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肉桂醛对大肠杆菌化学诱导诱变的抗诱变作用分析。

Analysis of the antimutagenic effect of cinnamaldehyde on chemically induced mutagenesis in Escherichia coli.

作者信息

Ohta T, Watanabe K, Moriya M, Shirasu Y, Kada T

出版信息

Mol Gen Genet. 1983;192(3):309-15. doi: 10.1007/BF00392167.

Abstract

The antimutagenic effect of cinnamaldehyde on mutagenesis was investigated using ten kinds of chemical mutagen in Escherichia coli WP2s (uvr A-). In addition, the frequency of mutation induction by each mutagen in an SOS repair deficient (umuC-) strain was compared with that in a wild-type (umuC+) strain. Cinnamaldehyde greatly suppressed the umuC-dependent mutagenesis induced by 4-nitroquinoline 1-oxide (4-NQO), furylfuramide or captan. However, cinnamaldehyde was less effective against the umuC-independent mutagenesis by alkylating agents such as N-methyl-N'-nitro-N-nitrosoguanidine and ethylmethanesulfonate. On the other hand, no inhibitory effect of cinnamaldehyde was observed on prophage induction or tif-mediated filamentous growth. These results suggest that a cinnamaldehyde does not prevent the induction of the SOS functions. Despite the decrease in the number of revertants, a remarkable increase was observed in the survival of 4-NQO-treated WP2s cells after exposure to cinnamaldehyde. The reactivation of survival suggests the promotion of some DNA repair system by cinnamaldehyde. This enhancement of survival was also observed in uvr B, polA, recF or umuC mutants and less in lexA or recB, C mutants. However, it was not observed in recA mutants. Therefore, we assume that cinnamaldehyde may enhance an error-free recombinational repair system by acting on recA-enzyme activity.

摘要

使用十种化学诱变剂在大肠杆菌WP2s(uvr A-)中研究了肉桂醛对诱变作用的抗诱变效果。此外,还比较了每种诱变剂在SOS修复缺陷型(umuC-)菌株和野生型(umuC+)菌株中诱导突变的频率。肉桂醛能显著抑制由4-硝基喹啉1-氧化物(4-NQO)、糠基糠酰胺或克菌丹诱导的依赖umuC的诱变作用。然而,肉桂醛对由烷基化剂如N-甲基-N'-硝基-N-亚硝基胍和甲基磺酸乙酯引起的不依赖umuC的诱变作用效果较差。另一方面,未观察到肉桂醛对原噬菌体诱导或tif介导的丝状生长有抑制作用。这些结果表明,肉桂醛不会阻止SOS功能的诱导。尽管回复突变体数量减少,但在暴露于肉桂醛后,观察到经4-NQO处理的WP2s细胞的存活率显著增加。存活率的恢复表明肉桂醛促进了某些DNA修复系统。在uvr B、polA、recF或umuC突变体中也观察到了这种存活率的提高,而在lexA或recB、C突变体中则较少。然而,在recA突变体中未观察到。因此,我们推测肉桂醛可能通过作用于recA酶活性来增强无差错重组修复系统。

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