Ziegler-Skylakakis K, Schwarz L R, Andrae U
Mutat Res. 1985 Nov-Dec;152(2-3):225-31. doi: 10.1016/0027-5107(85)90065-x.
The potential of N-hydroxyurea to induce gene mutations in V79 Chinese hamster cells was investigated. Upon metabolic activation by liver microsomes from phenobarbital-treated rats or by isolated rat hepatocytes co-cultured with the V79 cells, hydroxyurea caused a concentration-dependent increase in the frequency of HGPRT-deficient mutants. Hydroxyurea was not mutagenic in the absence of metabolic activation. Addition of catalase inhibited microsome-mediated mutagenicity, indicating that hydrogen peroxide was involved in the formation of the mutagenic DNA lesion. Acetohydroxamic acid and N-hydroxyurethane also induced hepatocyte-mediated mutagenicity, suggesting that the potential to elicit metabolism-dependent mutagenicity may be a common property of aliphatic hydroxamic acids.
研究了N-羟基脲在V79中国仓鼠细胞中诱导基因突变的潜力。经苯巴比妥处理的大鼠肝脏微粒体或与V79细胞共培养的分离大鼠肝细胞进行代谢活化后，羟基脲导致次黄嘌呤-鸟嘌呤磷酸核糖转移酶（HGPRT）缺陷型突变体频率呈浓度依赖性增加。在没有代谢活化的情况下，羟基脲没有致突变性。添加过氧化氢酶可抑制微粒体介导的致突变性，表明过氧化氢参与了诱变DNA损伤的形成。乙酰氧肟酸和N-羟基脲也诱导肝细胞介导的致突变性，提示引发代谢依赖性致突变性的潜力可能是脂肪族羟肟酸的共同特性。
