Toxicity mechanisms of polystyrene microplastics in marine mussels revealed by high-coverage quantitative metabolomics using chemical isotope labeling liquid chromatography mass spectrometry

Marine microplastic has become an important environmental issue of global concern due to its wide distribution and harmful impacts. However, there is still insufficient information on the toxicity mechanism of microplastics to marine organisms. In this study, we developed and applied a high-coverage quantitative metabolomics technique to investigate the toxicity mechanisms of the polystyrene microspheres (micro-PS) on marine mussels (Mytilus coruscus). A total of 3599 metabolites were quantified, including 163 positively identified metabolites, 318 high-confident putatively identified metabolites, and 2602 mass-matched metabolites from the hemolymph of mussels. Metabolomics analysis indicated that micro-PS disrupted the amino acid metabolism, particularly phenylalanine metabolism, which may lead to oxidative stress and neurotoxicity. Micro-PS at environmentally relevant concentrations induced oxidative stress and immunotoxicity in mussels. After 7 days of recovery, along with the significant clearance of micro-PS by mussels, both metabolite levels and biochemical indicators generally returned to the same level as the control group. Overall, the results showed that microplastics at environmentally-relevant concentrations can cause toxic effects on mussels but these influences are reversible. We envisage the usages of high-coverage metabolomics for investigating the toxicity of various types of microplastics under many different conditions, including those relevant to the marine environment.

Automated summary

The study used a high-coverage quantitative metabolomics technique to investigate the toxicity mechanisms of micro-PS on marine mussels, finding that micro-PS disrupted amino acid metabolism, leading to oxidative stress and neurotoxicity, and induced oxidative stress and immunotoxicity in mussels at environmentally-relevant concentrations. However, these effects were reversible, with metabolite levels and biochemical indicators returning to normal after a period of recovery.