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Background: Growing evidences reported that zinc oxide nanoparticles (ZnONPs) could reach the brain after oral ingestion; however, the “neurotoxicity of” ZnONPs after oral exposure has not been fully investigated. This study aimed to confirm the “neurotoxicity of” ZnONPs and the possible neuroprotective role of selenium.
Material and Methods: Post acclimatization, forty male albino rat were categorized into four groups (n= 10); G1: Healthy control, G2: Selenium-administered rats, 0.2 mg/kg/day, oral gavage and G3-G4: Treated groups, orally- given 1 g/kg/day ZnONPs by gastric tube for 5 consecutive days and divided as follows; G3: ZnONPs intoxicated rats., G4: ZnO NPs intoxicated rats with co-administration of selenium daily. Selenium was orally-given for 8 consecutive days, 3 days of them before the start of the experiment.
Results: The exposure of experimental animals to ZnO NPs confirmed the induction of an elevated percentage of apoptosis in the cerebellar tissue leading to damaged neurocytes in the three cortical layers. This could be detected via a significant increase in the immunoreactivity of caspase 3(an apoptosis marker) and morphometric analysis due to the subsequent release of reactive oxygen species (ROS. Concerning GFAP, a significant decrease in the immunoreactivity in astrocytes and glial nerve fibers was recorded as compared to control. These observations may be due to a focal loss of cerebellar glial nerve cells or associated with astrocyte damage due to ZnO NPs intoxication and the possible change in their functional properties and disability to synthesize GFAP protein.
However, these measurements were improved after nutritional co- supplemntation of 0.2 mg/kg b.w. with ZnO NPs exposure.
Conclusion: The present results confirmed the “neurotoxicity of” ZnONPs after recurrent oral exposure via oxidative stress and apoptosis. However, supplementation of Se restricted and minimized this effect owing to its antioxidant properties recording a protective role.