Duddy S K, Hsia M T
Department of Entomology, University of Wisconsin, Madison 53706.
Fundam Appl Toxicol. 1987 Aug;9(2):304-13. doi: 10.1016/0272-0590(87)90053-4.
This investigation was conducted to evaluate the effects of modulation of several phase I xenobiotic-metabolizing enzyme activities on the expression of precocene II-induced hepatotoxicity. Precocene II (175-200 mg/kg) was given intraperitoneally to male Sprague-Dawley rats that had been exposed previously to inducers (phenobarbital and 3-methylcholanthrene) or inhibitors (SKF 525-A and cimetidine) of oxidative xenobiotic metabolism. Hepatic damage was measured both biochemically (leakage of aspartate aminotransferase and alanine amino-transferase into the serum) and histologically. Significant protection from precocene II-induced hepatotoxicity was observed in all treated animals regardless of whether the modulator employed was an inducer or an inhibitor of microsomal oxidative enzymes. These results indicate that the level of activity of various forms of cytochrome P-450 significantly influences the severity of hepatic necrosis induced by precocene II. Furthermore, these results suggest that inducible non-P-450 factors, such as glutathione S-transferases, may be important in modulating precocene II-induced hepatotoxicity.
本研究旨在评估几种I相外源性物质代谢酶活性的调节对早熟素II诱导的肝毒性表达的影响。将早熟素II(175 - 200 mg/kg)腹腔注射给先前已接触过氧化外源性物质代谢诱导剂(苯巴比妥和3 - 甲基胆蒽)或抑制剂(SKF 525 - A和西咪替丁)的雄性Sprague - Dawley大鼠。通过生化方法(天冬氨酸转氨酶和丙氨酸转氨酶漏入血清)和组织学方法测量肝损伤。无论所使用的调节剂是微粒体氧化酶的诱导剂还是抑制剂,在所有接受治疗的动物中均观察到对早熟素II诱导的肝毒性有显著保护作用。这些结果表明,各种形式的细胞色素P - 450的活性水平显著影响早熟素II诱导的肝坏死的严重程度。此外,这些结果表明,可诱导的非P - 450因子,如谷胱甘肽S - 转移酶,可能在调节早熟素II诱导的肝毒性中起重要作用。