The detoxication of aflatoxin B1 with glutathione in the rat.
The detoxication of aflatoxin B1 with glutathione in the rat.
复制标题
谷胱甘肽对黄曲霉毒素B1在大鼠体内的解毒作用。
DOI：
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发表时间：
1979
期刊：
影响因子：
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通讯作者：
R. Dixon
中科院分区：
文献类型：
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作者：
G. Emerole;N. Nešković;R. Dixon
1.研究了谷胱甘肽(GSH)对大鼠黄曲霉毒素B1的灭活作用。黄曲霉毒素B1与[~3H]谷胱甘肽的代谢产物在体外与大鼠肝微粒体的结合不显著。与大鼠肝脏10000g上清液孵育后，结合力增加。在相同条件下，苯并(A)芘代谢产物与[~3H]谷胱甘肽的结合比与黄曲霉毒素B1的结合要强得多。2.预先给予黄曲霉毒素1(2 mg/kg)可引起大鼠肝脏GSH耗竭，6h最低，24 h恢复正常，GSH S-转移酶活性在6h略有升高，24 h恢复正常。3.肾GSH无明显下降，但肾脏GSH-S转移酶活性在6h突然升高，24 h基本恢复正常。5.大鼠肝脏和肾脏谷胱甘肽S转移酶活性在染毒后2小时最高，24小时后逐渐下降。6.谷胱甘肽对黄曲霉毒素B1代谢产物的亲核活性低于对苯并(A)芘代谢产物的亲核活性。
1. The deactivation of aflatoxin B1 by glutathione (GSH) has been investigated in rat. Binding of metabolites of aflatoxin B1 to [3H]glutathione in vitro with rat liver microsomes is insignificant. Incubation with rat liver 10 000 g supernatant results in increased binding. Under identical conditions, benzo(a)pyrene metabolites are bound to [3H]glutathione much more than is aflatoxin B1. 2. Pre-treatment of rats with aflatoxin 1 (2 mg/kg) caused depletion in GSH of rat liver with a minimum at 6 h but returning to above normal at 24 h. GSH S-transferase activity was marginally increased at 6 h also and returned to normal at 24 h. 3. Kidney GSH was not significantly decreased, but kidney GSH S-transferase activity showed a sudden increase in 6 h, returning to almost normal at 24 h. 4. Pre-treatment with benzo(a)pyrene (2 mg/kg) caused greater depletion of hepatic GSH than occurred with aflatoxin B1 but did not show any effect on kidney GSH. 5. Hepatic and kidney GSH S-transferase in benzo(a)pyrene-treated rats showed greatest activity at 2 h followed by a gradual fall through 24 h. 6. GSH was therefore a less efficient nucleophile for aflatoxin B1 metabolites than for benzo(a)pyrene metabolites.