Abstract
N-acetylcysteine (NAC) increases tissue levels of glutathione and has been widely investigated as a protective and antioxidative agent. This study evaluated the protective effect of NAC on under carbon tetrachloride (CCl4)-induced acute liver injury in the rat. Three-month-old Sprague-Dawley rats were intraperitoneally administered 4 mL/kg CCl4 (1:1 dissolved in olive oil, group 1) or 4 mL/kg CCl4 + NAC 150 mg/kg, 3 and 6 h after CCL4 (group 2) or 4 mL/kg olive oil (group 3, control). Twenty-four hours after administering CCl4, all of the rats were sacrificed. Biochemical assessment of serum transaminases and malonaldehyde (MDA) and tissue MDA, myeloperoxidase (MPO), and nitric oxide was done. Histopathological assessments were performed. Serum transaminases and tissue and serum MDA and tissue MPO were all increased in group 1 compared to control and were significantly decreased in the group treated with NAC. Histopathological comparison of the groups showed a decrease in congestion, polymorphonuclear leukocytes, mononuclear leukocytes, vacuolar degeneration of hepatocyte, and hepatocellular necrosis in the group treated with NAC. Our results suggest that NAC prevents experimental acute hepatic failure by preventing oxidative stress.
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