Sigler R E, Dominick M A, McGuire E J
Parke-Davis Pharmaceutical Research Division, Pathology and Experimental Toxicology, Ann Arbor, Michigan 48105.
Toxicol Pathol. 1992;20(4):595-602. doi: 10.1177/019262339202000406.
Wistar rats received an hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, a halogenated pyrrole designated PD 123244-15, orally by gavage for 14 days at 10, 50, 150, 300, and 600 mg/kg. Doses of 150-600 mg/kg caused death and marked systemic toxicity involving stomach, esophagus, liver, gonads, lymphoid tissues, and skeletal muscle. Histopathologic findings included hyperkeratosis in esophagus and forestomach, increased hepatic mitotic activity, ovarian follicular necrosis, testicular atrophy and arrested spermatogenesis, and skeletal muscle necrosis and regeneration. Elevated serum aspartate aminotransferase correlated with muscle necrosis and hepatocellular damage. Marked systemic effects associated with high plasma concentrations were consistent with toxicity defined for other HMG-CoA reductase inhibitors, with the exception of pathologic alterations in the esophagus and ovaries. Direct mucosal irritation may have contributed to forestomach and esophageal lesions induced by this halogenated pyrrole.
将Wistar大鼠通过灌胃口服给予一种羟甲基戊二酰辅酶A(HMG-CoA)还原酶抑制剂,一种名为PD 123244-15的卤代吡咯,剂量分别为10、50、150、300和600mg/kg,持续14天。150 - 600mg/kg的剂量导致死亡和明显的全身毒性,涉及胃、食管、肝脏、性腺、淋巴组织和骨骼肌。组织病理学发现包括食管和前胃的角化过度、肝脏有丝分裂活性增加、卵巢卵泡坏死、睾丸萎缩和精子发生停滞,以及骨骼肌坏死和再生。血清天冬氨酸氨基转移酶升高与肌肉坏死和肝细胞损伤相关。与高血浆浓度相关的明显全身效应与其他HMG-CoA还原酶抑制剂所定义的毒性一致,但食管和卵巢的病理改变除外。直接的黏膜刺激可能促成了这种卤代吡咯引起的前胃和食管病变。