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Background: 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. Materials and Methods: 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. Results: 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. Conclusion: 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.

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Background: It has been indicated that there is a relationship between vitamin B12 status and cognitive functioning. Measurement of serum vitamin B12 is routinely performed in patients with memory loss during initial diagnosis. Noticing the role of cholinergic system and vitamin B12 on memory, the aim of this experimental study was to examine the effect of the interactions between vitamin B12 and nicotine on memory retention in passive avoidance learning in adult male rats. Materials and Methods: The present study was an experimental one. Drugs, including vitamin B12 (0.01, 0.02, 0.03, 0.05, 0.1, and 1 µg/rat) and nicotine (0.1, 0.5, and 1 µg/rat) were administrated after training session intracerebroventriculary (i.c.v.). The drugs were used (i.c.v.) in a volume of 1µl/rat immediately after the training session. The level of memory retention was evaluated by passive avoidance learning. Twenty-four hours after training, a retention test was performed to determine long-term memory. Statistical analysis was carried out using one-way ANOVA test. Results: The results showed that the administration of vitamin B12 and nicotine significantly increased memory retention in rats. Nicotine significantly increased the response to vitamin B12 in memory retention process. Conclusion: Vitamin B12 through interaction with cholinergic system acts in memory retention process.