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Sabiha Sahin, Ozkan Alatas
Med Sci Tech 2010; 51(3-4): RA187-192
Background: Glutathione is an endogenous antioxidant and has an ubiquitous role in many of the body’s defences. Treatment with N-acetylcysteine (NAC) has been shown to increase levels of glutathione, and NAC has been proposed as a treatment for several illnesses. In recent years, N-acetyl-L-cysteine has been widely investigated as a potentially useful protective and antioxidative treatment for many diseases. The aim of the present study was to further evaluate the mechanisms of the NAC protective effect against carbon tetrachloride-induced acute liver injuries in rats.
Material/Methods: In an experimental study, 24 Sprague-Dawley albino rats were divided into 3 equal groups – Control, CCl4 and CCl4+NAC. Four ml/kg olive oil was administered intraperitoneally (i.p.) to the control group, and 4 ml/kg CCl4 (1.1 dissolved in olive oil) was administered i.p. to the CCl4 and CCl4+ NAC groups. Three and 6 hours later, 150 mg/kg NAC was administered i.p. to the NAC group. Twenty-four hours after administering CCl4, all of the groups were sacrificed. Biochemical assessments were performed using serum AST, ALT, tissue and serum MDA, tissue MPO and NO levels. Histopathological assessments were performed using hematoxylin and eosin staining in light microscopy.
Results: Serum AST, ALT, tissue and serum MDA, MPO, NO levels were all increased in the CCl4 group, but they were decreased in the group treated with NAC. There was a significant difference between the CCl4 and CCl4 +NAC groups (p<0.05), and NO reduction was found at a limited level.
Histopathological comparison of the groups showed a decrease in congestion, polymorphonuclear leukocytes, mononuclear leukocytes, vacuolar degeneration of hepatocytes and hepatocellular necrosis decreased in the group treated with NAC.
Conclusions: As NAC is currently used in humans intoxicated with paracetamol, it can be tested in acute hepatic failure for other reasons. Our results suggest that NAC prevents experimental acute hepatic failure by preventing oxidative stress.
Keywords: acute liver injury, , rat, , CCl4, , N-acetylcysteine