Biochemical Change in Pancreas Mitochondria Following ischemia
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概要
- 論文の詳細を見る
Little or nothing have been demonstrated to characterize the effects of ischemia on energy metabolism of pancreas. In this study, evidence was presented that the phosphorylating mechanism of pancreas mitochondria is very labile and is the first to be lost.<BR>Guinea pigs were exsanguinated by decapitation and allowed to remain at 22°C for certain periods. After 2 minutes ischemia, the maximal phosphorylation rates in pancreas and brain mitochondria fell to one third of the initial rates, whereas in mitochondria from other tissues the initial rates of phosphorylation remained almost constant for ten minutes. In addition, another remarkable feature of the pancreas mitochondria was observed under ischemia that state 3 respiration with glutamate as a substrate declined rapidly, whereas that with succinate plus glutamate was not significantly affected. Thus the G/S ratio (state 3 respiration in the presence of glutamate/state 3 respiration in the presence of glutamate and succinate) declined to less than one third of the original value. Those facts have never been observed with brain, liver, kidney and heart mitochondria. The pattern of decrease of the G/S ratio occurring after a few minutes of ischemia was very similar to the corresponding pattern in tightly coupled mitochondria of pancreas upon aging at 22°C.<BR>The progressive decrease in the G/S ratio observed under ischemia or aging was found to occur simultaneously with a fall in lecithin and a concomitant rise in lysolecithin due to endogenous phospholipase A.<BR>On the other hand, "aging" of liver mitochondria in the presence of lysolecithin, the amount of which is in the order of magnitude of that released by aging of pancreas mitochondria for 10 minutes at 22°C, resulted in a rapid and almost linear decrease of the G/S ratio, very similar to those obtained with aging of pancreas mitochondria.<BR>From the results, it has been suggested that inhibition of the G/S ratio of aged mitochondria of pancreas could be due to hydrolysis of an unstable lecithin compound associated with the system, transfering electron from NADH to cytochrome <I>b</I> through the action of endogenous phospholipase A and the product of endogenous phospholipase A action, i.e. lysolecithin.
- Japan Society of Clinical Chemistryの論文
著者
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小沢 和恵
京都大学医学部外科学教室第二講座
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高三 秀成
京都大学医学部第1外科学教室
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本庄 一夫
京都大学医学部本庄外科
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北村 脩
京都大学医学部本庄外科
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酒井 晃
京都大学医学部本庄外科
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大沢 忠嗣
京都大学医学部本庄外科
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小沢 和恵
京都大学医学部本庄外科
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高三 秀成
京都大学医学部本庄外科
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本庄 一夫
京都大学医学部外科学第1講座
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