The gut–brain axis in arsenic-induced toxicity: mechanisms, consequences, and therapeutic perspectives

Feb 5, 2026Metabolic brain disease

How gut and brain interactions relate to arsenic poisoning: causes, effects, and possible treatments

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Abstract

Chronic ingestion of arsenic from contaminated groundwater is associated with significant neurological health risks.

Arsenic disrupts gut microbiota by reducing beneficial bacteria and increasing harmful strains.
This disruption compromises gut barrier integrity and triggers inflammation and oxidative stress.
Alterations in metabolic pathways affecting neurotransmitter production and mitochondrial function may occur due to arsenic exposure.
Animal studies indicate chronic exposure leads to worsened cognitive and behavioral deficits alongside microbial dysbiosis.
Arsenic accumulation in brain tissues can impair neural signaling by increasing reactive oxygen species and inducing neuroinflammation.
Probiotic and prebiotic supplementation could restore microbiome balance and improve behavioral outcomes in experimental models.

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Chronic ingestion of arsenic frequently occurring in contaminated groundwater poses a serious dual threat to neurological health. Environmental toxicants present in groundwater are highly correlated with onset of neuropathological effects through complex gut-brain axis interactions. The systematic review of literature aims evaluate the neurobehavioural consequences and molecular outcome of a groundwater contaminant, arsenic with microbiota alteration involving animal studies and epidemiological data. Arsenic disrupts the gut microbiota, diminishing beneficial bacteria and promoting harmful strains, which in turn compromise gut barrier integrity, trigger inflammation and oxidative stress, leading to alteration in critical metabolic pathways involved in neurotransmitter production and mitochondrial function. Animal studies have shown that chronic exposure intensifies these effects, causing more pronounced microbial dysbiosis alongside worsened cognitive and behavioural deficits. Mechanistically, arsenic impairs neural signaling by elevating reactive oxygen species, disrupting synaptic and mitochondrial dynamics, and inducing neuroinflammation after its accumulation in brain tissues, while gut-derived neuroactive compounds exacerbate neuroinflammation and neuronal damage irrespective of significant arsenic deposition in the brain. Therapeutic strategies that reinforce gut health, such as targeted probiotic and prebiotic supplementation have demonstrated the ability to restore microbiome balance, strengthen barrier function, reduce neuroinflammatory markers and improve behavioural outcomes in experimental models. These microbiota-focused interventions, when combined with conventional measures like chelation to remove toxic metals and the deployment of water treatment infrastructure in affected regions, suggest a powerful integrated approach. By addressing both the source of contamination and the downstream biological consequences, this multimodal strategy holds significant promise for mitigating arsenic-induced neurotoxicity and protecting at-risk populations in affected communities.

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The gut–brain axis in arsenic-induced toxicity: mechanisms, consequences, and therapeutic perspectives

Abstract

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