Lead Acetate Induced Cerebral Tissue Damage; The Effect of Phoenix dactylifera Pits Extract

Abstract

This study investigates effect of Phoenix dactylifera pits extract (PdPE) on Lead acetate induced cerebral tissue damage. Wistar rats of average weight 150 g were divided into seven groups of six animals each. GRPI animals received distilled water only, GRPII received 60 mg/kg Lead acetate 5 times a week for 3 weeks then distilled water only for ten days (Negative control), GRPIII and GRPIV (treatment groups) received 60 mg/kg Lead acetate 5 times a week for 3 weeks then treated with 150 mg/kg PdPE and 300 mg/kg PdPE respectively for 10 days, Group V and Group VI (protective groups) received 150 mg/kg PdPE and 300 mg/kg PdPE respectively for 10 days then 60 mg/kg Lead acetate 5 times a week for 3weeks, while GRPVII animals received 60 mg/kg Lead acetate 5 times a week for 3 weeks then treated with 25 mg/kg Dimercaptosuccinic acid (DMSA) alone 4 times a week then distilled water for 3 days. Lead acetate induced cerebral tissue damage was evident from depleted reduced-glutathione and lipid peroxidation as shown by elevated malondialdehyde and nitrite concentration. Histological examination of the cerebral tissue showed congestion of the meningeal vessels and cellular infiltration. Malondialdehyde and nitrite were significantly reduced by 300 mg/kg PdPE (P<0.03). 300 mg/kg PdPE protective and treatment groups and 25 mg/kg DMSA ameliorates antioxidant depletion and showed significant protective effect against cerebral tissue damage. Memory assessment showed that 300 mg/kg PdPE and 25 mg/kg DMSA treatment significantly alleviate memory impairment induced by Lead acetate. Results from the study indicate that PdPE has the ability to alleviate lead acetate induced cerebral tissue damage in rats. PdPE may exert its protective and therapeutic effect against lead-induced cerebral damage possibly through its antioxidant mechanisms and due to the presence of membrane protecting unsaturated fatty acids.