Protective influence of diphenyl- p-phenylenediamine on hydrazine induced lipid peroxidation and hepatic injury

Abstract

Previous studies have demonstrated the ability of water soluble and/or lipid soluble antioxidants to reduce the toxicity as well as the biochemical, functional, and pathological changes induced by a variety of hepatotoxic agents. To further determine the ability of diphenyl- p-phenylenediamine (DPPD) to modify chemical induced hepatic injury, the influence of DPPD on hydrazine-induced hepatic toxicity was assessed. The administration of hydrazine to rats significantly increased liver triglycerides. Significant inhibition of triglyceride accumulation occurred in the DPPD-treated group. Hydrazine also caused an increase in hepatic lipid peroxidation as reflected by malonaldehyde (MDA) formation. The enhancement in MDA formation was prevented by DPPD treatment. In contrast to the profound hepatic necrosis observed following hydrazine, livers from DPPD treated rats which received hydrazine showed only mild architectural alterations. The hypoglycemia and retention of BSP which developed upon hydrazine administration was not modified by DPPD. The ability of the lipid soluble antioxidant, DPPD, to significantly inhibit hydrazine-induced fatty infiltration, necrosis, and lipid peroxidation further accents the potential of employment of appropriate antioxidants in the prevention of chemical-induced hepatic injury.