Acute toxic effects caused by the co-exposure of nanoparticles of ZnO and Cu in rainbow trout

Abstract

The toxic effects produced by the co-exposure to low- and non-toxic concentrations of zinc oxide (ZnONPs) and copper nanoparticles (CuNPs) was assessed in rainbow trout following the OECD Test Guideline 203. Four groups of trouts were exposed for 96 h to a range of concentrations (0.0425–0.34 mg/L) of CuNPs (50 nm) in combination with a fixed non-toxic concentration (1.25 mg/L) of ZnONPs (25 nm) determined from an independent concentration-response study. One additional group was exposed to the highest concentration of CuNPs alone. Behaviour and mortality were observed during the experiment. After 96 h exposure, accumulated levels of Cu and Zn in the fish were measured by ICP-MS and ICP-OES, respectively. The induction of oxidative stress in liver and gills was evaluated by the glutathione-S-transferase (GST) activity and the reduced glutathione (GSH) / oxidized glutathione (GSSG) ratio. The ethoxyresorufin-O-deethylase (EROD) activity was also assessed. The results showed that CuNPs at the highest tested concentration do not cause acute toxicity, whereas exposure to all mixtures caused mortality, which was inversely proportional to the concentration of CuNPs (from 28% to 86% survival). Accumulated levels of Cu and Zn in the fish increased with the increasing concentrations of CuNPs, suggesting that the presence of CuNPs favours the entry of Zn. In general, the GST activity increased significantly in the gills of co-exposed groups, whereas the GSH/GSSG ratio was altered in the liver. The EROD activity was not modified. In conclusion, the co-exposure to these NPs potentiates their toxicity, observing an alteration of the GST activity and GSH/GSSG ratio in gill and liver, which was more pronounced at the lowest concentration of CuNPs. The lower toxic effect observed with the highest concentrations of CuNPs coincides with a greater internalization of Zn.