DETERMINATION OF LD 50 OF NAJA ASHEI VENOM AND ITS EFFECTS ON THE HEART AND SERUM ELECTROLYTES IN BALB C MICE THROUGH I.P, S.C, AND I.M ROUTES

Objectives: This study aimed to determine the median lethal dose (LD₅₀) of Naja ashei venom in BALB/c mice following intraperitoneal, intramuscular, and subcutaneous administration, and to evaluate associated disturbances in serum electrolytes and cardiac function. Methodology: Fresh Naja ashei venom was collected, lyophilized, and physiochemically characterized. BALB/c mice received graded venom doses via intraperitoneal, intramuscular, or subcutaneous routes. LD₅₀ values were calculated using Reed-Muench method and confirmed by probit and dose–response analyses. Blood samples were obtained for serum sodium and potassium measurement. Cardiac injury was assessed using creatine kinase-MB and troponin assays, while histopathological examination of cardiac tissue was performed to confirm venom-induced myocardial damage. Results: Venom profiling demonstrated dominance of three-finger toxins (~69%) and phospholipase A₂ (~27%), supporting intense cytotoxic and systemic activity. Toxicity was route dependent, with intraperitoneal administration showing the lowest LD₅₀ (0.70mg/kg), followed by intramuscular (2.36mg/kg) and subcutaneous (2.69mg/kg) routes. Envenomation produced severe electrolyte disturbances, notably hyperkalemia (mean 7.8 mmol/L) with hyponatremia. Cardiac biomarkers were substantially elevated, with troponin and CK-MB increases indicating acute myocardial injury. Histology revealed myocardial necrosis, interstitial edema, and vascular congestion, confirming cardiotoxicity. Conclusion: Naja ashei venom exhibits high lethality and induces severe biochemical and cardiac disturbances in a route-dependent manner. The combined evidence of electrolyte imbalance and direct myocardial injury underscores the risk of rapid cardiovascular compromise following envenomation. These findings emphasize the need for prompt antivenom administration, early electrolyte correction, intensive cardiac monitoring, and inclusion of Naja ashei venom in antivenom development to improve clinical outcomes.