IS SUPEROXIDE AN INITIATOR OF MICROSOMAL LIPID-PEROXIDATION

被引:19
作者
AFANASEV, IB
DOROZHKO, AI
POLOZOVA, NI
KUPRIANOVA, NS
BRODSKII, AV
OSTRACHOVITCH, EA
KORKINA, LG
机构
[1] Vitamin Research Institute, 117820 Moscow
关键词
D O I
10.1006/abbi.1993.1199
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effects of 'pro-oxidant' quinones, doxorubicin, Fe3+-ADP-doxorubicin complex, and menadione, as well as of free radical scavengers possessing superoxide-dismuting activities, Fe3+-rutin and Cu2+-rutin, on superoxide production and lipid peroxidation in rat liver microsomes have been studied. All quinone compounds efficiently suppressed lucigenin-dependent chemiluminescence produced in NADPH-dependent microsomal lipid peroxidation, but exhibited different effects on cytochrome c reduction: Doxorubicin and Fe3+-ADP-doxorubicin weakly inhibited and menadione enhanced it. In accord with previous findings, menadione inhibited malondialdehyde (MDA) formation in microsomes, while Fe3-ADP-doxorubicin enhanced it. Efficiency of inhibition of MDA formation by the Fe3+-rutin and Cu2+-rutin complexes correlated well with their superoxide-dismuting activities in contrast to the findings obtained in nonenzymatic liposomal peroxidation, where the formation of superoxide ion is not expected. On these grounds, we propose that superoxide ion is an obligatory initiation species in microsomal lipid peroxidation; the effects of pro-oxidant quinones on lipid peroxidation depends on their ability to chelate iron ions and not on their redox-cycling activities. © 1993 Academic Press, Inc.
引用
收藏
页码:200 / 205
页数:6
相关论文
共 17 条