Incurrent societies, the riskof toxic liver damagehasmarkedly increased. The aimof thepresentwork was to carry out further research into the mechanism(s) of livermitochondrial damage inducedby acute (0.8 g/kgbodyweight, single injection) or chronic (1.6 g/ kg bodyweight, 30 days, biweekly injections) carbon tetrachloride–induced intoxication and to evaluate the hepatoprotective potential of the antioxidant, melatonin, as well as succinate and cranberryflavonoids in rats. Acute intoxication resulted in considerable impairment of mitochondrial respiratory parameters in the liver. The activity of mitochondrial succinate dehydrogenase (complex II) decreased (by 25%, pb0.05). Short-term melatonin treatment (10 mg/kg, three times) of rats did not reduce the degree of toxicmitochondrial dysfunction but decreased the enhanced NO production. After 30-day chronic intoxication, no significant change in the respiratory activity of livermitochondriawas observed, despite marked changes in the redox-balance of mitochondria. The activities of the mitochondrial enzymes, succinate dehydrogenase and glutathione peroxidase, as well as that of cytoplasmic catalase in liver cells were inhibited significantly. Mitochondria isolated from the livers of the rats chronically treated with CCl4 displayed obvious irreversible impairments. Long-term melatonin administration (10 mg/kg, 30 days, daily) to chronically intoxicated rats diminished the toxic effects of CCl4, reducing elevated plasma activities of alanine aminotransferase and aspartate aminotransferase and bilirubin concentration, prevented accumulation of membrane lipid peroxidation products in rat liver and resulted in apparent preservation of the mitochondrial ultrastructure. The treatment of the animals by the complex of melatonin (10 mg/kg) plus succinate (50 mg/kg) plus cranberryflavonoids (7 mg/kg) was even more effective in prevention of toxic liver injury and liver mitochondria damage