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[缺血期间离体心脏线粒体脂肪酸氧化紊乱的原因]

[Reasons for disorders of fatty acid oxidation in isolated heart mitochondria during ischemia].

作者信息

Balasiavichius R V, Dagis A I, Toleĭkis A I, Prashkiavichius A K

出版信息

Biull Eksp Biol Med. 1985 Mar;99(3):294-6.

PMID:3986334
Abstract

The influence of malate and cytochrome c on fatty acid oxidation under control and ischemic conditions was investigated. In the medium without malate, cytochrome did not make fatty acid oxidation decreased during ischemia return to normal. Oxidation in the media containing malate and cytochrome did not differ from control only when it was measured after preliminary oxidation of endogenous substrates. The ratio of palmitoyl-CoA and palmitoyl carnitine to the respiration rates at state 3 was unchanged at 60 min ischemia. Apparently, no changes in carnitine acyltransferase playing a role in oxidation of palmitoyl-CoA took place. Thus, the decrease of fatty acid oxidation at early periods of ischemia is largely caused by a reduction in the content of cytochrome c and intermediates of Krebs cycle in the mitochondria.

摘要

研究了苹果酸和细胞色素c在对照和缺血条件下对脂肪酸氧化的影响。在不含苹果酸的培养基中,细胞色素不会使缺血恢复正常期间的脂肪酸氧化减少。仅在对内源性底物进行初步氧化后进行测量时,含有苹果酸和细胞色素的培养基中的氧化与对照无差异。在缺血60分钟时,棕榈酰辅酶A和棕榈酰肉碱与状态3呼吸速率的比值未发生变化。显然,在棕榈酰辅酶A氧化中起作用的肉碱酰基转移酶没有变化。因此,缺血早期脂肪酸氧化的减少主要是由线粒体中细胞色素c和三羧酸循环中间体含量的降低引起的。

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