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[肝脏组织微粒体中NADP.H2和NAD.H2氧化途径的抑制作用分析]

[Analysis of inhibition in pathways of NADP.H2 and NAD.H2 oxidation in liver tissue microsomes].

作者信息

Archakov A I, Ahirnov G E, Karusina I I

出版信息

Vopr Med Khim. 1975 May-Jun;21(3):281-5.

PMID:1902
Abstract

Microsomal complexes of electron transfer were resistant to typical inhibitors of mitochondrial pathway of electron transport. In oxidation of NADP.H2 there were at least three point of molecular O2 reduction: NADP.H2-specific flavoprotein, Fe2+ participating in reactions of peroxidation of unsaturated fatty acids and cytochrome P-450. Efficiency of cytochrome P-450 inhibitors could not be evaluated by polarography as in the pathway several sites of molecular O2 activation were observed. In oxidation of NADP.H2 estimation of the rate of electron transfer reactions was carried out by monitoring of velocity of O2 absorption in presence of EDTA (inhibitor of the reaction of peroxidation) because about 50% of the total oxygen were utilized only in the process where NADP.H2 was oxidized. NAD.H2 oxidation, inhibited with EDTA, was activated by addition of Ca2+.

摘要

电子传递的微粒体复合物对电子传递线粒体途径的典型抑制剂具有抗性。在NADP.H2氧化过程中,分子氧还原至少有三个位点:NADP.H2特异性黄素蛋白、参与不饱和脂肪酸过氧化反应的Fe2+和细胞色素P-450。细胞色素P-450抑制剂的效率无法通过极谱法评估,因为在该途径中观察到了分子氧激活的多个位点。在NADP.H2氧化过程中,通过监测EDTA(过氧化反应抑制剂)存在下的氧气吸收速度来估计电子传递反应的速率,因为仅在NADP.H2氧化过程中就消耗了约50%的总氧气。被EDTA抑制的NAD.H2氧化通过添加Ca2+而被激活。

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