Sodium arsenite requires redox sensitization to cause developmental dopaminergic neurotoxicity in Caenorhabditis elegans

Developmental exposure of Caenorhabditis elegans to sodium arsenite causes dopaminergic neurotoxicity only when mitochondrial quality control or redox stress response is compromised, not under mild toxicity alone.

• Why it matters: Pollutants can impair mitochondria and neurotoxicity is often linked to mitochondrial dysfunction, but it is unclear whether Krebs cycle inhibition alone can produce developmental dopaminergic damage.
• What they did: Whole-development exposure to sodium arsenite or fluoroacetic acid was paired with assessments of neuronal morphology and function, dopaminergic ATP levels, and mitochondrial redox state, including genetic or chemical redox/mitochondrial challenges.
• The result: Sodium arsenite lowered dopaminergic ATP without altering mitochondrial redox state, and dopaminergic neurotoxicity plus dopamine-associated behavioral deficits emerged only with pink-1/PINK1 or sod-2/SOD2 loss, rotenone/antimycin A/buthionine sulfoximine co-exposure, or a 6-hydroxydopamine secondary challenge.

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