INCOMPLETE PALMITATE OXIDATION IN CELL-FREE SYSTEMS OF RAT AND HUMAN MUSCLES
INCOMPLETE PALMITATE OXIDATION IN CELL-FREE SYSTEMS OF RAT AND HUMAN MUSCLES
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DOI：
10.1016/0005-2760(83)90064-4
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发表时间：
1983-01-01
期刊：
影响因子：
--
通讯作者：
VANHINSBERGH, VWM
中科院分区：
文献类型：
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作者：
VEERKAMP, JH;VANMOERKERK, HTB;VANHINSBERGH, VWM
棕榈酸氧化能力测定在整个匀浆，核后馏分和线粒体馏分的各种大鼠和人类肌肉和大鼠肝，肾，脑和肺。在所有无细胞体系中，氧化速率（14 CO2和14 C标记的酸溶性中间产物的产生）为[1- 14 C]棕榈酸酯> [U-14 C]棕榈酸酯> [16- 14 C]棕榈酸酯。大鼠心脏和肝脏的氧化速率最高，肾脏、膈肌和心肌的氧化速率居中。[肌肉]四头肌和低的大脑和肺。人类心脏的容量远低于大鼠心脏，约为人类骨骼肌的两倍。省略L-肉碱和添加丙二酰辅酶A，KCN或抗霉素A降低整个匀浆和线粒体组分的氧化速率。抗霉素或KCN增加，丙二酰辅酶A降低[1- 14 C]-和[16- 14 C]棕榈酸酯的氧化速率比。肉毒碱浓度对该比值无显著影响。14 C-标记的十二烷酸和十四烷酸被确定在匀浆和线粒体组分的m。在存在和不存在抗霉素A的情况下，大鼠的四头肌和肝脏作为[16- 14 C]棕榈酸酯氧化的酸不溶性中间体。它们的回收量可以解释[1- 14 C]-和[16- 14 C]棕榈酸酯氧化速率的差异。在无细胞系统中的不完全棕榈酸氧化似乎主要是由过氧化物酶体氧化产物的线粒体降解不足引起的。
The palmitate oxidation capacity was determined in whole homogenates, postnuclear fractions and mitochondrial fractions of various rat and human muscles and in rat liver, kidney, brain and lung. The oxidaiton rate (production of 14CO2 and 14C-labeled acid-soluble intermediates) was [1-14C]palmitate > [U-14C]palmitate > [16-14C]palmitate in all cell-free systems. Oxidation rates were highest in rat heart and liver, intermediate in kidney, diaphragm and m. [musculus] quadriceps and low in brain and lung. The capacity of human heart was much lower than that of rat heart and about twice that of human skeletal muscles. Omission of L-carnitine and addition of malonyl-CoA, KCN or antimycin A decreasd the oxidation rates in whole homogenates and mitochondrial fractions. Antimycin or KCN increased and malonyl-CoA decreased the ratio of the oxidation rates with [1-14C]- and [16-14C]palmitate. The carnitine concentration had no significant effect on the ratio. 14C-labeled dodecanoic and tetradecanoic acids were identified in homogenates and mitochondrial fractions of m. quadriceps and liver of rat as acid-insoluble intermediates of [16-14C]palmitate oxidation in the presence and absence of antimycin A. Their amounts recovered can account for the differences in oxidation rates found with [1-14C]- and [16-14C]palmitate. The incomplete palmitate oxidation in cell-free systems appears to be mainly caused by an inadequate mitochondrial degradation of peroxisomal oxidation products.