The effect of sodium molybdate on decreasing CCl4-induced tissue injury in rats

Molybdenum is an essential trace element for both animals and plants. Molybdenum (Mo), which functions as a cofactor for a limited number of enzymes including xanthine dehyrogenase, aldehyde oxidase, and sulfite oxidase in mammals, is believed to be an essential trace element in animal nutrition. The aim of this study is to evaluate the hepatoprotective potential of sodium molybdate against carbon tetrachloride (CCl4) induced liver damage. In an experimental study, adult male rats received daily oral administrations of different doses of sodium molybdate (0.05, 0.1, and 0.2 g/kg bw) along with intrapertioneal CCl4 (50% CCl4 in olive oil, 1 ml/kg bw) twice a week for 28 consecutive days. Histopathological examinations in CCl4-treated rats showed extensive liver injuries characterized by extensive hepatocellular degeneration and necrosis, fat degeneration, and inflammatory cell infiltration while histopathological changes induced by CCl4 were significantly attenuated by sodium molybdate treatment. The results of this study suggest that sodium molybdate could protect liver against the CCl4-induced oxidative damage in rats, and this hepatoprotective effect might be contributed to the protection of liver by preventing the toxic chemical reactions which generate oxidative stress, lipid peroxidation, and molecular changes which ultimately lead to liver tissue necrosis.