Al-Bader A, Abul H, Hussain T, Al-Moosawi M, Mathew T C, Dashti H
Department of Pathology, Faculty of Medicine, Kuwait University Health Sciences Centre, Safat.
Mol Cell Biochem. 1998 Aug;185(1-2):1-6. doi: 10.1023/a:1006850514295.
Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.
研究了硫代乙酰胺诱导的大鼠硒缺乏效应。如预期的那样,饮用水中添加硫代乙酰胺(0.3 g/L)导致肝脏中硒显著流失。同时伴有肝硬化以及肝脏重量和肝体比显著增加。脾脏中硒的显著流失也伴随着其重量增加。然而,肺、睾丸和肾脏的重量不受硫代乙酰胺影响,其硒含量也没有变化。硫代乙酰胺处理组的血浆硒水平显著降低。所有这些变化都被证实是由硫代乙酰胺导致的硒缺乏引起的,因为补充硒可逆转这些变化。硒的作用方式尚不清楚,但可能涉及抗氧化防御机制。