Hesperidin restores experimentally induced neurotoxicity in Wistar rats.

Carbon tetrachloride (CCl4) is a highly toxic industrial solvent with pronounced systemic toxicity including brain. Neurotoxicity may be a direct result of hepatic dysfunction from CCl4 intoxication. Over the years CCl4 has been used as an excellent model for studying experimentally induced neurotoxicity in murine models. Hesperidin (HP) is a known cytoprotectant with comprehensive anti-oxidant and neuroprotective properties. The aim of the present study was to evaluate experimentally induced neurotoxicity by CCl4 and its abrogation by using antioxidant potential of HP. CCl4 caused a significant enhancement in the lipid peroxidation (LPO) levels and protein carbonyl (PC) content. HP supplementation significantly restored the LPO levels and PC content. It also replenished the altered enzymatic and non-enzymatic antioxidants in brain tissues of rats. The neurotoxicity markers were also restored to normalcy with HP treatment. It is suggested that HP, by attenuating neuronal oxidative stress, holds promise that can ameliorate CCl4-induced neurotoxicity. HP has the potential to be explored as a universal neuroprotectant in xenobiotically induced neurotoxicity mediated by oxidative stress.