Iba M M
Res Commun Chem Pathol Pharmacol. 1987 May;56(2):243-52.
The effect of pretreatment with 3,3'-dichlorobenzidine (DCB) on (i) enzymic and nonenzymic lipid peroxidation in hepatic microsomes--as measured by malondialdehyde (MDA) formation, and (ii) hepatic antioxidant status--as measured by the contents of vitamin E and reduced glutathione (GSH) and the activity of glutathione peroxidase, was examined in the rat. DCB-pretreatment (20 mg/kg/day, ip, for 2 days) caused an increase in NADPH-dependent (enzymic) lipid peroxidation, but had no effect on the linoleic acid hydroperoxide-dependent (nonenzymic) lipid peroxidation in microsomes. DCB-pretreatment also caused a 44% decrease in the content of vitamin E in microsomes, but had no effect on the content of GSH or the activities of glutathione peroxidases in the liver. The DCB-induced increase in in vitro microsomal lipid peroxidation is interpreted as resulting from the diminution of vitamin E induced by DCB in vivo.
研究了用3,3'-二氯联苯胺(DCB)预处理对大鼠(i)肝微粒体中酶促和非酶促脂质过氧化作用(通过丙二醛(MDA)形成来衡量)以及(ii)肝脏抗氧化状态(通过维生素E、还原型谷胱甘肽(GSH)含量和谷胱甘肽过氧化物酶活性来衡量)的影响。DCB预处理(20毫克/千克/天,腹腔注射,持续2天)导致依赖NADPH的(酶促)脂质过氧化增加,但对微粒体中依赖亚油酸氢过氧化物的(非酶促)脂质过氧化没有影响。DCB预处理还导致微粒体中维生素E含量降低44%,但对肝脏中GSH含量或谷胱甘肽过氧化物酶活性没有影响。DCB诱导的体外微粒体脂质过氧化增加被解释为是由于DCB在体内导致维生素E减少所致。