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短链有机酸对大肠杆菌K12的抑制作用:缺乏诱导SOS反应的证据。

Inhibition of Escherichia coli K12 by short-chain organic acids: lack of evidence for induction of the SOS response.

作者信息

Cherrington C A, Hinton M, Pearson G R, Chopra I

机构信息

Department of Veterinary Medicine, University of Bristol, Langford, Avon, UK.

出版信息

J Appl Bacteriol. 1991 Feb;70(2):156-60. doi: 10.1111/j.1365-2672.1991.tb04441.x.

DOI:10.1111/j.1365-2672.1991.tb04441.x
PMID:2019550
Abstract

Sublethal concentrations of formic acid (10 mmol/l) and propionic acid (5 mmol/l) at pH 5.0 preferentially inhibit DNA synthesis and stop cell multiplication in the absence of a corresponding cessation in the increase of culture turbidity. The possibility that the acids induce the SOS response by starving cells of thymine or by causing physical damage to the DNA molecule has now been investigated. Accumulation of thymine into the cytoplasm of whole cells was not inhibited by either acid. Mutants defective in excision repair (uvr A6), recombination repair (rec A56) and polymerase activity (pol A1) were not more sensitive to the acids than their isogenic parent. No significant increase in cell length was observed from measurements of transmission electron microscope images of acid-treated cells. It is concluded, therefore, that sublethal concentrations of formic and propionic acid inhibit DNA synthesis without physically damaging DNA molecule, or starving the cell of essential thymine or otherwise inducing an SOS response.

摘要

在pH 5.0条件下,亚致死浓度的甲酸(10 mmol/l)和丙酸(5 mmol/l)优先抑制DNA合成并阻止细胞增殖,同时培养液浊度的增加并未相应停止。目前已经研究了这些酸是通过使细胞缺乏胸腺嘧啶还是对DNA分子造成物理损伤来诱导SOS反应的可能性。两种酸均未抑制胸腺嘧啶在全细胞胞质中的积累。切除修复缺陷型(uvr A6)、重组修复缺陷型(rec A56)和聚合酶活性缺陷型(pol A1)的突变体对这些酸的敏感性并不比其同基因亲本更高。通过对酸处理细胞的透射电子显微镜图像测量,未观察到细胞长度有显著增加。因此得出结论,亚致死浓度的甲酸和丙酸抑制DNA合成,但不会对DNA分子造成物理损伤,也不会使细胞缺乏必需的胸腺嘧啶或以其他方式诱导SOS反应。

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Inhibition of Escherichia coli K12 by short-chain organic acids: lack of evidence for induction of the SOS response.短链有机酸对大肠杆菌K12的抑制作用:缺乏诱导SOS反应的证据。
J Appl Bacteriol. 1991 Feb;70(2):156-60. doi: 10.1111/j.1365-2672.1991.tb04441.x.
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