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在受到氧化应激毒害的大肠杆菌中糖异生作用的持续性

Persistence of gluconeogenesis in Escherichia coli poisoned by oxidant stress.

作者信息

Brown O R

机构信息

Department of Veterinary Biomedical Sciences, School of Medicine, University of Missouri, Columbia 65211.

出版信息

Microbios. 1990;62(252-253):179-86.

PMID:2195303
Abstract

The poisoning (inhibition of growth rate) of Escherichia coli by 4.2 atmospheres of hyperbaric oxygen was less when the culture energy source was glucose, fructose-6-phosphate, or glycerol, compared to pyruvate, oxaloacetate, or amino acids. This was consistent with previous indirect data which pointed to impaired gluconeogenesis in the toxicity mechanism. However, the three enzymes unique to gluconeogenesis (fructose-1, 6-diphosphatase, phosphoenolpyruvate synthase and phosphoenolpyruvate carboxyl-kinase) were not decreased in specific activity to a biologically significant extent in cell-free extract of cells poisoned by hyperbaric oxygen. Net glycogen synthesis in vivo was not decreased from glycerol, pyruvate or oxaloacetate, compared to glucose in cells exposed to oxidant stress from hyperbaric oxygen or 1 mM aerobic paraquat with cells exposed as exponentially growing cells prior to assay or as resting cells during the assay.

摘要

当培养能量源为葡萄糖、6-磷酸果糖或甘油时,与丙酮酸、草酰乙酸或氨基酸相比,4.2个大气压的高压氧对大肠杆菌的毒害作用(生长速率抑制)较小。这与之前的间接数据一致,这些数据表明糖异生受损存在于毒性机制中。然而,在高压氧中毒细胞的无细胞提取物中,糖异生特有的三种酶(果糖-1,6-二磷酸酶、磷酸烯醇丙酮酸合酶和磷酸烯醇丙酮酸羧激酶)的比活性并未降低到具有生物学意义的程度。与在测定前以指数生长细胞或在测定期间以静止细胞暴露于高压氧或1 mM需氧百草枯的氧化应激下的细胞中的葡萄糖相比,体内由甘油、丙酮酸或草酰乙酸合成的糖原净量并未减少。

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