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<p>Researchers have implicated mercury (Hg) exposure in the pathogenesis of autism spectrum disorder (ASD) through multiple mechanisms, including oxidative stress, mitochondrial dysfunction, and glutamatergic dysregulation. This review delineates the molecular and cellular pathways by which Hg exerts neurotoxic effects, emphasizing its disruption of the glutamate–glutamine–GABA cycle and the resulting excitotoxic activation of NMDA receptors. The selenium (Se)–glutathione (GSH) axis is central to these processes, which play a pivotal role in Hg detoxification and the maintenance of redox balance. Individuals with ASD frequently exhibit impairments in these systems, increasing their susceptibility to Hg-induced neurotoxicity. Nutritional strategies to restore Se and GSH levels may mitigate oxidative stress and neurobehavioral abnormalities in ASD. By integrating findings from molecular studies, animal models, and clinical research, this paper proposes a targeted therapeutic framework to address environmentally mediated biochemical vulnerabilities in ASD.</p>

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Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium–glutathione axis

  • 期刊论文

  • 发表日期：

    2026年2月26日

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  • Afaf El-Ansary,
  • Laila Al-Ayadhi,
  • Ahmed Dewedar,
  • Ramesa Shafi Bhat,
  • Ramiz Saad,
  • Geir Bjørklund

摘要

Researchers have implicated mercury (Hg) exposure in the pathogenesis of autism spectrum disorder (ASD) through multiple mechanisms, including oxidative stress, mitochondrial dysfunction, and glutamatergic dysregulation. This review delineates the molecular and cellular pathways by which Hg exerts neurotoxic effects, emphasizing its disruption of the glutamate–glutamine–GABA cycle and the resulting excitotoxic activation of NMDA receptors. The selenium (Se)–glutathione (GSH) axis is central to these processes, which play a pivotal role in Hg detoxification and the maintenance of redox balance. Individuals with ASD frequently exhibit impairments in these systems, increasing their susceptibility to Hg-induced neurotoxicity. Nutritional strategies to restore Se and GSH levels may mitigate oxidative stress and neurobehavioral abnormalities in ASD. By integrating findings from molecular studies, animal models, and clinical research, this paper proposes a targeted therapeutic framework to address environmentally mediated biochemical vulnerabilities in ASD.