Abstract
BACKGROUND: Heavy metal interactions within aquatic ecosystems significantly affect fish physiology. This study evaluated the protective role of selenium against cadmium-induced hematological, biochemical, and electrophoretic alterations in goldfish. METHODS: A total of 120 goldfish individuals were divided into four groups: control, cadmium chloride-treated (2.8 mg/L), sodium selenite-treated (2 mg/L), and a combined cadmium and selenium-treated group. After 14 days, blood samples were collected and analyzed for hematological parameters, biochemical markers, and serum protein electrophoresis. RESULTS: Cadmium exposure led to significant reductions in red blood cell (RBC) and white blood cell (WBC) counts, hemoglobin (Hb), and hematocrit (HCT) (p < 0.001). Selenium supplementation alleviated these declines and improved overall hematological function. Additionally, cadmium exposure decreased albumin and total protein levels while elevating aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, indicating liver damage. Selenium co-treatment reduced cadmium accumulation and mitigated liver toxicity. Elevated urea and creatinine levels in cadmium-exposed fish were also significantly lowered in the combined treatment group (p < 0.0001). Furthermore, selenium supplementation enhanced antioxidant defense mechanisms by increasing catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activity while reducing malondialdehyde (MDA) levels, effectively counteracting cadmium-induced oxidative stress. CONCLUSION: Sodium selenite at a dose of 2 mg/L effectively mitigated the toxic effects of cadmium chloride on hematological, biochemical, and oxidative stress markers in goldfish, demonstrating its protective potential against heavy metal toxicity.