Relative and Combined Effects of Selenium, Protein Deficiency and Ethanol on Hepatocyte Ballooning and Liver Steatosis

Abstract

Oxidative damage plays a key role in alcohol-mediated liver alterations. Selenium, a potent antioxidant, is decreased in alcoholics. This study was conducted to analyse if the supplementation with selenium may alter liver changes in a murine model fed ethanol and/or a 2 % protein-containing diet, following the Lieber-DeCarli design. Adult male Sprague Dawley rats were divided into eight groups which received the Lieber-DeCarli control diet; an isocaloric, 36 % ethanol-containing diet; an isocaloric, 2 % protein-containing diet; and an isocaloric diet containing 2 % protein and 36 % ethanol diet; and other similar four groups to which selenomethionine (1 mg/kg body weight) was added. After sacrifice (5 weeks later), liver fat amount and hepatocyte areas of pericentral and periportal cells were measured, and liver and serum selenium, activity of liver glutathione peroxidase (GPX), and liver malondialdehyde were determined. Ethanol-fed rats showed increased hepatocyte areas and fat accumulation especially when ethanol was added to a 2 % protein diet. Selenium caused a decrease in hepatocyte ballooning and liver fat amount, but an increase in GPX activity, and a marked increase in serum and liver selenium. The present study demonstrates that selenium, added to the diet of rats in the form of seleniomethionine, prevents the appearance of early signs of ethanol-mediated liver injury under the conditions of the Lieber-DeCarli experimental design.