Toxicological, Hematological, and Pathological Effects of Acute Copper and Lead Intoxication in Grass Carp (Ctenopharyngodon idella).

Environmental contamination by heavy metals, particularly fish poisoning, is a growing concern due to its impact on aquatic ecosystems. Fish serve as bioindicators and play a crucial role in the food chain. This study evaluated the toxic effects of acute copper and lead exposure in Ctenopharyngodon idella, analyzing hematological, biochemical, and pathological alterations. Fifty-six grass carp were exposed for 96 h to copper and lead (2, 3, and 4 mg/L). Blood samples were analyzed for hematological and oxidative stress parameters, while brain, gills, liver, and kidneys were assessed for enzymatic activity (acetylcholinesterase, catalase, glutathione S-transferase) and histopathology. Data were analyzed using ANOVA and Tukey's test (p < 0.05). Significant increases in gill glutathione S-transferase (GST) activity (Cu2 and Cu3, p < 0.05) and catalase activity (Pb3 e Pb4, p < 0.05) indicated oxidative stress. Lead exposure caused a significant reduction in erythrocyte count (Pb2, p < 0.05). Although not statistically significant, erythrocyte osmotic fragility increased at higher metal concentrations. Histopathology revealed epithelial hyperplasia, inflammatory infiltrates, and edema in gills, hepatocellular degeneration, and subcapsular/interstitial renal hemorrhages in all exposed groups. These renal lesions diverge from typical heavy metal nephrotoxicity, usually characterized by tubular degeneration. These findings highlight the systemic effects of copper and lead, particularly their oxidative impact and unexpected renal damage. These findings underscore the complex toxicopathological effects of copper and lead in fish, particularly their impact on oxidative stress.