Highlights
- Ocean acidification disrupts calcium homeostasis in the mantle of mussels.
- Ocean acidification and N-NPs together intensify the inhibition of calcification.
- Surface charge determines distinct, mechanism-specific response pathways.
- Both omics reveal key roles for calcium transport, CA, and ECM synthesis.
Abstract
Ocean acidification (OA) and nanoplastics (NPs) increasingly co-occur in coastal ecosystems, yet their combined mechanistic impacts on calcifying invertebrates remain poorly resolved. Here, the mussel Mytilus coruscus was exposed for 30 days to factorial combinations of OA (pH 7.7 vs 8.1), surface-modified polystyrene NPs at a concentration of 100 μg/L (positively and negatively charged), and experimental shell damage to assess effects on shell repair, ion homeostasis, and energy metabolism. OA reduced shell repair quality by thinning repair layers, increasing porosity, and lowering calcium content, effects that were further enhanced by co-exposure to NPs, particularly negatively charged particles. OA and NPs jointly altered Ca2+ and Mg2+ levels, alkaline phosphatase activity, Ca2+Mg2+-ATPase activity, and key indicators of energy metabolism, including ATP content and cellular energy allocation. Transcriptomic and proteomic analyses revealed enrichment of ion transport, extracellular matrix, TGF-β signaling and other pathways, with divergent patterns linked to NPs surface charge. Together, these results suggest that nanoplastic surface charge under OA may impair mussel shell repair through associated alterations in ion homeostasis and energy metabolism. These findings highlight that particle surface properties shape how organisms respond to combined environmental stressors in acidifying marine environments.
Sun R., Hu M., PMaszczyk P., Khan F. U., Singh N., Khor W., Fazhan H., Lee J.-S., Bock C., Fang J. K.-H., Ding R., Li X., Sharifinia M. & Wang Y., 2026. Ocean acidification and nanoplastics disrupt mussel calcification in synergy: a multi-omics analysis,. Water Biology and Security: 100712. doi: 10.1016/j.watbs.2026.100712. Article.
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