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与二丁基亚硝胺相关的烷基-(ω-羟烷基)亚硝胺的致突变性

Mutagenicity of alkyl-(omega-hydroxyalkyl) nitrosamines related to dibutylnitrosamine.

作者信息

Olajos E J, Maverakis N, Cornish H H

出版信息

Mutat Res. 1978 Jan;56(3):219-23. doi: 10.1016/0027-5107(78)90188-4.

DOI:10.1016/0027-5107(78)90188-4
PMID:342939
Abstract

Various alkyl-(omega-hydroxyalkyl) derivatives related to dibutylnitrosamine (DBN) were investigated for mutagenicity in the absence of liver-activation system. Butyl-(4-hydroxybutyl)-, butyl-(3-hydroxypropyl)-, and butyl-(2-hydroxyethyl)-nitrosamines were so tested and found to be mutagenic for TA 1535 strain of Salmonella typhimurium. In all cases, a simple dose-response relationship was observed. Furthermore, no significant (p less than 0.05) differences in the mutagenicity of the various test compounds were observed as the alkyl sidechain possessing the OH group increased in length. From these results it is siggested that mutagenesis in S. typhimurium by the higher dialkylnitrosamines is partially due to the formation of omega-hydroxylated derivatives in addition to the major mutagenic metabolite derived from alpha-carbon dealkylation.

摘要

在没有肝激活系统的情况下,研究了与二丁基亚硝胺(DBN)相关的各种烷基-(ω-羟烷基)衍生物的致突变性。对丁基-(4-羟丁基)-、丁基-(3-羟丙基)-和丁基-(2-羟乙基)-亚硝胺进行了测试,发现它们对鼠伤寒沙门氏菌TA 1535菌株具有致突变性。在所有情况下,都观察到了简单的剂量反应关系。此外,随着含有OH基团的烷基侧链长度增加,未观察到各种测试化合物的致突变性有显著(p小于0.05)差异。从这些结果表明,除了由α-碳脱烷基产生的主要诱变代谢物外,较高的二烷基亚硝胺在鼠伤寒沙门氏菌中的诱变作用部分归因于ω-羟基化衍生物的形成。

相似文献

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Mutagenicity of alkyl-(omega-hydroxyalkyl) nitrosamines related to dibutylnitrosamine.与二丁基亚硝胺相关的烷基-(ω-羟烷基)亚硝胺的致突变性
Mutat Res. 1978 Jan;56(3):219-23. doi: 10.1016/0027-5107(78)90188-4.
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High mutagenicity of N-(alpha-acyloxy)alkyl-N-alkylnitrosamines in S. typhimurium: model compounds for metabolically activated N,N-dialkylnitrosamines.N-(α-酰氧基)烷基-N-烷基亚硝胺在鼠伤寒沙门氏菌中的高诱变性:代谢活化的N,N-二烷基亚硝胺的模型化合物
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引用本文的文献

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Interaction of mutagenic spermidine-nitrous acid reaction products with uvr- and recA-dependent repair systems in Salmonella.鼠伤寒沙门氏菌中诱变亚精胺-亚硝酸反应产物与uvr和recA依赖性修复系统的相互作用
J Bacteriol. 1980 Apr;142(1):191-5. doi: 10.1128/jb.142.1.191-195.1980.