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关于小鼠腹水肿瘤细胞中巴斯德效应的机制。

On the mechanism of the Crabtree effect in mouse ascites tumor cells.

作者信息

Sauer L A

出版信息

J Cell Physiol. 1977 Nov;93(2):313-6. doi: 10.1002/jcp.1040930218.

DOI:10.1002/jcp.1040930218
PMID:563409
Abstract

The addition of glucose to ELD and ELT/B1 mouse ascites tumor cell suspensions caused a 2.3-fold increase in the phosphorylation state ratio, (ATP)/(ADP) (Pi), because of a decrease in the intracellular Pi concentration. The addition of glucose to these cell suspensions has been reported by Chance and Hess ('59) to cause an increase in the study state reduction of cytochrome b and an increase in the steady state oxidation of cytochrome c. On a quantitative basis these two independent measurements suggest that a near equilibrium exists between the oxidation-reduction state of the mitochondrial electron carriers and the reactions of ATP synthesis (as expressed by the phosphorylation state ratio) both before and after glucose addition. We conclude that the mechanism of the inhibition of respiration by glycolysis (the Crabtree effect) is a decrease in the rate of electron transport caused by the mass action effect of the elevated phosphorylation state ratio.

摘要

向ELD和ELT/B1小鼠腹水肿瘤细胞悬液中添加葡萄糖,由于细胞内无机磷酸(Pi)浓度降低,导致磷酸化状态比(ATP)/(ADP)(Pi)增加了2.3倍。Chance和Hess(1959年)报道,向这些细胞悬液中添加葡萄糖会导致细胞色素b的研究状态还原增加,以及细胞色素c的稳态氧化增加。从定量角度来看,这两项独立测量表明,添加葡萄糖前后,线粒体电子载体的氧化还原状态与ATP合成反应(以磷酸化状态比表示)之间存在近乎平衡的状态。我们得出结论,糖酵解对呼吸作用的抑制机制(即克氏效应)是由于升高的磷酸化状态比的质量作用效应导致电子传递速率降低。

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On the mechanism of the Crabtree effect in mouse ascites tumor cells.关于小鼠腹水肿瘤细胞中巴斯德效应的机制。
J Cell Physiol. 1977 Nov;93(2):313-6. doi: 10.1002/jcp.1040930218.
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