Fang S C, Chen R W, Fallin E
Chem Biol Interact. 1976 Sep;15(1):51-7. doi: 10.1016/0009-2797(76)90127-7.
The effect of dietary selenite on the binding characteristics of serum proteins was investigated with rats. In the control serum, the maximal binding of phenylmercuric acetate (PMA) and methylmercuric chloride (MMC) to rat serum protein was approx. 18 and 9 nmoles per mg protein, respectively. The binding of Hg2+ was biphasic and it did not reach a maximum at the concentrations used. Selenite treatment caused a reduction in binding capacity of serum proteins to Hg2+ and PMA, and an increase in the binding affinities. However, there were no such changes for the binding of MMC. Selenite protection from mercury toxicity, therefore, acts not only via a change in tissue distribution and a change in the formation of seleno-proteins but, also, via a change in the binding characteristics to some mercury compounds. In the case of methylmercury, a different mechanism of protection must exist as the modification of tissue distribution, its binding to subcellular and soluble proteins and the binding characteristics remained equivocal.
用大鼠研究了膳食亚硒酸盐对血清蛋白结合特性的影响。在对照血清中，醋酸苯汞（PMA）和氯化甲基汞（MMC）与大鼠血清蛋白的最大结合量分别约为每毫克蛋白18和9纳摩尔。Hg2+的结合是双相的，在所使用的浓度下未达到最大值。亚硒酸盐处理导致血清蛋白与Hg2+和PMA的结合能力降低，结合亲和力增加。然而，MMC的结合没有这种变化。因此，亚硒酸盐对汞毒性的保护作用不仅通过组织分布的改变和硒蛋白形成的改变，还通过对某些汞化合物结合特性的改变来实现。对于甲基汞，由于其组织分布的改变、与亚细胞和可溶性蛋白的结合以及结合特性仍不明确，必然存在不同机制的保护作用。
