Balint G A
Department of Neurology and Psychiatry, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Exp Toxicol Pathol. 1998 Mar;50(1):9-11. doi: 10.1016/S0940-2993(98)80051-1.
Exogenously administered prostaglandins are reported to be involved in hepatic regeneration, i.e. they hinder liver cell injury and cell-death induced by different toxic noxae. In the pertinent literature no data are available regarding the role of endogenous (tissue) prostaglandins in hepatotoxic processes. In subchronic carbon-tetrachloride intoxication (800 mg/kg twice a week, s.c., for 12 weeks) the endogenous prostacyclin level showed a transient and significant elevation signalling (similarly to the gastrointestinal tract) the process of protective mechanisms. This tenet was further strengthened by the concomitant decrease of serum ALT and AST levels. Continuing the carbon-tetrachloride treatment, finally not only the endogenous prostacyclin synthesising capacity of the liver but the hepatic cells themselves were also destroyed. According to the author's best knowledge these are the first data in the literature which try to enlighten the protective role of endogenous prostacyclin in hepatotoxic processes.
据报道，外源性给予的前列腺素参与肝脏再生，即它们可抑制由不同毒性物质诱导的肝细胞损伤和细胞死亡。在相关文献中，尚无关于内源性（组织）前列腺素在肝毒性过程中作用的数据。在亚慢性四氯化碳中毒（每周两次，皮下注射800mg/kg，共12周）时，内源性前列环素水平出现短暂且显著升高，这表明（与胃肠道类似）存在保护机制。血清谷丙转氨酶（ALT）和谷草转氨酶（AST）水平的同时降低进一步强化了这一观点。持续进行四氯化碳处理，最终不仅肝脏的内源性前列环素合成能力被破坏，肝细胞本身也遭到破坏。据作者所知，这些是文献中首批试图阐明内源性前列环素在肝毒性过程中保护作用的数据。
