VITAMIN E-DEFICIENCY IN GUINEA PIG - EFFECT OF SUCCINATE ON MITOCHONDRIAL NAD-LINKED OXIDATION

被引:3
作者
CARABELLO, FB
BIRD, JWC
机构
[1] Department of Physiology, Biochemistry Rutgers University, New Brunswick, NJ
基金
美国国家卫生研究院;
关键词
D O I
10.1016/0006-291X(69)90533-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Control of β-hydroxybutyrate oxidation by succinate occurred via two mechanisms in E+ liver mitochondria and one of these was energy-dependent (reversal of electron transport). Addition of an energy trapping system (Pi-acceptor) to E+ mitochondria resulted in loss of energy-dependent control by succinate. Pi-acceptor had no effect on control in E- mitochondria, indicating that reversal of electron transport was not functional in these preparations. ATP was inefficient as an energy source for succinate control in E- mitochondria. Menadione inhibited control of β-hydroxybutyrate oxidation in both E- and E+ mitochondria. The effect of menadione is consistent with its capacity to by-pass the NADH-Coenzyme Q reductase segment of the respiratory chain. © 1969.
引用
收藏
页码:92 / +
页数:1
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