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[肝内质网中混合功能氧化酶系统破坏的机制。膜磷脂过氧化的作用]

[Mechanisms of mixed-function oxidase system breakdown in the hepatic endoplasmic reticulum. The role of membrane phospholipid peroxidation].

作者信息

Kagan V E, Novikov K N, Savov V M, Serbinova E A, Kozlov Iu P

出版信息

Nauchnye Doki Vyss Shkoly Biol Nauki. 1984(3):21-32.

PMID:6713028
Abstract

It has been shown that endogenous lipid peroxidation (LPO) is an effective mechanism participating in the destruction of endoplasmic reticulum membranes (cytochrome P450) in liver. Antioxidants are able to control the rate of degradation of cytochrome P450 in vivo. Stock of the constitutive cytochrome P450 as compared with induced P450 is more resistive to LPO in vivo and in vitro. Spontaneous as well as induced by Fe2+--ADP+ +NADPH system destruction of cytochrome P450 due to accumulation of LPO products malonic dialdehyde (MDA) occurs during incubation of isolated rats hepatocytes. The LPO inhibitors (4-methyl-2,6- ditretbutilphenol , pyrogallol) stabilize cytochrome P450 preventing accumulation MDA hepatocytes. Degradation of cytochrome P450 in microsomes during trypsin proteolysis has been found to be enhanced by PLO induction. Efficiency of proteolysis depends on the way of induction and decreases in such an order: NADPH-- HNDH --ascorbate-dependent LPO. LPO may be considered as a trigger mechanism that makes some forms of cytochrome P450 available for endogenous proteases.

摘要

研究表明,内源性脂质过氧化(LPO)是参与肝脏内质网膜(细胞色素P450)破坏的一种有效机制。抗氧化剂能够在体内控制细胞色素P450的降解速率。与诱导型P450相比,组成型细胞色素P450储备在体内和体外对LPO更具抗性。在离体大鼠肝细胞孵育期间,由于LPO产物丙二醛(MDA)的积累,细胞色素P450会发生自发的以及由Fe2 + - ADP + + NADPH系统诱导的破坏。LPO抑制剂(4 - 甲基 - 2,6 - 二叔丁基苯酚、邻苯三酚)可稳定细胞色素P450,防止肝细胞中MDA的积累。已发现胰蛋白酶蛋白水解过程中微粒体中细胞色素P450的降解会因PLO诱导而增强。蛋白水解效率取决于诱导方式,并按以下顺序降低:NADPH - HNDH - 抗坏血酸依赖性LPO。LPO可被视为一种触发机制,使某些形式的细胞色素P450可被内源性蛋白酶作用。

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