Selenite toxicity, depletion of liver S-adenosylmethionine, and inactivation of methionine adenosyltransferase.
Selenite toxicity, depletion of liver S-adenosylmethionine, and inactivation of methionine adenosyltransferase.
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亚硒酸盐毒性、肝脏 S-腺苷甲硫氨酸耗竭以及甲硫氨酸腺苷转移酶失活。
DOI：
10.1016/0003-9861(77)90096-0
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发表时间：
1977
影响因子：
3.9
通讯作者：
J. L. Hoffman
中科院分区：
文献类型：
--
作者：
J. L. Hoffman
探讨了二甲基硒的产生消耗肝脏-腺苷蛋氨酸作为亚硒酸盐毒性的生化基础的可能性。亚硒酸盐（25 nmol/ g体重）的毒性剂量可迅速降低小鼠肝脏腺苷基蛋氨酸，增加腺苷基同型半胱氨酸，表明转甲基化率增加。然而，在二甲基硒合成停止后，s -腺苷蛋氨酸水平仍处于低水平，这表明亚硒酸盐灭活了蛋氨酸腺苷转移酶。通过测量分级剂量亚硒酸盐对蛋氨酸类似物乙硫氨酸转化为s -腺苷基蛋氨酸的影响，发现这是体内酪蛋白。体外研究也表明亚硒酸盐能使这种酶失活。如上所述，注射25 nmol /g亚硒酸盐的小鼠肝脏匀浆的蛋氨酸腺苷转移酶活性低于注射盐水的对照组的50%。
The possibility that dimethyl selenide production depletes liverS-adenosylmethionine was explored as a biochemical basis for selenite toxicity. Toxic doses of selenite (25 nmol/ g body weight) were found to rapidly decrease mouse liverS-adenosylmethionine and increaseS-adenosylhomocysteine, indicative of an increased rate of transmethylation. However,S-adenosylmethionine levels remained depressed beyond the time when dimethyl selenide synthesis ceased, suggesting that selenite inactivated methionine adenosyltransferase. This was found to be the casein vivoby measuring the effect of graded doses of selenite on the conversion of the methionine analog, ethionine, toS-adenosylethionine.In vitrostudies also indicated inactivation of this enzyme by selenite. Liver homogenates from mice injected with 25 nmol of selenite/g, as above, were found to have less than 50% of the methionine adenosyltransferase activity of saline-injected controls.