Abstract

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.