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硒诱导镉与组织蛋白结合的重新分布:一种可能的抵御镉毒性的保护机制。

Selenium - induced redistribution of cadmium binding to tissue proteins: a possible mechanism of protection against cadmium toxicity.

作者信息

Chen R W, Whanger P D, Weswig P H

出版信息

Bioinorg Chem. 1975 Jan;4(2):125-33. doi: 10.1016/s0006-3061(00)81021-2.

Abstract

The mechanisms involved in the protection by Se against Cd toxicity in the rat were investigated. Se was found to significantly increase the Cd content in the blood and the testis, while decreasing that in the liver and kidney. Se diverted almost all the Cd in the soluble fraction of the testis from low-molecular-weight (MW) proteins to larger ones. Since the soluble fraction was the major subcellular Cd-binding component, the diversion of Cd by Se appears to be a mechanism involved in the protection by this element against the Cd-induced testicular injury. The diversion in binding of the Cd in the soluble fraction to higher MW proteins was also observed in the kidney and liver, and may be a second mechanism involved in the protection of these organs against Cd by Se, in addition to the reductive effect of Se on the tissue Cd concentration. Se was also found in these higher MW Cd-binding proteins. Based on a similarity of MW of about 115,000, the Cd-binding, Se-containing proteins found in these organs appear to be similar. A diversion of Cd from lower MW proteins to larger ones by Se was also found in the plasma, but the Cd-binding, Se-containing proteins in plasma appear to be different from those found in the other organs since they have a larger MW.

摘要

研究了硒对大鼠镉毒性的保护作用机制。发现硒显著增加血液和睾丸中的镉含量,同时降低肝脏和肾脏中的镉含量。硒将睾丸可溶部分中几乎所有的镉从低分子量(MW)蛋白质转移到较大分子量的蛋白质上。由于可溶部分是亚细胞镉结合的主要成分,硒对镉的转移似乎是该元素保护睾丸免受镉诱导损伤的一种机制。在肾脏和肝脏中也观察到可溶部分的镉与较高分子量蛋白质结合的转移,这可能是硒保护这些器官免受镉损伤的第二种机制,此外还有硒对组织镉浓度的还原作用。在这些较高分子量的镉结合蛋白中也发现了硒。基于约115,000的相似分子量,在这些器官中发现的结合镉、含硒的蛋白质似乎相似。在血浆中也发现硒使镉从较低分子量蛋白质转移到较大分子量蛋白质上,但血浆中结合镉、含硒的蛋白质似乎与其他器官中发现的不同,因为它们的分子量更大。

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