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<p>The underlying mechanism for the environmental factor-induced autism spectrum disorder (ASD) remains largely unclear. Considering the recent reports that mitochondria-associated amino acid metabolism contributes to ASD development, we explored the roles of hydrogen sulfide (H<sub>2</sub>S), a gaseous product of sulfur-containing amino acid metabolism, in the social deficits of ASD mice induced by the environmental factor double-hit (DH). We detected synaptic and mitochondrial dysfunction, elevation of H<sub>2</sub>S, dysregulation of sulfur-containing metabolites, and upregulation of cystathionine-β-synthase (CBS) in the anterior cingulate cortex of DH mice. Inhibiting mitochondrial function induced H<sub>2</sub>S accumulation in wild-type neurons, whereas introducing healthy mitochondria suppressed H<sub>2</sub>S levels in DH neurons. Knocking down CBS or restricting sulfur intake significantly ameliorated synaptic dysfunction, social impairments, and anxiety-like behaviors in DH mice. Similar H<sub>2</sub>S accumulation was detected in human DH neurons and ASD patients. Our data demonstrated a role of H<sub>2</sub>S overload in the social dysfunction of environmental factor-induced ASD.</p>

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Elevation of H2S Underlies Social Deficits in Environmental Factor Double-Hit Autism Model

  • 期刊论文

  • 发表日期：

    2026年3月23日

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  • Hongyu Ma,
  • Qing Xu,
  • Songqi Dong,
  • Mengxin Guo,
  • Hanze Liu,
  • Taozhi Wang,
  • Mengmeng Wang,
  • Yazhou Wang,
  • Shengxi Wu

摘要

The underlying mechanism for the environmental factor-induced autism spectrum disorder (ASD) remains largely unclear. Considering the recent reports that mitochondria-associated amino acid metabolism contributes to ASD development, we explored the roles of hydrogen sulfide (H2S), a gaseous product of sulfur-containing amino acid metabolism, in the social deficits of ASD mice induced by the environmental factor double-hit (DH). We detected synaptic and mitochondrial dysfunction, elevation of H2S, dysregulation of sulfur-containing metabolites, and upregulation of cystathionine-β-synthase (CBS) in the anterior cingulate cortex of DH mice. Inhibiting mitochondrial function induced H2S accumulation in wild-type neurons, whereas introducing healthy mitochondria suppressed H2S levels in DH neurons. Knocking down CBS or restricting sulfur intake significantly ameliorated synaptic dysfunction, social impairments, and anxiety-like behaviors in DH mice. Similar H2S accumulation was detected in human DH neurons and ASD patients. Our data demonstrated a role of H2S overload in the social dysfunction of environmental factor-induced ASD.