Introduction: Arsenic (As) is one of the heavy metals and it is widely present in our environment polluting the food and water consumed by the human. Chronic exposure to As leads to arsenic toxicity that produces certain undesirable effects on the human body including substantia nigra (SN) dopaminergic cells neurotoxicity. Selenium (Se) has many protective effects on the human body against toxic substances that include antidegenerative effects proved on the substantia nigra of the midbrain.
The Aim of the Work: The current study was carried out for evaluation of the possible neuroprotective role of selenium in arsenic-induced midbrain substantia nigra neurotoxicity in guinea pig model.
Material and Methods: In the current study, sixty adult male guinea pigs were used. The animals were left for 7 days to acclimate in the new environment then, divided randomly into equal 4 groups with fifteen animals per group. Group A (Control group); received distilled water orally daily. Group B (Se-treated group); received sodium selenite at a single daily orally dose of 0.25 mg/kg/day. Group C (As-treated group); received sodium arsenite at a single daily orally dose of 2.5 mg/kg/day. Group D (As & Se-treated group); received sodium arsenite at a single daily orally dose of 2.5 mg/kg/day followed after 2 hours by sodium selenite at a single daily orally dose of 0.25 mg/kg/day. The drugs were given daily for successive 8 weeks.
Results: The Arsenic exposure resulted in deformed dopaminergic neurons, many neurons with vacuolated cytoplasm and congested blood vessels. However, the co-administration of selenium showed normal multiple pyramidal dopaminergic neurons, no obvious cytoplasmic vacuoles or dilated vessels.
Conclusion: Selenium proved a protective effect on neurodegenerative toxic morphological changes induced by arsenic in dopaminergic neurons of SN of midbrain in guinea pig model.