用大肠杆菌CM89菌株对三种化学物抗突变作用的研究  

Antimutagenic Effects of Three Chemicals in Escherichia coli Strain CM891

作　　者：郭峻[1] 金中初[1] 梅汝焕[1] 陈星若[1] 

机构地区：[1]浙江医科大学病理生理教研室,杭州310006

出　　处：《卫生毒理学杂志》1993年第1期16-19,共4页Journal of Health Toxicology

基　　金：国家自然科学基金

摘　　要：本文以 E.coli CM891为靶细胞,用细菌内抗突变作用模式研究了肉桂醛,鞣酸,二烯丙三硫的抗4NQO 突变性及其作用机制。含质粒 pKM101的 CM891的高抗株(抗50μg/ml 氨苄青霉素)能提高该菌株的自发突变率和4NQO 诱发的突变率以及对鞣酸的杀伤抗性。肉桂醛的抗突变性不依赖质粒 pKM101效应,但与暂时性生长延搁有关。鞣酸及二烯丙三硫的抗突变机制可能包括质粒 pKM101介导的易误修复。上述三种化学物中每二种联合应用均显示抗4NQO 突变性的协同效应及对靶细胞的毒性杀伤作用。Antimutagenic effects of cinnamaldehyde,tannic acid and diallyl trisulfide on 4-Nitroqu-inoline-l-oxide(4NQO)induced mutagenesis and their mechanisms were investigated with abio-antimutagenic model in Escherichia coli strain CM891.The CM891 strain carring plasmidpKM101 to a high dose(50μg/ml)ampenicillin resistance could increase spontaneous or 4 NQO-induced reversion mutation(trp^-→trp^+)and resistance to tannic acid—killing.Antimutageniceffect of cinnamaldehyde was due to a transient growth retardation,but not dependent on pl-asmid PKM101—mediated effects.Antimutagenic mechanisms of tannic acid and diallyl trisu- lfide might be involved in suppression to PKM101—mediated effects,via an analogical error—prone Pathway.Associating with each two of three chemicals mentioned above,their antimut-agenic and toxic effects on target cells were enhanced.

关 键 词：抗突变 肉桂醛 二烯丙三硫 

分 类 号：R730.1[医药卫生—肿瘤]