Abstract
Simple Summary
Copper oxide nanoparticles (CuONPs) are increasingly manufactured because of their wide range of biomedical uses and industrial applications. Nonetheless, their release into the aquatic ecosystems is predictably increased, which will sequentially induce serious toxicological influences on the exposed aquatic biota. Several research studies have been published on CuONPs toxicity in fish; however, the mechanisms of their toxicity at the molecular levels in Nile tilapia (Oreochromis niloticus) are not completely described. The current study investigated the influences of sub-lethal CuONPs levels on serum biochemical indices, histopathological alterations, and transcriptomic responses in the hepatic and gill tissues of Nile tilapia juveniles.
In the present study, fish were exposed to sub-lethal doses of CuONPs (68.92 +/- 3.49 nm) (10 mg/L, 20 mg/L, and 50 mg/L) for a long exposure period (25 days). Compared to the control group (0.0 mg/L CuONPs), a significant dose-dependent elevation in blood urea and creatinine values, serum alanine transaminase, aspartate transaminase, and alkaline phosphatase enzyme activities were evident in CuONPs-exposed groups (p < 0.05). Fish exposure to 50 mg/L CuONPs significantly upregulated the transcription of pro-inflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, interleukin 12, and interleukin 8), heat shock protein 70, apoptosis-related gene (caspase 3), and oxidative stress-related (superoxide dismutase, catalase, and glutathione peroxidase) genes in liver and gills of the exposed fish in comparison with those in the control group (p < 0.05). Moreover, varying histopathological injuries were noticed in the hepatopancreatic tissues, posterior kidneys, and gills of fish groups correlated to the tested exposure dose of CuONPs. In summary, our results provide new insights and helpful information for better understanding the mechanisms of CuONPs toxicity in Nile tilapia at hematological, molecular levels, and tissue levels.