Ascorbic acid and glutamate as therapeutics for oxidative stress and behavioral dysfunction in rats exposed to zinc nanoparticles

Oxidative stress is the main manifestation of several neurodegenerative diseases. The same metabolic and behavioral scheme can be seen in neurotoxicity. Several factors are likely to induce oxidative stress. Metallic oxides nanoparticles (NPs) induce the formation of reactive oxygen species, which may seriously affect the brain despite the blood-brain barrier. However, the strategies to protect the brain and/or to restore its physiological equilibrium following neurotoxicity induced by NPs are still under investigation.

Here we use eight groups of rats to show how oxidative damage from zinc oxide can be mitigated. The neurotoxicity can be mitigated by the intervention of ascorbic acid (AA) and glutamate (Glu) to restore the activity of the antioxidative system and mitigate the behavioral disorder caused by zinc oxide NPs (ZnO-NPs).

Biochemical analysis shows that the administration of ZnO-NPs at 25 mg/Kg causes an oxidative response in the brain which alters the serum biochemical parameters and induces serious disorders in the behavior of animals.

The combined treatments using AA and Glu with nanoparticles proved to be corrective at the biochemical level. Using the elevated plus maze (EPM) test, we demonstrated that AA and AA + Glu cure the anxious state and ameliorate the damage to the learning and memory of rats caused by ZnO-NPs.