Toxicity of flavoglaucin from Aspergillus chevalieri in rabbits

Female rabbits were injected intraperitoneally (i.p.) with purified flavoglaucin from Aspergillus chevalieri. After 2 h the rabbits were bled and the livers removed for enzyme assays. No changes were found for plasma lactate dehydrogenase (LDH) and its isozymes or liver transketolase (TK) activities. A small but not statistically significant increase was found in plasma glutamate pyruvate transaminase activity. A highly significant increase in plasma glutamic oxaloacetate transaminase activity was observed along with an increase in liver LDH which was, however, not quite significant. The liver also showed some histological evidence of hepatic damage.     

亚慢性2,3,7,8四氯二苯并二噁英暴露对大鼠肝脏的毒性

目的：了解亚慢性2,3,7,8四氯二苯并二噁英（TCDD）暴露对大鼠肝脏的毒性作用。方法：1月龄SD大鼠随机分为阴性对照组（予玉米油）和3个TCDD（2、10和50 ng.kg-1.d-1）实验组,每组30只,雌雄各半,连续暴露13周后测定血清丙氨酸氨基转移酶（ALT）和天门冬氨酸氨基转移酶（AST）活性,观察肝脏病理组织学变化。结果：亚慢性TCDD暴露对大鼠体质量和主要脏器相对重量无明显影响;血清AST和ALT活性在实验组升高：雌鼠AST和ALT在10和50 ng.kg-1.d-1组高于对照组和2 ng.kg-1.d-1组（P〈0.05）;雄鼠AST在50 ng.kg-1.d-1组高于其它3组（P〈0.05）,ALT在各组间差异无统计学意义;病理观察发现实验组肝组织坏死,肝血窦瘀血和肝细胞空泡样变。结论：亚慢性TCDD暴露对大鼠肝脏具有毒性作用,且雌鼠比雄鼠的肝脏对TCDD的毒性更敏感。     

Examination of the protective effect of ICRF-187 and dimethyl sulfoxide against acetaminophen-induced hepatotoxicity in Syrian golden hamsters

The protective activity of 1,2-bis(3,5-dioxopiperazin-l-yl)propane (ICRF-187) and dimethyl sulfoxide (DMSO) was tested against acetaminophen-induced hepatotoxicity. Male Syrian golden hamsters injected intraperitoneally between 18:00 h and 20:00 h for 2 consecutive days with acetaminophen (N-acetyl-p-aminophenol) (300 mg/kg) displayed signs of hepatotoxicity as evidenced by increases in enzyme activity and cellular damage. Forty-eight hours after the second acetaminophen dose, the activities of serum glutamic-pyruvic transaminase and alkaline phosphatase were increased compared with levels found in hamsters given only saline. In addition, hepatocellular necrosis was evident in acetaminophen-treated animals. ICRF-187 (300 mg/kg) given 1 h before acetaminophen attenuated the increases in enzyme activities, and both DMSO (7.3 g/kg) and ICRF-187 reduced the incidence and severity of acetaminophen-induced hepatocellular injury. Both ICRF-187 and DMSO are capable of altering free radical-mediated toxicity in other experimental systems. Whether these compounds reduce acetaminophen-induced liver toxicity by a similar mechanism remains to be determined.