article · Animals
Exposing Nile tilapia to sub-lethal concentrations of copper oxide nanoparticles over a 25-day period causes multi-organ toxic effects. The study examined nanoparticle concentrations of 10, 20, and 50 milligrams per litre. Fish exhibited dose-dependent increases in blood urea and creatinine, alongside elevated activities of serum enzymes including alanine transaminase, aspartate transaminase, and alkaline phosphatase, indicating kidney and liver damage. At the highest concentration of 50 milligrams per litre, there was significant upregulation of genes associated with inflammation, heat shock protein 70, apoptosis, and oxidative stress across liver and gill tissues. Microscopic examination confirmed dose-dependent histopathological alterations in the hepatopancreatic tissue, posterior kidneys, and gills. These findings detail the physiological, molecular, and cellular pathways through which prolonged exposure to copper oxide nanoparticles harms aquatic organisms, providing baseline toxicological data for this fish species.
Nanoparticles increasingly enter aquatic ecosystems through various industrial and agricultural pathways. This research demonstrates how prolonged contact with sub-lethal levels of copper oxide nanoparticles compromises the organ health, immune signalling, and stress responses of Nile tilapia. Such toxicological insights help environmental regulators and aquaculture managers identify cellular and biochemical markers of nanoparticle contamination before catastrophic stock losses or broader ecosystem decline occur.
This is early-stage toxicological research that does not offer a direct product or commercial process. The abstract indicates an exploratory study into toxicity mechanisms rather than a market-ready tool. However, the identified biochemical indices and gene expression alterations could inform environmental monitoring frameworks, risk assessment protocols, or safety guidelines used by ecotoxicologists, aquaculture producers, and chemical safety regulators assessing nanoparticle hazards in aquatic environments.
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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 (<i>p</i> < 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 (<i>p</i> < 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.
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DOI: 10.3390/ani11030652
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