氢过氧化枯烯引起离体线粒体脂质过氧化作用的初步研究

Preliminary Study on Cumene Hydroperoxide-Induced Mltochondrial Lipid Peroxidation in Vitro

氢过氧化桔烯(CHP)能非常显著地引起小鼠肝离体线粒体脂质过氧化作用(LP)、CHP在低浓度时.脂质过氧化物(LPO)与CHP浓度成线性增加,CHP在150μmol/L时,LPO形成达最大.-LPO与温育时间(20 mim内)成线性增加.以后保持在较高不变水平.还原型谷胱甘肽(GSH),维生素E(Vit.E)和依地酸(EDTA)能非常昱著地抑制CHP引起的线粒体LP而且GSH含量减少,Vit.E几乎不变.用二甲基亚砜(DMSO)和超氧化物岐化酶(SOD)排除了OH-及O2-的形成.本文讨论了CHP引起LP的可能机理及抗氧化剂的作用.

Cumene Hydroperoxide(CHP)-induced mouse mitochondrial lipid peroxides (LPO) are significantly higher than those of the normal mitochondria ( P<0. 01) .Those LPO increase lineally with the CHP at the lower concentration . The LPO appear the maxium at CHP being 5-400 μmol/L . The LPO increase lineally with the incubation time within the first 20 min , and keep on a higher constant Ievel aftcr that time . Reduced glutathione (GSH), vitamin E (Vit E) and ethylenediamine tetraacetic acid (EDTA) inhibit the LPO production significantly (P<0. 01) . Moreover , GSH content decreases tnarkedly , bui Vit E doesn't change when it is incubated with CHP . Dimethyl sulphoxidc(DMSO) and superoxide dismutase (SOD) wthout inhibiting effect on CHP-induced LPO cxclude the for-mation of hydroxyl radical and superoxide anion .The possible mechanism of CHP -induced LPO and antioxidant effects of GSH and Vit E is discussed .