Toxic and bioaccumulative effects of zinc nanoparticle exposure to goldfish, Carassius auratus (Linnaeus, 1758)

The widespread use of produced metal oxide nanoparticles (NPs) has increased major concerns about their impact on human as well as aquatic animal health. The present study shows that exposure to different concentrations of zinc oxide (ZnO) NPs led to high accumulations of Zn ions in the metabolic organs of fish (liver and gills), resulting in severe oxidative stress in Carassius auratus. The goldfish (C. auratus) was chosen as an aquatic species for the evaluation of the potential toxicity of aqueous ZnO-NPs (Treatments of hemoglobin and neutrophils (0, 0.5, 1, and 1.5 mg L− 1) following 14 days of exposure. A range of histological and hematological factors were examined. Exposure to the NPs produced significant reduction of red blood cell and white blood cell counts, hematocrit) were found to produce no significant differences in lymphocyte, monocyte, and eosinophil counts; as well as the mean corpuscular hemoglobin concentrations index (P > 0.05). Moreover, the results revealed significant alterations in serum biochemical parameters, hepatic enzyme levels, and immune and antioxidant responses; except for total protein and superoxide dismutase (SOD) of C. auratus exposed to ZnO-NPs, particularly at the 1 and 1.5 mg L− 1 concentrations. Fish exposed to 1 and 1.5 mg L−1 ZnO-NPs displayed a significant reduction in alternative complement pathway activity, lysozyme, and total protein contents of mucus compared to those in the control group. The results showed that hepatic SOD and catalase, and gill catalase activity were significantly decreased, and their malondialdehyde levels increased at 1 and 1.5 mg L−1 ZnO-NPs compared to the control group (P < 0.05). Significant accumulations of ZnO-NPs were observed in the liver, kidney, and gill tissues of fish leading to severe histopathological alterations in these organs. These results suggest that water-borne ZnO-NPs can easily accumulate in metabolic organs and lead to oxidative stress and destructive effects on the physiological features of C. auratus.