Bernacchi A S, de Castro C R, de Toranzo E G, de Ferreyra E C, de Fenos O M, Castro J A
Xenobiotica. 1987 Feb;17(2):223-8. doi: 10.3109/00498258709043932.
Administration of CCl4 i.p. to Leghorn chickens did not promote lipid peroxidation of liver microsomal lipids, as evidenced by either increased diene conjugation or by decreased arachidonic acid content. The hepatotoxin did not produce liver necrosis 24 h after dosing, but decreased the cytochrome P-450 content, and aminopyrine N-demethylase and glucose 6 phosphatase activities at 1, 3, 6 and 24 h. CCl4 administration produced dilation of the rough endoplasmic reticulum and detachment of ribosomes from their membranes. These observations suggest that lipid peroxidation is not the key event in the production of these biochemical and ultrastructural alterations, elicited by CCl4.
对来亨鸡腹腔注射四氯化碳(CCl4),并未促进肝微粒体脂质的脂质过氧化,这一点可通过二烯共轭增加或花生四烯酸含量降低得以证明。给药24小时后,这种肝毒素并未导致肝坏死,但在给药后1、3、6和24小时降低了细胞色素P - 450含量、氨基比林N - 脱甲基酶和葡萄糖6磷酸酶的活性。给予CCl4导致粗面内质网扩张以及核糖体从其膜上脱离。这些观察结果表明,脂质过氧化并非由CCl4引发的这些生化和超微结构改变产生过程中的关键事件。