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本文以硝普钠（ＳＮＰ）为ＮＯ供体药物，研究慢性升高的ＮＯ对哺乳动物细胞的诱变作用和微核形成的影响。结果ＳＮＰ（２－８ｍＭ，不加或加Ｓ９）处理，均以剂量—反应方式诱发ｇ１２细胞ｇｐｔ位点突变，在最高受试剂量，诱变率分别超过本底１３和２５倍。在处理组还观察到含微核的双核细胞数显著增多。在０．５－４ｍＭ（＋Ｓ９）或２－８ｍＭ（－Ｓ９）ＳＮＰ剂量范围内，双核微核细胞率、微核率及含多微核的双核细胞比率均以剂量—依存方式增加。结果表明ＳＮＰ释放的ＮＯ过量积累可能是导致ｇ１２细胞遗传毒性的主要原因。
In this paper, sodium nitroprusside (SNP) as a NO donor drug to study the effects of chronic elevated NO on mammalian cell mutagenesis and micronucleus formation. Results SNP (2-8mM, without or with S9) all induced gpt site mutation in g12 cells by dose-response method. At the highest doses, the mutagenesis rates exceeded 13 and 25 times of the background, respectively. There was also a significant increase in the number of micronucleated binucleated cells in the treatment group. In the dose range of 0.5-4mM (+ S9) or 2-8mM (-S9) SNP, binucleate micronuclei, micronuclei and micronuclei containing binucleate cells both increased in a dose-dependent manner. The results show that SNP release of excessive accumulation of NO may be the main cause of genotoxicity of g12 cells.