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Polystyrene nanoplastics exacerbate cadmium-induced bioenergetic impairment and oxidized phospholipid accumulation in the mussel Mytilus coruscus
Summary
Scientists found that tiny plastic particles (nanoplastics) can act like a "delivery truck" for the toxic heavy metal cadmium, helping it build up in shellfish tissue and causing more cell damage than cadmium alone. This matters because it shows how plastic pollution and heavy metals in our oceans can team up to harm marine life more severely than either would separately, and since mussels and other seafood are part of the human food chain, this combined contamination could eventually affect the food we eat.
The coexistence of nanoplastics and conventional heavy metals poses a serious ecological threat to marine ecosystems, yet the specific mechanisms underlying their synergistic toxicity remain unclear. This study employed a comprehensive approach, encompassing tissue cadmium quantification, biochemical assays, real-time quantitative PCR, non-targeted metabolomics, and molecular docking, to investigate the combined toxic effects of polystyrene nanoplastics (PS-NPs) and cadmium (Cd) in the thick-shelled mussels (Mytilus coruscus). The results revealed a significant carrier effect: compared to the gills, PS-NPs promoted anomalous and tissue-specific accumulation of Cd in the digestive glands; this elevated toxic load led to severe dysfunction in bioenergetic metabolism. Concurrently, despite strong compensatory activation of the Nrf2/GST detoxification axis, the cellular antioxidant capacity was substantially depleted, ultimately triggering BAX/BCL-2-mediated apoptosis and resulting in irreversible tissue damage. Crucially, metabolomic analysis highlighted severe disruption of cellular membrane structural lipids under combined exposure. Mechanistically, integrative analysis indicated that Cd-driven intense oxidative stress led to the massive accumulation of oxidized phospholipids (OxPLs). These OxPLs may not be merely metabolic by-products but candidate endogenous danger-associated molecular patterns (DAMPs) with the potential to trigger the TLR4/MyD88/TRAF6 immune-inflammatory cascade, as supported by metabolomic evidence and molecular docking predictions. The molecular mechanisms proposed in this study provide new scientific insights for the ecological risk assessment of complex multi-stressor pollution.