内源性32p在脑膜炎奈瑟菌中的掺入。1 .二氧化碳和电子通量的影响。

S. Jyssum, K. Jyssum
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引用次数: 1

摘要

在Mg44和ADP存在的情况下,脑膜炎球菌提取物介导32P的掺入,EDTA的加入改善了这种掺入。这种结合的主要部分是由于多核苷酸磷酸化酶的活性,并且与电子通量无关。但是内源性呼吸也伴随着磷酸化。当细胞色素氧化酶被KCN抑制时,细胞色素氧化酶的磷酸化与添加的哺乳动物铁细胞色素c的内源性减少同时发生。当系统中含有KHCO3时,这种磷酸化几乎翻了一番。在以NADH、NADPH或铁细胞色素c作为电子源的脑膜炎球菌提取物中,不可能证明电子-氧运输水平上的氧化磷酸化。讨论了与电子通量相关的磷酸化,以及KHCO3对其的增强作用与脑膜炎奈瑟菌典型的CO2需求有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endogenous incorporation of 32 P in Neisseria meningitidis. I. The effects of CO2 and electron flux.
Meningococcal extracts mediate an incorporation of 32P in the presence of Mg44 and ADP which is improved by the addition of EDTA. A major part of this incorporation is due to a polynucleotide phosphorylase activity, and is independent of electron flux. But the endogenous respiration is also accompanied by a phosphorylation. When the cytochrome oxidase is inhibited by KCN phosphorylation occurs concomitantly with the endogenous reduction of added mammalian ferricytochrome c. This phosphorylation is nearly doubled when KHCO3 is included in the system. It has not been possible to demonstrate an oxidative phosphorylation on the electron-oxygen transport level in meningococcal extracts with NADH, NADPH or ferrocytochrome c as electron sources. The phosphorylation connected with electron flux, and its enhancement by KHCO3 have been discussed in relation to the CO2 requirements typical for N. meningitidis.
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