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从链霉菌属代谢产物中分离出的N-甲基-缬氨酰氨甲蝶呤(BA-2)的抗诱变作用

Antimutagenic effects of N-methyl-valyl-amiclenomycin (BA-2) isolated from the metabolites of Streptomyces sp.

作者信息

Yamada T, Osawa T, Kawakishi S, Udaka S, Ohta T

机构信息

Department of Food Science and Technology, Nagoya University, Japan.

出版信息

Mutat Res. 1993 Apr;286(2):293-7. doi: 10.1016/0027-5107(93)90194-k.

DOI:10.1016/0027-5107(93)90194-k
PMID:7681541
Abstract

A novel antimutagenic factor, BA-2, active against UV-induced mutagenesis in Escherichia coli WP2 was isolated from the metabolites of Streptomyces sp. strain AJ9455. BA-2 also suppressed mutations induced by 4-nitroquinoline N-oxide (4-NQO) and furylfuramide (AF-2) in E. coli WP2s (uvrA) without any decrease of cellular viability. BA-2 strongly inhibited the UV induction of SOS repair functions when it was monitored by beta-galactosidase activity expressed from the sulA::lacZ fusion gene of strain PQ37. It is assumed that the antimutagenic effect of BA-2 on mutagenesis induced by UV, 4-NQO or AF-2 was the result of inhibition of induction of the inducible error-prone SOS repair. The structure of BA-2 was considered to be N-methyl-valyl-amiclenomycin, and the structural unit of 4-amino-2,5-cyclohexadiene must be essential for the antimutagenic activity, since deamination by heating results in the loss of antimutagenic activity of BA-2.

摘要

从链霉菌属菌株AJ9455的代谢产物中分离出一种新型抗诱变因子BA - 2,它对大肠杆菌WP2中紫外线诱导的诱变具有活性。BA - 2还能抑制4 - 硝基喹啉N - 氧化物(4 - NQO)和呋喃基糠酰胺(AF - 2)在大肠杆菌WP2s(uvrA)中诱导的突变,且不会降低细胞活力。当通过菌株PQ37的sulA::lacZ融合基因表达的β - 半乳糖苷酶活性监测时,BA - 2强烈抑制紫外线诱导的SOS修复功能。推测BA - 2对紫外线、4 - NQO或AF - 2诱导的诱变的抗诱变作用是抑制诱导型易错SOS修复诱导的结果。BA - 2的结构被认为是N - 甲基 - 缬氨酰 - 氨甲环霉素,4 - 氨基 - 2,5 - 环己二烯的结构单元对于抗诱变活性必定是必不可少的,因为加热脱氨会导致BA - 2失去抗诱变活性。

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