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Dissolution and bandgap paradigms have been proposed for predicting the ability of metal oxide nanoparticles (NPs) to induce oxidative stress in differentin vitro and in vivomodels. Here, we addressed the effectiveness of these paradigmsin vivoand under conditions typical of the marine environment, a final sink for many NPs released through aquatic systems. We used ZnO and MnO2NPs as models for dissolution and bandgap paradigms, respectively, and CeO2NPs to assess reactive oxygen radical (ROS) production via Fenton-like reactionsin vivo. Oyster embryos were exposed to 0.5–500 μM of each test NP over 24 h and oxidative stress was determined as a primary toxicity pathway across successive levels of biological complexity, with arrested development as the main pathological outcome. NPs were actively ingested by oyster larvae and entered cells. Dissolution was a viable paradigm for predicting the toxicity of NPs in the marine environment, whereas the surface reactivity based paradigms (i.e. bandgap and ROS generation via Fenton-like reaction) were not supported under seawater conditions. Bio-imaging identified potential cellular storage-disposal sites of solid particles that could ameliorate the toxicological behavior of non-dissolving NPs, whilst abiotic screening of surface reactivity suggested that the adsorption-complexation of surface active sites by seawater ions could provide a valuable hypothesis to explain the quenching of the intrinsic oxidation potential of MnO2NPs in seawater. [ABSTRACT FROM PUBLISHER]

Cerium oxide nanoparticles (CeO2NPs) exhibit fast valence exchange between Ce(IV) and Ce(III) associated with oxygen storage and both pro and antioxidant activities have been reported in laboratory models. The reactivity of CeO2NPs once they are released into the aquatic environment is virtually unknown, but this is important to determine for assessing their environmental risk. Here, we show that amphipods (Corophium volutator) grown in marine sediments containing CeO2NPs showed a significant increase in oxidative damage compared to those grown in sediments without NPs and those containing large-sized (bulk) CeO2particles. There was no exposure effect on survival, but significant increases in single-strand DNA breaks, lipid peroxidation and superoxide dismutase activity were observed after a 10-day exposure to 12.5 mg L−1CeO2. Characterisation of the CeO2NPs dispersed in deionised or saline exposure waters revealed that more radicals were produced by CeO2NPs compared with bulk CeO2. Electron energy loss spectroscopy (EELS) analysis revealed that both CeO2NPs were predominantly Ce(III) in saline waters compared to deionised waters where they were predominantly Ce(IV). In both types of medium, the bulk CeO2consisted mainly of Ce(IV). These results support a model whereby redox cycling of CeO2NPs between Ce(III) and Ce(IV) is enhanced in saline waters, leading to sublethal oxidative damage to tissues in our test organism. [ABSTRACT FROM AUTHOR]