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首页> 外文期刊>Mutation Research, C. Mutation Research Letters >SYNERGISTIC ACTION OF N-NITROSODIALKYLAMINES AND NEAR-UV IN THE INDUCTION OF CHROMOSOME ABERRATIONS IN CHINESE HAMSTER LUNG FIBROBLASTS IN VITRO
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SYNERGISTIC ACTION OF N-NITROSODIALKYLAMINES AND NEAR-UV IN THE INDUCTION OF CHROMOSOME ABERRATIONS IN CHINESE HAMSTER LUNG FIBROBLASTS IN VITRO

机译：N-亚硝基苯乙酰胺和近紫外光在体外诱导中国仓鼠成纤维细胞染色体异常协同作用

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N-Nitrosodialkylamines are promutagens and proclastogens, requiring metabolic activation for their actions. Previously, we showed that direct-acting bacterial mutagens can be formed from N-nitrosodialkylamines on exposure to near-UV. We have now found that N-nitrosodialkylamines with near-UV irradiation are clastogenic to Chinese hamster lung cells. When the cells in culture were irradiated with near-UV for 3h in the presence of N-nitrosodimethylamine (NDMA), N-nitrosodiethylamine (NDEA), N-nitrosopyrrolidine (NPYR), N-nitrosopiperidine (NPIP) or N-nitrosomorpholine (NMOR), and then further incubated for a total period of 24h with the N-nitrosodialkylamines, chromosome aberrations were induced. Neither the N-nitrosodialkylamine nor near-UV alone were clastogenic. Severe clastogenicity(> 50% of cells examined showing aberrations) was observed for 0.5 mM NDEA, NPYR and NPIP. The order of the clastogenic activity was NDEA, NPYR > NPIP, NDMA > NMOR. This order differed from that of bacterial mutagenicity previously reported for these N-nitrosodialkylamines plus near-UV, in which NMOR gave the strongest activity. The chromosome aberrations induced by the NPYR and NDEA plus near-UV in CHL-cells were inhibited by superoxide dismutase, glutathione and L-cysteine. Dimethylsulfoxide or D-mannitol, scavengers of hydroxy radical, and L-histidine, a scavenger of singlet oxygen, were ineffective. These results suggest that superoxide formed by a synergistic action of an N-nitrosodialkylamine and near-UV is the cause of the chromosome aberrations observed, an assumption consistent with the known ability of superoxide to cleave DNA.
机译：N-亚硝基二烷基胺是promutagens和proclastogens，需要代谢激活才能发挥作用。以前，我们表明暴露于近紫外光时，N-亚硝基二烷基胺可形成直接作用的细菌诱变剂。现在我们发现，具有近紫外线照射的N-亚硝基二烷基胺对中国仓鼠肺细胞具有致死作用。当在N-亚硝基二甲胺（NDMA），N-亚硝基二乙胺（NDEA），N-亚硝基吡咯烷（NPYR），N-亚硝基哌啶（NPIP）或N-亚硝基吗啉（NMOR）存在下用近紫外线照射培养的细胞3小时），然后与N-亚硝基二烷基胺共孵育24小时，诱导染色体畸变。单独的N-亚硝基二烷基胺和近紫外光都不会造成致死作用。对于0.5 mM NDEA，NPYR和NPIP，观察到了严重的致胶性（> 50％的细胞显示出畸变）。致胶凝活性的顺序是NDEA，NPYR> NPIP，NDMA> NMOR。该顺序不同于先前报道的这些N-亚硝基二烷基胺加近紫外光的致突变性，其中NMOR具有最强的活性。超氧化物歧化酶，谷胱甘肽和L-半胱氨酸可抑制NPYR和NDEA加上CHL细胞中的近紫外线诱导的染色体畸变。二甲基亚砜或D-甘露糖醇（羟基自由基的清除剂）和L-组氨酸（单线态氧的清除剂）无效。这些结果表明，由N-亚硝基二烷基胺和近紫外光的协同作用形成的超氧化物是观察到的染色体畸变的原因，该假设与已知的超氧化物裂解DNA的能力一致。

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