Vengerovskiĭ A I, Saratikov A S
Vopr Med Khim. 1989 May-Jun;35(3):87-91.
Release of lysosomal hydrolases (including phospholipase A), increase in content of lysophosphatidyl choline and cardiolipin and decrease in content of phosphatidyl choline and phosphatidyl ethanolamine, activation of lipid peroxidation, inhibition of the cell antioxidant system, inhibition of tricarboxylic acid cycle enzymes and of beta-hydroxybutyrate dehydrogenase in mitochondria were detected in hepatocytes of rats after acute poisoning with necrosogenic toxins D-galactosamine, allyl alcohol and apamide. Hydrazine and ethanol caused an extensive steatosis of liver tissue parenchyma, decreased moderately the activity of mitochondrial enzymes, stimulated lipid peroxidation without impairment of antiradical activity of the lipids, contributed to accumulation of cardiolipin and to a decrease in phosphatidyl choline content.
在大鼠经坏死性毒素D-半乳糖胺、烯丙醇和蜂毒明肽急性中毒后,肝细胞中检测到溶酶体水解酶(包括磷脂酶A)的释放、溶血磷脂酰胆碱和心磷脂含量的增加以及磷脂酰胆碱和磷脂酰乙醇胺含量的减少、脂质过氧化的激活、细胞抗氧化系统的抑制、线粒体中三羧酸循环酶和β-羟基丁酸脱氢酶的抑制。肼和乙醇导致肝组织实质广泛脂肪变性,适度降低线粒体酶的活性,刺激脂质过氧化而不损害脂质的抗自由基活性,促使心磷脂积累并导致磷脂酰胆碱含量降低。