| This study investigated the acute toxicological effects of Indoxacarb (IDX) in mice by evaluating clinical signs, toxicity scores, and biochemical markers. IDX, a modern oxadiazine insecticide, exerts its action by blocking voltage-gated sodium channels in insect neurons, leading to paralysis and death. A total of 81 healthy mice (20–32 g, 8–12 weeks old) were used. The oral median lethal dose (LD₅₀) was determined as 1292.25 mg/kg body weight, classifying IDX as moderately toxic. Clinical observations revealed the rapid onset of neurological symptoms, including convulsions, ataxia, Straub tail, rolling, piloerection, hindlimb paralysis, and abnormal posture within 10–45 minutes post-exposure. Toxicity was dose-dependent, with severity scores of 15 and 24 recorded in groups treated with 700 and 900 mg/kg B.W., respectively, within 24 h, indicating a marked increase in neurotoxic effects at higher doses. Blood samples were collected from the retro-orbital plexus, and brain and liver tissues were excised for biochemical evaluation. Plasma analysis demonstrated significant hepatotoxicity, as evidenced by elevated AST, ALT, and ALP activities, indicating hepatocellular damage. Blood glucose levels increased by 67.8%, reflecting stress-induced hyperglycemia and metabolic disruption. Indoxacarb also markedly inhibited acetylcholinesterase (AChE) activity across tissues. Plasma AChE was most affected, with inhibition of 72.4% and 82.1% at 700 and 900 mg/kg B.W. after 4 h, followed by partial recovery at 24 h. Liver AChE inhibition was moderate (25.9–31.0%), while brain tissue showed greater sensitivity (39.6–49.4%). In conclusion, Indoxacarb induced acute, dose-dependent neurotoxic, hepatotoxic, and metabolic alterations, highlighting potential health risks and the importance of strict safety measures. |