Abstract
The use of nanoscale materials is growing exponentially, but there are also concerns about the environmental hazard to aquatic biota. Metal-containing engineered nanoparticles (NPs) are an important group of these new materials, and are often made of one metal (e.g., Cu-NPs and Ag-NPs), metal oxides (e.g., ZnO and TiO 2 NPs), or composite of several metals. The physiological effects and toxicity of trace metals in the traditional dissolved form are relatively well known and the overall aim of this review was to use our existing conceptual framework of metal toxicity in fish to compare and contrast the effects of nanometals. Conceptually, there are some fundamental differences that relate to bioavailability and uptake. The chemistry and behaviour of nanometals involves dynamic aspects of aggregation theory, rather than the equilibrium models traditionally used for free metal ions. Some NPs, such as Cu-NPs, may also release free metal ions from the surface of the particle. Biological uptake of NPs is not likely via ion transporters, but endocytosis is a possible uptake mechanism. The body distribution, metabolism, and excretion of nanometals is poorly understood and hampered by a lack of methods for measuring NPs in tissues. Although data sets are still limited, emerging studies on the acute toxicity of nanometals have so far shown that these materials can be lethal to fish in the mg–μg l −1 range, depending on the type of material. Evidence suggests that some nanometals can be more acutely toxic to some fish than dissolved forms. For example, juvenile zebrafish have a 48-h LC 50 of about 0.71 and 1.78 mg l −1 for nano- and dissolved forms of Cu respectively. The acute toxicity of metal NPs is not always explained, or only partly explained, by the presence of free metal ions; suggesting that other novel mechanisms may be involved in bioavailability. Evidence suggests that nanometals can cause a range of sublethal effects in fish including respiratory toxicity, disturbances to trace elements in tissues, inhibition of Na +K +-ATPase, and oxidative stress. Organ pathologies from nanometals can be found in a range of organs including the gill, liver, intestine, and brain. These sublethal effects suggest some common features in the sublethal responses to nanometals compared to metal salts. Effects on early life stages of fish are also emerging, with reports of nanometals crossing the chorion (e.g., Ag-NPs), and suggestions that the nano-forms of some metals (Cu-NPs and ZnO NPs) may be more toxic to embryos or juveniles, than the equivalent metal salt. It remains possible that nanometals could interfere with, and/or stimulate stress responses in fish; but data has yet to be collected on this aspect. We conclude that nanometals do have adverse physiological effects on fish, and the hazard for some metal NPs will be different to the traditional dissolved forms of metals.
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