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野生型大肠杆菌K-12对甲基乙二醛毒性浓度的积累。

Accumulation of toxic concentrations of methylglyoxal by wild-type Escherichia coli K-12.

作者信息

Ackerman R S, Cozzarelli N R, Epstein W

出版信息

J Bacteriol. 1974 Aug;119(2):357-62. doi: 10.1128/jb.119.2.357-362.1974.

Abstract

Wild-type strains of Escherichia coli K-12 accumulate toxic concentrations of methylglyoxal when grown in medium containing adenosine 3',5'-monophosphate and either d-xylose, l-arabinose, or d-glucose-6-phosphate, independent of the presence of other carbon sources. Mutations at a locus called cxm specifically block methylglyoxal formation from xylose in the presence of adenosine 3',5'-monophosphate. Accumulation in medium containing xylose, studied in some detail, is dependent on the ability to utilize xylose and is associated with an increased rate of xylose utilization without changes in levels of xylose isomerase. These results suggest that adenosine 3',5'-monophosphate results in induction of excessively high levels of an early rate-limiting step in xylose metabolism. This step may be the transport of xylose into the cell. The resulting excessive rates of xylose catabolism could stimulate methylglyoxal formation by overburdening late steps in glycolysis.

摘要

当在含有3',5'-单磷酸腺苷以及d-木糖、l-阿拉伯糖或6-磷酸-d-葡萄糖的培养基中生长时,野生型大肠杆菌K-12菌株会积累有毒浓度的甲基乙二醛,这与其他碳源的存在无关。在一个名为cxm的位点发生的突变,在3',5'-单磷酸腺苷存在的情况下,能特异性地阻止木糖形成甲基乙二醛。在含有木糖的培养基中的积累情况已得到较为详细的研究,它取决于利用木糖的能力,并且与木糖利用率的提高相关,而木糖异构酶水平并无变化。这些结果表明,3',5'-单磷酸腺苷会导致木糖代谢中一个早期限速步骤的水平被过度诱导升高。这个步骤可能是木糖转运进入细胞。由此导致的木糖分解代谢速率过高,可能会因使糖酵解后期步骤负担过重而刺激甲基乙二醛的形成。

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