Quercetin mitigates lead acetate-induced behavioral and histological alterations via suppression of oxidative stress, Hsp-70, Bak and upregulation of Bcl-2

- Lead acetate (LA) induced motor and somatosensory impairments and oxidative stress.
- LA have shown upregulation of Hsp-70 and Bak and downregulation of Bcl-2.
- Quercetin successfully protected the histological architecture of brain.
- Quercetin reduced the lead-induced oxidative stress and inhibited the apoptosis.

Lead toxicity is of major health concern due to its persistence in environment that induces cognitive impairment and neuronal degeneration. The present study was conducted to investigate the efficacy of quercetin, a ubiquitous bioflavonoid against lead-induced neurotoxicity in Wistar rats. Briefly, lead acetate (20 mg/kg) was injected i.p., followed by oral administration of quercetin (50 and 100 mg/kg) once daily for five consecutive days. On 6th day, rats were assessed for motor co-ordination, grip strength and sensorimotor impairment (by adhesive removal test). Lead treated rats have shown marked behavioral impairment with increased oxidative stress. Quercetin reduced lead-induced oxidative burden in brain, thus maintained the normal behavioral functions of lead-intoxicated rats. The lead administered group showed severely vacuolated and pyknotic nuclei with high expressions of Bak and Hsp-70. The expression of anti-apoptotic Bcl-2 was observed to be reduced in lead intoxicated group. Quercetin however, restored the normal morphology of brain and the expressions of Bak, Bcl-2 and Hsp-70. In conclusion, quercetin mitigates the toxic effect of lead effectively and thus, may be an important compound for developing effective therapeutic intervention against metal toxicity.