Pesticides and heavy metals are ubiquitous pollutants that often co-exist in natural environments; at levels beyond safety thresholds, they may generate severe cytotoxicity in fish. Considering this, a 42-day trial experiment was set up in which Nile tilapia ( Oreochromis niloticus ) fingerlings were exposed to sub-toxic levels of fenitrothion (Fen.) and mercury (Hg), either separately or in combination, to evaluate their effects on hematology, gill and liver tissue morphology, antioxidant, and immune functions. Three different water-delivered treatments were designed, namely Fen. (0.3 mg/L), Hg (0.03 mg/L), Fen. + Hg (0.3 mg/L + 0.03 mg/L), with a control, each replicated three times. At the end of the 42-day trial, the co-exposure group exhibited the highest mortality than the single-exposure treatments. Moreover, the co-exposure group showed significant alterations in blood physiology characterized by elevated glucose (121.17 ± 4.94 mg/dL; p < 0.05) and decreased hemoglobin (8.40 ± 0.88 g/dL; p < 0.05); and increased incidence of erythrocytic cellular and nuclear abnormalities. Co-exposed fish exhibited severe gill and liver deformities, as identified through histo-architectural assessment, compared with controls and single-contaminant treatments. At the mRNA level, hepatic transcriptional profiling revealed that co-exposure to fenitrothion and mercury triggered oxidative stress, as shown by elevated expression of antioxidant genes (SOD and CAT; p < 0.05), which suggests a weakened antioxidant defense mechanism in the exposed fish. Concurrently, immune‑related genes ( TNF‑α, IFN‑γ , and IL‑1β; p < 0.05) were significantly suppressed, indicating an impairment of immune competence. Together, Nile tilapia fingerlings in the co-exposure group showed greater impairment in hematological biomarkers, tissue morphology, and antioxidant-immune gene expression, as confirmed by principal component analysis (PCA).
Mondal et al. (Mon,) studied this question.
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