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<p>Microplastics (MPs) threaten aquatic ecosystems and pose potential risks to organismal health through bioaccumulation in aquatic species. This study reveals that 14-day exposure to 5 μm polystyrene microplastics (PS-MPs) (500 μg/L) induces neurocognitive impairment in rainbow trout (<i>Oncorhynchus mykiss</i>), a globally consumed aquaculture species. MPs accumulated in brain and gut tissues, causing blood-brain barrier structural alterations, intestinal mucosal damage, and oxidative stress. Multi-omics analysis revealed associations between gut microbiota dysbiosis (reduced <i>Ralstonia</i>, increased <i>Acinetobacter</i>) to suppressed neuroactive pathways, particularly GABA synthesis and transport. Downregulation of monocarboxylate transporters (<i>mct1/2</i>) and GABA-related enzymes (GAD1/2) disrupted gut-to-brain GABA homeostasis, neurobehavioral deficits. These findings establish the gut microbiota-GABA axis as a critical mediator of MPs neurotoxicity, highlighting risks to seafood safety and necessitating urgent regulation of microplastic contamination in aquatic food chains.</p>

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Gut microbiota–GABA axis dysregulation underlies polystyrene microplastic (PS-MP) neurotoxicity in rainbow trout: a role for oxidative stress and blood–brain barrier disruption

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月7日

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  • Fang Ma,
  • Pan Zheng,
  • Wenli Wang,
  • Jiaxuan Dong,
  • Xiangjun Zhou,
  • Zhiyun Lin,
  • Xiajiao Nian

摘要

Microplastics (MPs) threaten aquatic ecosystems and pose potential risks to organismal health through bioaccumulation in aquatic species. This study reveals that 14-day exposure to 5 μm polystyrene microplastics (PS-MPs) (500 μg/L) induces neurocognitive impairment in rainbow trout (Oncorhynchus mykiss), a globally consumed aquaculture species. MPs accumulated in brain and gut tissues, causing blood-brain barrier structural alterations, intestinal mucosal damage, and oxidative stress. Multi-omics analysis revealed associations between gut microbiota dysbiosis (reduced Ralstonia, increased Acinetobacter) to suppressed neuroactive pathways, particularly GABA synthesis and transport. Downregulation of monocarboxylate transporters (mct1/2) and GABA-related enzymes (GAD1/2) disrupted gut-to-brain GABA homeostasis, neurobehavioral deficits. These findings establish the gut microbiota-GABA axis as a critical mediator of MPs neurotoxicity, highlighting risks to seafood safety and necessitating urgent regulation of microplastic contamination in aquatic food chains.