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人胎盘线粒体对外源NADH氧化的一些特性

Some properties of external NADH oxidation by human placental mitochondria.

作者信息

Scislowski P, Swierczyński J

出版信息

Experientia. 1976 Sep 15;32(9):1118-20. doi: 10.1007/BF01927578.

DOI:10.1007/BF01927578
PMID:183977
Abstract

Isolated human term placenta mitochondria catalyse oxidation of external NADH in the presence of cytochrome c. This reaction is insensitive to the respiratory chain inhibitors such as rotenone and antimycin A, and is not coupled to phosphorylation. Comparison of the effect of Mg++ ion on NADH plus cytochrome c oxidation by human term placental, human skeletal muscle and rat skeletal mitochondria showed that Mg++ ion exerts an inhibitory effect in the case of human mitochondria and a stimulatory effect in the case of rat skeletal muscle mitochondria.

摘要

分离出的人类足月胎盘线粒体在细胞色素c存在的情况下催化外部NADH的氧化。该反应对鱼藤酮和抗霉素A等呼吸链抑制剂不敏感,且与磷酸化不偶联。比较Mg++离子对人类足月胎盘线粒体、人类骨骼肌线粒体和大鼠骨骼肌线粒体中NADH加细胞色素c氧化的影响,结果表明Mg++离子对人类线粒体有抑制作用,而对大鼠骨骼肌线粒体有刺激作用。

相似文献

1
Some properties of external NADH oxidation by human placental mitochondria.人胎盘线粒体对外源NADH氧化的一些特性
Experientia. 1976 Sep 15;32(9):1118-20. doi: 10.1007/BF01927578.
2
Oxidation of NADH via an "external" pathway in skeletal-muscle mitochondria and its possible role in the repayment of lactacid oxygen debt.骨骼肌线粒体中通过“外部”途径氧化NADH及其在偿还乳酸氧债中的可能作用。
Int J Biochem. 1984;16(12):1231-5. doi: 10.1016/0020-711x(84)90221-0.
3
Antimycin A treatment decreases respiratory internal rotenone-insensitive NADH oxidation capacity in potato leaves.抗霉素A处理降低了马铃薯叶片中对鱼藤酮不敏感的呼吸性NADH氧化能力。
BMC Plant Biol. 2004 May 12;4:8. doi: 10.1186/1471-2229-4-8.
4
Mg(2+) induces intermembrane electron transport by cytochrome c desorption in mitochondria with the ruptured outer membrane.镁离子通过细胞色素c从外膜破裂的线粒体中解吸来诱导膜间电子传递。
FEBS Lett. 2000 Apr 21;472(1):5-8. doi: 10.1016/s0014-5793(00)01419-8.
5
Mitochondria from human term placenta. II. Characterization of respiratory pathways and coupling mechanisms.来自人类足月胎盘的线粒体。II. 呼吸途径和偶联机制的特征
Biochim Biophys Acta. 1975 Mar 20;376(3):436-45. doi: 10.1016/0005-2728(75)90165-6.
6
[Activation of the external pathway of NADH oxidation in mitochondria at decreased pH].[在pH值降低时线粒体中NADH氧化的外部途径的激活]
Biokhimiia. 1981 Nov;46(11):1945-56.
7
Estimation of NADH oxidation in human skeletal muscle mitochondria.人体骨骼肌线粒体中NADH氧化的估计
Clin Chim Acta. 1986 Mar 28;155(3):263-73. doi: 10.1016/0009-8981(86)90246-9.
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Reducibility of cytochromes b in aerobic beef-heart mitochondria treated with antimycin.用抗霉素处理的需氧牛心线粒体中细胞色素b的可还原性
Biochim Biophys Acta. 1972 Dec 14;283(3):395-402. doi: 10.1016/0005-2728(72)90257-5.
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The effect of respiratory inhibitors on NADH, succinate and malate oxidation in corn mitochondria.呼吸抑制剂对玉米线粒体中NADH、琥珀酸和苹果酸氧化的影响。
Plant Physiol. 1969 Sep;44(9):1335-41. doi: 10.1104/pp.44.9.1335.
10
Regulating effect of mitochondrial lactate dehydrogenase on oxidation of cytoplasmic NADH via an "external" pathway in skeletal muscle mitochondria.
Int J Biochem. 1992 Apr;24(4):657-61. doi: 10.1016/0020-711x(92)90343-y.

本文引用的文献

1
Phosphorylation coupled to oxidation of dihydrodiphosphopyridine nucleotide.磷酸化与二氢二磷酸吡啶核苷酸的氧化相偶联。
J Biol Chem. 1951 May;190(1):345-59.
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Oxidation of external DPNH by mitochondria from human and rat skeletal muscle.
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An electron-transport system associated with the outer membrane of liver mitochondria. A biochemical and morphological study.与肝线粒体外膜相关的电子传递系统。一项生化与形态学研究。
J Cell Biol. 1967 Feb;32(2):415-38. doi: 10.1083/jcb.32.2.415.
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Intramitochondrial distribution of magnesium.镁在线粒体内的分布
Biochem Biophys Res Commun. 1971 Sep 17;44(6):1330-7. doi: 10.1016/s0006-291x(71)80231-0.
5
Inhibition of anion transport across with mitochondrial membrane by amytal.巴比妥对阴离子跨线粒体膜转运的抑制作用。
Biochim Biophys Acta. 1974 Nov 27;373(1):66-75. doi: 10.1016/0005-2736(74)90106-0.
6
Intermembrane electron transfer in mitochondrial and microsomal systems.线粒体和微粒体系统中的膜间电子转移。
FEBS Lett. 1974 Feb 15;39(2):239-42. doi: 10.1016/0014-5793(74)80059-1.
7
High activity of alpha-glycerophosphate oxidation by human placental mitochondria.人胎盘线粒体α-甘油磷酸氧化活性高。
Biochim Biophys Acta. 1976 Mar 11;429(1):46-54. doi: 10.1016/0005-2744(76)90028-0.