[Oxidative stress of deltamethrin on rat nervous system]

Huang-yuan Li1, Nian Shi, Dan Chen

  • 1Department of Health Toxicology, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province 430030, China.

Abstract

Insights

Deltamethrin (DM) exposure induces oxidative stress in rat brain tissues, evidenced by increased lipid peroxidation and altered antioxidant enzyme activities. Decreased gamma-glutamylcysteine synthetase and glutathione reductase activities may drive reduced glutathione levels in the hippocampus.

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Context:

  • Pesticide exposure and its neurological effects are a growing public health concern.
  • Deltamethrin (DM) is a widely used pyrethroid insecticide with known neurotoxic potential.
  • Understanding the specific mechanisms of DM neurotoxicity is crucial for risk assessment and mitigation.

Purpose:

  • To investigate the impact of deltamethrin on lipid peroxidation and antioxidant defense systems in the rat cerebral cortex and hippocampus.
  • To elucidate the biochemical pathways underlying deltamethrin-induced neurotoxicity.

Summary:

  • Administration of deltamethrin to Wistar male rats at doses of 3.125 and 12.500 mg/kg/day for 5 days.
  • Assessed malondialdehyde (MDA) levels, and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px), glutathione reductase (GR), reduced glutathione (GSH), and gamma-glutamylcysteine synthetase (gamma-GCS).
  • Deltamethrin exposure increased MDA content, decreased SOD and CuZn-SOD activities in the cerebral cortex, and altered GSH levels and gamma-GCS and GR activities in both brain regions, suggesting oxidative stress.

Impact:

  • This study identifies oxidative stress as a key mechanism in deltamethrin neurotoxicity.
  • The findings highlight the role of altered antioxidant enzyme activities, particularly gamma-GCS and GR, in deltamethrin-induced GSH depletion in the hippocampus.
  • Results contribute to a better understanding of pesticide-induced neurological damage and inform safety guidelines.

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