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小鼠核黄素缺乏及恢复过程中肝脏线粒体氧化代谢与形态的关系

Relationship between hepatic mitochondrial oxidative metabolism and morphology during riboflavin deficiency and recovery in mice.

作者信息

Hoppel C L, Tandler B

出版信息

J Nutr. 1976 Jan;106(1):73-6. doi: 10.1093/jn/106.1.73.

Abstract

Changes in hepatic mitochondrial oxidative metabolism were examined during the development of severe riboflavin deficiency in mice, and during recovery from this deficiency. There was a marked reduction in oxidative rates for all substrates tested, with the decline being most pronounced with palmitoyl-1-carnitine. These effects were not enhanced by addition of galactoflavin to the riboflavin-deficient diet. Treatment of the deficient mice with riboflavin restored hepatic mitochondrial oxidation to normal within 24 hours in those mice fed a simple riboflavin-deficient diet, but required 72 hours in galactoflavin-supplemented mice. These metabolic changes in hepatic mitochondria appear to be temporally independent of the striking morphological changes occurring in these organelles during ariboflavinosis and recovery.

摘要

在小鼠严重核黄素缺乏症的发展过程中以及从这种缺乏症恢复的过程中,对肝脏线粒体氧化代谢的变化进行了研究。所有测试底物的氧化速率均显著降低,其中以棕榈酰-1-肉碱的下降最为明显。在核黄素缺乏的饮食中添加半乳糖黄素并不能增强这些作用。用核黄素治疗缺乏症小鼠时,对于喂食简单核黄素缺乏饮食的小鼠,肝脏线粒体氧化在24小时内恢复正常,但对于补充半乳糖黄素的小鼠则需要72小时。肝脏线粒体中的这些代谢变化在时间上似乎与核黄素缺乏病和恢复过程中这些细胞器发生的显著形态变化无关。

相似文献

9
Riboflavin deficiency.核黄素缺乏症
Prog Clin Biol Res. 1990;321:233-48.

引用本文的文献

1
Megamitochondria formation - physiology and pathology.巨型线粒体的形成——生理学与病理学
J Cell Mol Med. 2002 Oct-Dec;6(4):497-538. doi: 10.1111/j.1582-4934.2002.tb00452.x.

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