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Abstract

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.

Contents and Uptake Rates of Mn, Fe, Co, Zn, and Se in Se-Deficient Rat Liver Cell Fractions

“…The percentage of liver weight to body weight was significantly larger in the SeD rats than in the normal rats. In a previous study by Al-Bader et al, 24 rats administered thioacetamide (which is known to cause Sedeficiency) developed liver cirrhosis and showed significant increases in both liver weight and the ratio of liver-to-body weight. In this study, the total amounts of each dry cell fraction for the INAA samples and each wet cell fraction for the MTA samples were weighed.…”

The possible role of selenium concentration in hepatitis B and C patients

“…[26] observed a significant decrease of serum selenium concentration accompanied by liver cirrhosis in rats when they were given thioacetamide, and the changes were reversed when selenium supplementation was introduced. On the other hand, Buljevac et al .…”

SelW protects against H2O2-induced liver injury in chickens via inhibiting inflammation and apoptosis

“…4 Se deciency can decrease the liverelimination abilities of toxic substances, which causes liver damage characterized by hepatomegaly or liver atrophy, a rough surface with red and yellow, liver cells having fatty degeneration, cytoplasm disappearance, and diffuse cellular debris. 5,6 The production of reactive oxygen species (ROS) is a natural consequence of a variety of essential biochemical reactions; however, excessive ROS is implicated in the pathogenesis of several diseases, such as alcoholic liver diseases, 7 non-alcoholic fatty liver disease, 8 liver brosis 9 and hepatitis. 10 ROS not only initiates MAPK activation, but also potently regulates the pro-inammatory transcription factor NF-kB.…”