Bacterial mutagenicity of cigarette smoke and its interaction with ethanol.
Bacterial mutagenicity of cigarette smoke and its interaction with ethanol.
复制标题
香烟烟雾的细菌致突变性及其与乙醇的相互作用。
作者：
S. Flora;R. Balansky;Laura Gasparini;A. Camoirano
采用鼠伤寒沙门菌和大肠埃希菌电池，研究了香烟主流烟雾（CS）、香烟烟气冷凝物（CSC）和吸烟者尿液的诱变性。当使用经典菌株TA98和TA100的硝基还原酶特别是o -乙酰转移酶过量衍生物时，s9介导的CSC致突变性显著增强，敏感性等级如下：YG1024 > YG1029 > YG1021 > TA98NR > YG1026 > TA98 > TA100 > TA100- dnp6 > TA100NR > TA98-1,8- dnp6。在我们的实验条件下，使用YG1024，在一根香烟中回收的烟雾冷凝物只有1/110的情况下，观察到自发回复物的两倍。同样，在TA98和TA100的o -乙酰转移酶过量衍生物YG1024和YG1029中，主流CS的s9介导的诱变性也显著增加。在没有S9混合物的情况下，来自5名吸烟者的23份尿液标本的浓缩物不能恢复鼠伤寒沙门氏菌TA98和YG1024，并且对大肠杆菌WP2和其修复缺陷的对应物CM871 （uvrA-, recA-, lexA-）是等量的。S9混合存在时，所有标本均具有诱变性，平均YG1024:TA98比值为6.6:1。这些模式表明，与烟相关的复杂混合物的细菌诱变性主要是由于芳香胺。与亲本菌株TA100相比，多环芳烃苯并[a]芘（BP）和烟草特异性亚硝胺4-（甲基亚硝胺）-1-（3-吡啶基）-1-丁酮（NNK）的诱变性在过量产生o -乙酰转移酶的菌株YG1029中没有明显增强。此外，BP和NNK在高剂量联合使用时诱导的诱变反应小于添加剂。（摘要删节250字）
The mutagenicities of mainstream cigarette smoke (CS), a cigarette smoke condensate (CSC) and smokers' urines were investigated by using batteries of Salmonella typhimurium and Escherichia coli strains. The S9-mediated mutagenicity of CSC was remarkably enhanced when using nitroreductase- and especially O-acetyltransferase-overproducing derivatives of the classical strains TA98 and TA100, with the following rank of sensitivity: YG1024 > YG1029 > YG1021 > TA98NR > YG1026 > TA98 > TA100 > TA100-DNP6 > TA100NR > TA98-1,8-DNP6. With YG1024, a doubling of spontaneous revertants was observed with as little as 1/110 of the smoke condensate recovered from one cigarette under our experimental conditions. Similarly, the S9-mediated mutagenicity of mainstream CS was considerably increased in YG1024 and YG1029, the O-acetyltransferase-overproducing derivatives of TA98 and TA100, respectively. In the absence of S9 mix, the concentrates of 23 urine specimens from five smokers failed to revert S. typhimurium TA98 and YG1024, and were equitoxic in E. coli WP2 and its repair-deficient counterpart CM871 (uvrA-, recA-, lexA-). In the presence of S9 mix, all specimens were mutagenic, with an average YG1024:TA98 ratio of 6.6:1. These patterns suggest that the bacterial mutagenicity of smoke-associated complex mixtures is mainly due to aromatic amines. The mutagenicities of other typical constituents of CS, i.e. the polycyclic aromatic hydrocarbon benzo[a]pyrene (BP) and the tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), were not appreciably enhanced in the O-acetyltransferase-overproducing strain YG1029, compared to its parental strain TA100. Moreover, BP and NNK induced less than additive mutagenic responses when combined at high doses.(ABSTRACT TRUNCATED AT 250 WORDS)