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Numerous studies have reported the involvement of oxidative stress in CCl<jats:sub>4<\/jats:sub>\u2010induced liver damage and the hepato\u2010protective effects mediated by different antioxidants. The present study examined the effects of diphenyl diselenide, (PhSe)<jats:sub>2<\/jats:sub>, on hepatotoxicity induced by CCl<jats:sub>4 <\/jats:sub>in rats. To this end, male Wistar rats received (PhSe)<jats:sub>2<\/jats:sub> by oral route at the dosage of 31.2\u00a0mg\/kg for one or two days. After the second day of treatment, rats received CCl<jats:sub>4<\/jats:sub> orally in a single dose. The liver and kidney were utilized for determination of histopathology, biochemical [aspartate (ALT) and alanine (AST) aminotransferases, alkaline phosphatase (ALP), total bilirrubin (TB) and gamaglutamyl transferase (GGT)] and toxicological parameters [thiobarbituric reactive species (TBARS) levels, catalase activity, ascorbic acid, nonprotein thiols (NPSH) and aminolevulinate dehydratase (<jats:italic>\u03b4<\/jats:italic>\u2010ALA\u2010D) activity]. Repeated administration of (PhSe)<jats:sub>2 <\/jats:sub>caused a marked potentiation of hepatotoxicity induced by CCl<jats:sub>4 <\/jats:sub>exposure, as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of TBARS levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid. Pre\u2010treatment with a single dose of (PhSe)<jats:sub>2 <\/jats:sub>prevented the effect of strychnine, a substrate for CYPs, abolishing lethality in mice. This result indicates that (PhSe)<jats:sub>2<\/jats:sub> prevented animal death, suggesting an activator action of (PhSe)<jats:sub>2<\/jats:sub> in CYPs. This study clearly indicates that (PhSe)<jats:sub>2 <\/jats:sub>potentiated acute hepatic damage induced by CCl<jats:sub>4<\/jats:sub>. 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