MICROPLASTIC exposure was associated with widespread brain metabolic abnormalities, mitochondrial dysfunction, and behavioural impairment in fruit flies, according to an experimental study investigating the neurological effects of chronic dietary exposure to polystyrene microplastics.
The findings identified alterations in oxidative stress, neurotransmitter activity, and neuronal viability, providing insights into potential mechanisms underlying microplastic-associated neurotoxicity.
Researchers investigated the neurological effects of chronic dietary exposure to polystyrene microplastics in Drosophila melanogaster, using an integrated metabolomic, biochemical, histological, and behavioural approach.
Fruit flies were exposed to polystyrene microplastics at concentrations of 10 ppm and 50 ppm to examine changes in brain metabolism and neurological function.
At both concentrations, chronic exposure was associated with reduced locomotor activity, impaired climbing ability, altered feeding behaviour, and diminished circadian amplitude.
Untargeted brain metabolomic analysis revealed widespread disturbances affecting amino acid, nitrogen, kynurenine, polyamine, and central carbon metabolism.
Notably, researchers identified reduced putrescine concentrations alongside elevated spermidine and spermine levels.
Alterations were also observed in glycolytic and tricarboxylic acid cycle intermediates, suggesting disruption of pathways involved in cellular energy metabolism.
Biochemical analyses demonstrated increased oxidative stress and impaired antioxidant defences following microplastic exposure.
Catalase activity decreased by 46%, while superoxide dismutase activity declined by 40%, indicating substantial reductions in antioxidant enzyme activity.
Researchers also identified evidence of mitochondrial impairment, including increased mitochondrial reactive oxygen species, reduced membrane potential, diminished electron transport, and altered nicotinamide adenine dinucleotide redox balance.
These abnormalities were accompanied by reduced metabolic viability, suggesting disruption of cellular energy regulation.
Histological examination further revealed increased brain tissue damage and decreased neuronal viability following chronic microplastic exposure.
Beyond metabolic and mitochondrial abnormalities, researchers observed changes in neurotransmitter-associated markers.
Polystyrene microplastic exposure was associated with reduced tyrosine hydroxylase and dopamine levels, indicating alterations in dopaminergic pathways.
Levels of γ-aminobutyric acid, an inhibitory neurotransmitter, were also reduced, suggesting broader disturbances in neurotransmitter regulation.
Together, these findings demonstrated associations between chronic microplastic exposure and multiple neurological abnormalities in the experimental model.
Although the results highlighted potential mechanisms of microplastic-associated neurotoxicity, the study was conducted in fruit flies and did not establish equivalent effects in humans.
Further investigation is needed to determine the relevance of these metabolic and neurological changes to human brain health.
References
Rathor P et al. Brain metabolomics reveals metabolic alterations associated with chronic polystyrene microplastic-induced neurotoxicity in Drosophila melanogaster. NeuroToxicology. 2026.
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