LAUSR

Objective(s): The goal of this study was to evaluate the neuroprotective effects of vit B12 on paraquat-induced neurotoxicity. Materials and Methods: Thirty-six male mice were randomly divided into six groups. Three groups were treated intraperitoneally with paraquat (10 mg/kg) twice a week (with a 3-day interval) for 3 weeks. Normal saline, vit B12 (1 mg /kg), or vit C (50 mg/kg) was injected 30 min before paraquat administration. Other groups only received normal saline (control), vit B12, or vit C in the same protocol. Motor performance and coordination were assayed by challenging beam traversal, pole, open field, and rotarod tests. The hippocampus and serum samples were isolated to evaluate the oxidative stress (GSH and ROS), apoptosis (caspase 3), and inflammatory markers (TNF-α and IL-1β). Results: Administration of paraquat leads to induction of motor deficits, which were improved by treatment with vit B12. In addition, vit B12 could prevent oxidative damage, apoptosis, and inflammation caused by paraquat. Conclusion: It seems that vit B12 could be a novel therapeutic agent in the management of paraquat induced-neurotoxicity.