The Effect of N-acetylcysteine on Pyrrolized Protein, Lipid Hydroperoxide and Thiol Levels in the Carbon Tetrachloride Hepatotoxicity

Author(s): C. Yazici, K. Kose, E. Delibas, K. Deniz and I. Gunturk
Department of Medical Biochemistry, 1Department of Pathology, Erciyes University, Faculty of Medicine, 38039−Kayseri, Turkey

Correspondence Address:
K. KÖSE Department of Medical Biochemistry, Erciyes University, Faculty of Medicine, 38039−Kayseri, Turkey E-mail: [email protected]

This study was performed, on the rat model, to form oxidative stress by carbon tetrachloride (CCl4) and to reveal the relationship between toxicity and oxidative/thiol stresses through lipid/protein oxidation and to investigate the effects of N-acetylcysteine on the hepatotoxicity induced oxidative stress. Wistar albino male rats were divided into four groups as CCl4, N-acetylcysteine, CCl4-N-acetylcysteine and Control, each of ten rats. CCl4 (1.0 ml, 800 mg/kg; single dose) and N-acetylcysteine (200 mg; three doses) were intraperitoneally applied to corresponding groups as per kg of rat weight. Hepatotoxicity was identified with histopathological methods. Besides the thiol levels in plasma/tissue samples, pyrrolized protein and total lipid hydroperoxide levels in serum samples were measured. CCl4-induced hepatotoxic lesions remarkably improved in the presence of N-acetylcysteine. There was no significant difference between Control and N-acetylcysteine groups, in terms of parameters measured in serum/plasma and tissue samples. When compared to these groups, pyrrolized protein and total lipid hydroperoxide levels were found to be higher; whereas plasma/tissue thiol levels lower in the CCl4 group. N-acetylcysteine in combination with CCl4 significantly lowered pyrrolized protein and total lipid hydroperoxide levels, and increased thiol levels, so that the values were reached to those of Control and N-acetylcysteine groups. As reflected by higher pyrrolized protein and total lipid hydroperoxide, and lower thiol levels, enhanced free radical production in the CCl4 hepatotoxicity may lead to oxidative and thiol stresses mediated lipid/protein oxidation. In addition, N-acetylcysteine, a powerful antioxidant, may be added as a thiol source to the treatment protocols of several diseases whose pathogenesis is of oxidative and thiol stress.

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