用氢氧化甲基汞预处理对四氯化碳诱导的肝毒性的保护作用。

Protection against carbon tetrachloride-induced hepatotoxicity by pretreatment with methylmercury hydroxide.

作者信息

Carlson G P

出版信息

Toxicology. 1975;4(1):83-9. doi: 10.1016/0300-483x(75)90024-4.

Abstract

Pretreatment of rats with methylmercury hydroxide (MMH) (15 mg/kg s.c. for 2 days) protected against hepatotoxicity due to the inhalation of CCl4 vapor (4800-6100 ppm for 2 h). This was evidenced by lessening of the changes due to CCl4 in liver glucose-6-phosphatase, serum glutamic oxalacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), serum isocitrate dehydrogenase and serum sorbitol dehydrogenase. Decreases in p-nitroanisole demethylation and cytochrome P-450 were also altered. Lipid peroxidation due to CCl4 was decreased by MMH. These biochemical indices of protection were supported by histopathological observations. These results lend further support to the concept that metabolism of CCl4 is necessary for its hepatoxicity.

摘要

用氢氧化甲基汞（MMH）（15毫克/千克，皮下注射，持续2天）对大鼠进行预处理，可预防因吸入四氯化碳蒸汽（4800 - 6100 ppm，持续2小时）所致的肝毒性。这一点可通过减轻四氯化碳对肝脏葡萄糖-6-磷酸酶、血清谷草转氨酶（SGOT）、血清谷丙转氨酶（SGPT）、血清异柠檬酸脱氢酶和血清山梨醇脱氢酶的影响得到证明。对硝基苯甲醚去甲基化和细胞色素P - 450的降低也发生了改变。MMH降低了四氯化碳所致的脂质过氧化。这些保护的生化指标得到了组织病理学观察结果的支持。这些结果进一步支持了四氯化碳代谢对其肝毒性是必要的这一概念。