Neuro-protective and redox potential of troxerutin against cypermethrin-induced neurotoxicity and oxidative stress in mice

The present study was designed to evaluate the protective efficacy of troxerutin against cypermethrin-induced behavioral defects, motor function abnormalities, and oxidative stress in mice. Twenty-four adult female albino mice were randomly divided into four equal groups. The first group served as control, the second group was treated with cypermethrin (20 mg/kg b.w) intraperitoneally at day 21, and the remaining two groups were orally supplemented with TRX (150, 300 mg/kg b.w) for 20 days and with cypermethrin (20 mg/kg b.w) intraperitoneally at day 21. Behavior activities recorded after cypermethrin exposure showed significantly impaired motor function (p <= 0.05) as evidenced by the beam balance and pole test. The cypermethrin was also found to cause significant memory dysfunction. Moreover, the oxidative stress in terms of increased tissue malondialdehyde level (p <= 0.05) was recorded in the cypermethrin group. The antioxidant activities of catalase and glutathione peroxidase were decreased (p <= 0.05) after cypermethrin exposure. Troxerutin supplementation significantly improved the cypermethrin-induced motor impairment and memory dysfunction. The supplementation of troxerutin significantly restored the redox status. Troxerutin attenuates the neurotoxic and behavioral deficits cypermethrin-induced oxidative stress by improving the oxidative stress markers.