Low-dose triclosan induces neurotoxicity in zebrafish via gut microbiota disruption.

Summary

This experimental study used germ-free zebrafish and fecal microbiota transplantation to establish that triclosan exposure causes neurotoxicity primarily through gut microbiota disruption at environmentally relevant low doses. Three-month exposure to 0.4–4.0 μg/L triclosan enriched Proteobacteria and increased lipopolysaccharide levels, which crossed a compromised blood-brain barrier to trigger neuroinflammation and behavioural changes; higher doses (40 μg/L) engaged both microbiota-dependent and independent mechanisms. The work highlights the gut-brain axis as a critical pathway for triclosan's neurotoxic effects in female zebrafish, though the authors note sex-specific responses require further investigation.

Regional applicability

Although conducted in a zebrafish model, this mechanistic study is relevant to United Kingdom and global food safety and environmental health policy, as triclosan is an antimicrobial widely detected in environmental samples and human biological fluids. The findings support the rationale for triclosan restrictions already in place in several UK and EU consumer products, and point to the need for consideration of gut-mediated neurotoxicity in risk assessment frameworks for antimicrobial agents in food and water systems.

Key measures

Gut bacterial composition (16S rRNA sequencing), lipopolysaccharide (LPS) levels, blood-brain barrier integrity, neuroinflammatory markers, behavioural metrics, gene expression (transcriptomics)

Outcomes reported

The study established a causal link between triclosan-induced gut dysbiosis and neurotoxicity in zebrafish, demonstrating that environmentally relevant triclosan concentrations alter gut bacterial composition and lipopolysaccharide levels, triggering neuroinflammation and behavioural abnormalities via the gut-brain axis.

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