rather than by short lived radicals, and that AsA reacts efficiently with long-lived radicals, resulting in a decrease of the mutations and transformations induced.

摘要

利用电子自旋共振(ESR),我们在细胞中发现了一种新型自由基,其具有较长的寿命(T1/2>20小时),并且在诱导突变和转化方面可能比活性短寿命的H或OH自由基发挥更重要的作用。当细胞在照射前用二甲基亚砜(DMSO)和L-抗坏血酸(AsA)处理时,短寿命自由基被有效清除。另一方面,如果细胞在照射后20分钟用清除剂处理,那么AsA可以清除长寿命自由基,但DMSO不能。照射开始后20分钟进行AsA处理可显著降低人类细胞中次黄嘌呤鸟嘌呤磷酸核糖转移酶(HGPRT)位点的突变频率以及小鼠m5S细胞中的形态转化频率,但DMSO处理则没有这种效果。此外,照射后20小时进行AsA处理也降低了人类细胞中的突变频率。这些结果表明,突变和形态转化可能是由细胞中长寿命自由基的存在引起的,而不是短寿命自由基,并且AsA能与长寿命自由基有效反应,从而导致诱导的突变和转化减少。

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