El-Hawari A M, Plaa G L
Toxicol Lett. 1983 Jul;17(3-4):293-300. doi: 10.1016/0378-4274(83)90241-2.
Thioacetamide-induced hepatoxicity was potentiated in male Sprague-Dawley rats rendered diabetic by alloxan or streptozotocin. The response was more striking in alloxan-diabetic rats. Insulin administration prevented the potentiation following alloxan pretreatment. Fasting also resulted in an enhanced hepatotoxic response to thioacetamide, but the increase was much less than that observed in rats given the diabetogenic agents. The ketosis produced by alloxan was more severe than that induced by streptozotocin, but was unlike that caused by fasting. Pretreatment with phenobarbital, 3-methylcholanthrene or 3,4-benzpyrene did not enhance thioacetamide liver injury.
用四氧嘧啶或链脲佐菌素使雄性斯普拉格-道利大鼠患糖尿病后,硫代乙酰胺诱导的肝毒性增强。在四氧嘧啶诱导的糖尿病大鼠中,这种反应更为明显。给予胰岛素可预防四氧嘧啶预处理后的毒性增强。禁食也会导致对硫代乙酰胺的肝毒性反应增强,但增加程度远小于给予致糖尿病药物的大鼠。四氧嘧啶产生的酮症比链脲佐菌素诱导的更严重,但与禁食引起的不同。用苯巴比妥、3-甲基胆蒽或3,4-苯并芘预处理不会增强硫代乙酰胺对肝脏的损伤。