Low-c oncentration exposure to glyphosate-based herbicide modulates the complexes of the mitochondrial respiratory chain and induces mitochondrial hyperpolarization in the Danio rerio brain

Summary

This laboratory study examined neurotoxic effects of glyphosate-based herbicide (GBH Scout®) in adult zebrafish (Danio rerio) exposed in vivo to three concentrations (0.065–10.0 mg L⁻¹) for 7 days, complemented by in vitro assays with pure glyphosate. The findings demonstrate that GBH induces mitochondrial dysfunction in brain tissue, evidenced by inhibition of respiratory chain complex activity, altered gene expression, mitochondrial hyperpolarisation, and increased reactive species production; these effects were accompanied by decreased cell viability and behavioural impairments. The research identifies mitochondria as a critical target of GBH toxicity, supporting concern about neurotoxic mechanisms not captured in standard regulatory toxicity assays.

Regional applicability

This is a laboratory study using zebrafish as a model organism and does not directly assess UK agricultural practice or food safety context. However, the findings on glyphosate-based herbicide neurotoxicity are relevant to UK food safety policy and pesticide residue monitoring, given widespread use of glyphosate in UK agriculture and potential for low-level exposures through the food chain.

Key measures

Cell viability, mitochondrial respiratory chain complex enzymatic activity, gene expression of mitochondrial complexes, mitochondrial membrane potential, reactive species production, behavioural repertoire

Outcomes reported

The study measured acute toxicity, mitochondrial respiratory chain complex activity and gene expression, mitochondrial membrane potential, reactive species formation, and behavioural changes in zebrafish brain exposed to glyphosate-based herbicide. Exposure induced decreased cell viability, inhibited mitochondrial complex activity, modulated gene expression, increased reactive species production, and promoted mitochondrial hyperpolarisation.

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