Abstract

<p>Some nanoparticles (NPs) may induce adverse health effects in exposed organisms, but to date the evidence for this in wildlife is very limited. Silver nanoparticles (AgNPs) can be toxic to aquatic organisms, including fish, at concentrations relevant for some environmental exposures. We applied whole mount <i>in-situ</i> hybridisation (<i>WISH</i>) in zebrafish embryos and larvae for a suite of genes involved with detoxifying processes and oxidative stress, including metallothionein (<i>mt2</i>), glutathionine <i>S</i>-transferase pi (<i>gstp</i>), glutathionine <i>S</i>-transferase mu (<i>gstm1</i>), haem oxygenase (<i>hmox1</i>) and ferritin heavy chain 1 (<i>fth1</i>) to identify potential target tissues and effect mechanisms of AgNPs compared with a bulk counterpart and ionic silver (AgNO<sub>3</sub>). AgNPs caused upregulation in the expression of <i>mt2, gstp</i> and <i>gstm1</i> and down regulation of expression of both <i>hmox1</i> and <i>fth1</i> and there were both life stage and tissue-specific responses. Responding tissues included olfactory bulbs, lateral line neuromasts and ionocytes in the skin with the potential for effects on olfaction, behaviour and maintenance of ion balance. Silver ions induced similar gene responses and affected the same target tissues as AgNPs. AgNPs invoked levels of target gene responses more similar to silver treatments compared to coated AgNPs indicating the responses seen were due to released silver ions. In the <i>Nrf2</i> zebrafish mutant, expression of <i>mt2</i> (24 hpf) and <i>gstp</i> (3 dpf) were either non-detectable or were at lower levels compared with wild type zebrafish for exposures to AgNPs, indicating that these gene responses are controlled through the Nrf2-Keap pathway.</p

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