Selenium nanoparticles impart robust neuroprotection against deltamethrin-induced neurotoxicity in male rats by reversing behavioral alterations, oxidative damage, apoptosis, and neuronal loss

Neurotoxicology. 2022 Jul:91:329-339. doi: 10.1016/j.neuro.2022.06.006. Epub 2022 Jun 23.

Abstract

This study investigated the neuroprotective role of selenium nanoparticles (SeNPs) on deltamethrin-induced neurotoxicity in rats. A total of 32 adult male Wister rats were allocated into the following four groups: 1) control, 2) deltamethrin (0.6 mg/kg), 3) SeNPs (0.5 mg/kg), and 4) deltamethrin + SeNPs. All agents were administered orally three times per week for 2 months. Locomotor behavior, anxiety-like behavior, biochemical parameters, including brain oxidative damage biomarkers (Malondialdehyde (MDA) and reduced glutathione (GSH)), brain acetylcholinesterase (AChE), and brain genotoxicity were evaluated. The gene expression levels of IGF-1 and Bcl2 were also determined. Moreover, a brain histopathological examination associated with the immunohistochemical determination of Bax in brain tissue was performed. Deltamethrin-intoxicated rats showed a reduction in the locomotor activity associated with a highly anxious state. They also displayed a disturbance in the brain redox state with a decrease in the brain AChE levels and a high DNA fragmentation percentage. Furthermore, they showed a decrement in the immunohistochemical GFAP levels as well as IGF-1 and Bcl2 gene expression levels with an increase in the immunohistochemical Bax levels. All these changes were confirmed by brain histopathology. Interestingly, SeNPs ameliorated all these changes and restored the normal brain architecture. In conclusion. SeNPs possess a potent medicinal activity due to their antioxidant and anti-inflammatory activity. Therefore, SeNPs can be a potential agent in ameliorating deltamethrin-induced neurotoxicity.

Keywords: Anxiety; Apoptosis; Deltamethrin; Neurotoxicity; Oxidative stress; Selenium nanoparticles.

MeSH terms

  • Acetylcholinesterase / metabolism
  • Animals
  • Antioxidants / pharmacology
  • Apoptosis
  • Insulin-Like Growth Factor I / metabolism
  • Male
  • Nanoparticles* / toxicity
  • Neuroprotection
  • Neurotoxicity Syndromes* / etiology
  • Neurotoxicity Syndromes* / metabolism
  • Neurotoxicity Syndromes* / prevention & control
  • Nitriles
  • Oxidative Stress
  • Pyrethrins
  • Rats
  • Rats, Wistar
  • Selenium* / pharmacology
  • bcl-2-Associated X Protein / genetics
  • bcl-2-Associated X Protein / metabolism

Substances

  • Antioxidants
  • Nitriles
  • Pyrethrins
  • bcl-2-Associated X Protein
  • decamethrin
  • Insulin-Like Growth Factor I
  • Acetylcholinesterase
  • Selenium