3-氨基-1,2,4-三唑和二硫化碳在苯巴比妥处理的饥饿大鼠中的肝毒性。

The hepatotoxicity of 3-amino-1,2,4-triazole and carbon disulphide in phenobarbitone-treated starved rats.

作者信息

Magos L, Butler W H, Snowden R

出版信息

Toxicology. 1978 Feb;9(1-2):103-7. doi: 10.1016/0300-483x(78)90035-5.

Abstract

In phenobarbitone-treated starved male rats 1 g/kg 3-amino-1,2,4-triazole produced moderate liver necorsis and increased the serum glutamic-pyruvic transaminase activity. If half an hour after the administration of aminotriazole animals were exposed for 4 h to 2.0 mg/l CS2, the necrotic damage in the liver was larger and the serum glutamic-pyruvic transaminase activity higher than in rats not exposed to CS2. Carbon-disulphide in phenobarbitone-treated starved male rats caused only a very slight increase in the serum transminase activity in spite of the widespread hydropic degeneration in the liver. These experiments indicated that increase in serum transaminase activity is the consequence of necrosis and not hydropic degeneration; aminotriazole is hepatotoxic in rats when microsomal enzymes are induced and the hepatotoxicity of aminotriazole and carbon disulphide is potentiated by the administration of the other compound.

摘要

在苯巴比妥处理的饥饿雄性大鼠中，1克/千克的3-氨基-1,2,4-三唑可产生中度肝坏死，并增加血清谷丙转氨酶活性。如果在给予氨基三唑半小时后，将动物暴露于2.0毫克/升的二硫化碳中4小时，肝脏的坏死损伤比未暴露于二硫化碳的大鼠更大，血清谷丙转氨酶活性也更高。尽管肝脏中广泛存在水样变性，但在苯巴比妥处理的饥饿雄性大鼠中，二硫化碳仅使血清转氨酶活性略有增加。这些实验表明，血清转氨酶活性的增加是坏死的结果而非水样变性；当微粒体酶被诱导时，氨基三唑对大鼠具有肝毒性，并且氨基三唑和二硫化碳的肝毒性可因另一种化合物的给药而增强。