ArticleInternational journal of biological sciences2026
Synergistic Neurotoxicity of environmental Cadmium and Paraquat in Parkinsonism: Unveiling the Mito-ROS/OPA1/Caspase-3/GSDME-driven Apoptosis Axis.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Plasma proteomics reveals the molecular features in rapidly progressive pneumoconiosis.Frontiers in immunology · 2026Article
- Exercise modulation of BDNF/TrkB signaling in Parkinson's disease: an evidence-calibrated review of neuroprotective mechanisms, biomarker limitations, and translational gaps.Frontiers in neurologyReview
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16 authors.
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Abstract
The increasing environmental presence of cadmium (Cd) and paraquat (PQ), driven by industrial emissions and overuse of herbicide, poses heightened risks for neurodegenerative disorders. Although each of these toxins can independently induce neuronal damage, the synergistic neurotoxic effects resulting from chronic, low-dose co-exposure to Cd and PQ remain inadequately understood. This study demonstrates that exposure to subtoxic levels of Cd and PQ concurrently induces neuronal cell death and contributes to Parkinson's disease (PD)-like symptoms. Mechanistically, chronic co-exposure to Cd and PQ triggers a marked overproduction of mitochondrial ROS (mito-ROS), which impairs OPA1 processing and results in mitochondrial fragmentation. This mitochondrial dysfunction subsequently triggers caspase-3 activation, leading to GSDME cleavage and its translocation to the mitochondria, ultimately promoting neuronal apoptosis. Furthermore, our
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