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Due to their antimicrobial, electrical and magnetic properties, copper nanoparticles (NPs) are suitable for a vast array of applications. Copper can be toxic to biota, making it necessary to assess the potential hazard of copper nanomaterials. Zebrafish ( Danio rerio) were exposed to 10 µg Cu/L of CuO NPs of ≈100 nm (CuO-poly) or ionic copper to compare the effects provoked after 3 and 21 days of exposure and at 6 months post-exposure (mpe). At 21 days, significant copper accumulation was only detected in fish exposed to ionic copper. Exposure to both copper forms caused histopathological alterations that could reduce gill functionality, more markedly in the case of ionic copper. Nevertheless, at 6 mpe higher prevalences of gill lesions were detected in fish previously exposed to CuO-poly NPs. No relevant histological alterations were detected in liver, but the lysosomal membrane stability test showed significantly impaired general health status after exposure to both metal forms that lasted up to 6 mpe. 69 transcripts appeared regulated after 3 days of exposure to CuO-poly NPs, suggesting that NPs could produce oxidative stress and reduce metabolism and transport processes. Thirty transcripts were regulated after 21 days of exposure to ionic copper, indicating possible DNA damage. Genes of the circadian clock were identified as the key genes involved in time-dependent differences between the two copper forms. In conclusion, each copper form showed a distinct pattern of liver transcriptome regulation, but both caused gill histopathological alterations and long lasting impaired health status in adult zebrafish. [ABSTRACT FROM AUTHOR]

We aimed to determine the effects of changes in polycyclic aromatic hydrocarbon (PAH) and polychlorinated biphenyl (PCB) bioavailability on peroxisome proliferation and antioxidant enzymes to assess their potential use as pollution biomarkers. For this, mussels (Mytilus galloprovincialis) were sampled in Txatxarramendi and transplanted to Arriluze, Muskiz, and Plentzia (northern Spain), and vice versa. Arriluze was the most heavily polluted site, followed by Plentzia, Txatxarramendi, and Muskiz. Animals transplanted from a polluted station to a cleaner station lost contaminant load in three to six weeks, and when transplanted to a more polluted station, they accumulated PAHs and PCBs accordingly. Peroxisomal acyl-A oxidase (AOX) activity was the highest in animals from Arriluze, and animals transplanted to Arriluze showed increased AOX activity, reaching the levels of native mussels. Mussels from Txatxarramendi showed the lowest peroxisomal volume density (Vvp). Among mussels from Txatxarramendi, only those transplanted to Plentzia showed increased Vvp, whereas animals from Arriluze and Muskiz transplanted to Txatxarramendi after 2 d and six weeks, respectively, had decreased Vvp. Two days after transplant, superoxide dismutase and glutathione peroxidase activities were significantly lower in mussels from Arriluze and Muskiz, respectively, than in those from Txatxarramendi and than in animals transplanted to Txatxarramendi from these stations. In conclusion, transplant experiments with mussels are useful to assess the effects of pollution. Peroxisome proliferation, measured as induction of AOX or increased Vvp, shows great potential as a biomarker of pollution to be included in pollution monitoring programs. In the present work, we have demonstrated that peroxisome proliferation is a reversible phenomenon in mussels. [ABSTRACT FROM AUTHOR]

Exposure of marine animals to certain organic and metal pollutants is thought to enhance reactive oxygen species (ROS) production with concomitant alterations of antioxidant defence mechanisms. Some of these organic pollutants cause peroxisome proliferation, a process resulting also in possible enhanced production of ROS. The aim of this study was to investigate the effects of two organic xenobiotics, benzo(a)pyrene (B(a)P) and di(2-ethylhexyl)phthalate (DEHP), as well as the effects of cadmium (Cd), on antioxidant and peroxisomal enzymes and on peroxisomal volume density in the digestive gland of mussel, Mytilus galloprovincialis Lmk., experimentally exposed for 21 days. Special attention was paid to the interactive effects of organic and metal compounds by exposing one group of mussels to a mixture of B(a)P and Cd. Exposure of mussels to Cd caused a decrease in superoxide dismutase (SOD) activity, in Mn-SOD protein levels and in volume density of peroxisomes. B(a)P exposure significantly increased catalase and glutathione peroxidase (GPX) and inhibited Mn-SOD after 21 days of exposure. B(a)P also caused a slight increase in acyl-CoA oxidase (AOX) activity and peroxisomal volume density after 21 days of exposure. Cd tended to inhibit changes provoked by B(a)P, indicating that responses to organic xenobiotics can be modulated by concomitant exposure to metal contaminants. Exposure to DEHP increased catalase and AOX and inhibited SOD activity and Mn-SOD protein levels. In conclusion, peroxisome proliferation, measured as an increase of the peroxisomal enzymes catalase and AOX (up to 1.53-fold for AOX), is a specific response to organic contaminants such as B(a)P and DEHP, whereas Cd does not cause peroxisome proliferation. Thus, peroxisome proliferation may be a specific biomarker of organic pollutants in mussels. Both organic and metal pollutants inhibited SOD activity and protein levels (up to 0.21-fold for Mn-SOD protein levels), the latter offering potential as general marker of pollution. [ABSTRACT FROM AUTHOR]