Amacher David E, Schomaker Shelli J, Boldt Sherri E, Mirsky Michael
World-wide Safety Sciences, Pfizer Global Research and Development, Groton, CT 06340, USA.
Food Chem Toxicol. 2006 Apr;44(4):528-37. doi: 10.1016/j.fct.2005.08.027. Epub 2005 Nov 7.
The purpose of this investigation was to examine the relationship among hepatic microsomal enzyme induction, liver weight, histological evidence of hepatic injury, and serum clinical chemistry markers of hepatic origin in the cynomolgus monkey. We report here the results from independent toxicology studies for 10 investigative drug candidates representing four therapeutic classes. Study conditions were selected to elicit target organ toxicity. We found that six of the 10 compounds altered cytochrome P450-associated activities in both male and female monkeys, two in females only, and one altered similar activities in males only. Frequently, significant treatment-related elevations in NADPH cytochrome c reductase and ethylmorphine N-demethylase were noted. When the results from all 10 studies were pooled, 14 cytochrome P450-associated activities were significantly increased and five were decreased in males compared to 15 significantly increased and three decreased in the females. Treatment-associated liver weight increases were noted in four studies. Except for hepatocellular hypertrophy in one study, no significant treatment-related microscopic changes in liver and no elevations of serum biomarkers commonly associated with liver toxicity were observed in any of the studies that demonstrated significant hepatic enzyme induction. Compared to parallel rat studies, one compound was an inducer only in monkeys and one was an inducer only in rats. Significant elevations of microsomal drug-metabolizing enzymes in the cynomolgus monkey liver are not accompanied by substantial hepatic changes except for hepatomegaly. These alterations in the hepatic drug-metabolizing enzyme system were benign based the absence of histopathological lesions and serum biomarkers of hepatobiliary toxicity.
本研究的目的是探讨食蟹猴肝脏微粒体酶诱导、肝脏重量、肝损伤的组织学证据以及肝脏来源的血清临床化学标志物之间的关系。我们在此报告了针对代表四个治疗类别的10种研究性候选药物的独立毒理学研究结果。选择研究条件以引发靶器官毒性。我们发现,10种化合物中有6种改变了雄性和雌性猴子中与细胞色素P450相关的活性,2种仅在雌性中改变,1种仅在雄性中改变了类似的活性。经常观察到与治疗相关的NADPH细胞色素c还原酶和乙基吗啡N-脱甲基酶显著升高。当汇总所有10项研究的结果时,与雌性相比,雄性中有14种与细胞色素P450相关的活性显著增加,5种降低,而雌性中有15种显著增加,3种降低。在四项研究中观察到与治疗相关的肝脏重量增加。除了一项研究中有肝细胞肥大外,在任何显示出显著肝酶诱导的研究中,均未观察到与治疗相关的肝脏微观显著变化,也未观察到通常与肝毒性相关的血清生物标志物升高。与平行的大鼠研究相比,一种化合物仅在猴子中是诱导剂,一种仅在大鼠中是诱导剂。食蟹猴肝脏微粒体药物代谢酶的显著升高,除了肝肿大外,没有伴随实质性的肝脏变化。基于缺乏组织病理学病变和肝胆毒性的血清生物标志物,肝脏药物代谢酶系统的这些改变是良性的。