Vinogradova L F, Mirzoian Zh A, Kharlitskaia E V, Beketova T P
Farmakol Toksikol. 1989 Mar-Apr;52(2):62-6.
The pathogenetic mechanisms of hepatotoxicity of an anthelminthic drug chloxyl as compared with the mechanisms of CCl4 hepatotoxicity were studied on the basis of the change of the liver content of the primary (conjugated dienes) and secondary (malondialdehyde) products of lipid peroxidation. the activity of alanine aminotransferase and aspartate aminotransferase in the blood serum of rats and on the basis of the change of the liver structure. The pathogenetic mechanisms of chloxyl hepatotoxicity are close to those of CCl4 and consist in the activation of membrane lipid peroxidation, that is, an increase of the liver contents of the primary and secondary products of lipid peroxidation, an impairment of permeability of membranes of hepatocytes and their destruction with the release in the blood of cytoplasmic enzymes of alanine aminotransferase and aspartate aminotransferase.
基于脂质过氧化的初级产物（共轭二烯）和次级产物（丙二醛）在肝脏中的含量变化、大鼠血清中丙氨酸转氨酶和天冬氨酸转氨酶的活性以及肝脏结构的变化，研究了驱虫药氯硝柳胺肝毒性的发病机制，并与四氯化碳肝毒性机制进行了比较。氯硝柳胺肝毒性的发病机制与四氯化碳相似，在于膜脂质过氧化的激活，即脂质过氧化的初级和次级产物在肝脏中的含量增加，肝细胞细胞膜通透性受损并遭到破坏，导致丙氨酸转氨酶和天冬氨酸转氨酶等细胞质酶释放入血。
