Siegers C P, Heger B, Baretton G, Younes M
Institute of Toxicology, Medical University of Lübeck, F.R.G.
Toxicology. 1988 Dec 30;53(2-3):213-8. doi: 10.1016/0300-483x(88)90214-4.
In mice, the synthetic prostaglandin derivative misoprostol failed to protect against liver damage induced by acetaminophen, carbon terachloride,1,1-dichloroethylene or thioacetamide. In rats, misoprostol (20-100 micrograms/kg p.o.) markedly reduced early increments of plasma enzyme activities (glutamate-pyruvate-transaminase, GPT; sorbitol dehydrogenase, SDH) in a model of halothane-induced liver injury; the most effective dose in this respect (20 micrograms/kg) significantly depressed halothane-induced ethane exhalation indicating in vivo lipid peroxidation. Repeated treatment with misoprostol (20 micrograms/kg p.o.) still diminished halothane-induced elevations of enzyme activities over 48 h, but failed to prove hepatoprotection by histomorphological examinations. It is concluded that the antiperoxidative properties of misoprostol are not paralleled by an hepatoprotection, which was indicated by significant reductions of liver-specific plasma enzyme activities, but not confirmed by the morphological picture.
在小鼠中，合成前列腺素衍生物米索前列醇未能预防对乙酰氨基酚、四氯化碳、1,1 - 二氯乙烯或硫代乙酰胺所致的肝损伤。在大鼠中，米索前列醇（20 - 100微克/千克，口服）在氟烷诱导的肝损伤模型中显著降低了血浆酶活性（谷氨酸丙酮酸转氨酶，GPT；山梨醇脱氢酶，SDH）的早期升高；在这方面最有效的剂量（20微克/千克）显著降低了氟烷诱导的乙烷呼出，表明体内脂质过氧化。用米索前列醇（20微克/千克，口服）重复治疗在48小时内仍能减轻氟烷诱导的酶活性升高，但组织形态学检查未能证明其具有肝保护作用。结论是，米索前列醇的抗过氧化特性与肝保护作用并不平行，肝保护作用通过肝脏特异性血浆酶活性的显著降低得以体现，但未得到形态学图像的证实。
