STIMULATION OF RESPIRATORY-CHAIN OF RAT-LIVER MITOCHONDRIA BETWEEN CYTOCHROME C1 AND CYTOCHROME-C BY GLUCAGON TREATMENT OF RATS
STIMULATION OF RESPIRATORY-CHAIN OF RAT-LIVER MITOCHONDRIA BETWEEN CYTOCHROME C1 AND CYTOCHROME-C BY GLUCAGON TREATMENT OF RATS
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DOI：
10.1042/bj1720399
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发表时间：
1978-01-01
影响因子：
4.1
通讯作者：
HALESTRAP, AP
中科院分区：
文献类型：
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作者：
HALESTRAP, AP
高血糖素处理的大鼠线粒体氧化琥珀酸，而不是抗坏血酸+四甲基苯二胺，在非偶联状态下，比对照线粒体氧化得更快。在两种底物存在下的氧气吸收速率等于单独存在其中一种底物时氧气吸收速率的总和。结论：线粒体呼吸链在细胞色素带之间的某一点受到限制，这一步受高血糖素的调节。在琥珀酸和鱼藤酮存在的非偶联条件下，细胞色素光谱的测量表明，对照线粒体与胰升糖素处理的大鼠相比，细胞色素c1和细胞色素c1发生了交叉，对照线粒体的细胞色素被更多地氧化，细胞色素c1被更多地减少。在研究丙酮酸代谢的条件下，对照线粒体一般比高血糖素处理的大鼠线粒体氧化程度更高，细胞色素B-566的氧化还原状态与蔗糖介质中丙酮酸代谢的速度有关。然而，当考虑到线粒体的氧化还原状态时，细胞色素和c1之间的交叉再次明显。细胞色素的光谱是复杂的，但细胞色素B-562似乎比对照组线粒体中细胞色素B-566的减少更严重。这可以用胰升糖素处理的大鼠体内存在一种更碱性的基质来解释，即细胞色素的氧化还原电位对pH敏感。结论：胰升糖素可刺激细胞色素1和细胞色素C之间的电子流动。对这些发现的生理学意义进行了讨论。
Mitochondria from glucagon-treated rats oxidize succinate, but not ascorbate plus tetramethylphenylenediamine, faster in the uncoupled state than do control mitochondria. The rate of O2uptake in the presence of both substrates is equal to the sum of the rates of the O2uptake in the presence of either substrate alone. It is concluded that the mitochondrial respiratory chain is limited at some point between cytochromesbandcand that this step is regulated by glucagon. Measurement of the cytochrome spectra under uncoupled conditions in the presence of succinate and rotenone demonstrates a crossover between cytochromescandc1when control mitochondria are compared with those from glucagon-treated rats, cytochromecbeing more oxidized and cytochromec1more reduced in control mitochondria. Under conditions where pyruvate metabolism is studied the control mitochondria are generally more oxidized than those from glucagon-treated rats, the redox state of cytochromeb-566 correlating with the rate of pyruvate metabolism in sucrose medium. However, when the redox state of the mitochondria is taken into account, a crossover between cytochromescandc1is again apparent. The spectra of thebcytochromes are complex, but cytochromeb-562 appears to become more reduced relative to cytochromeb-566 in mitochondria from glucagon-treated rats than in control mitochondria. This can be explained by the existence of a more alkaline matrix in glucagon-treated rats, the redox potential for cytochromebbeing pH-sensitive. It is concluded that glucagon stimulates electron flow between cytochromesc1andc. The physiological significance of these findings is discussed.