Aminoguanidine attenuates arsenic-induced hepatic oxidative stress: Dose-dependent effects in a mouse model.

Background: Arsenic exposure through environmental contamination poses significant public health concerns via oxidative stress-mediated toxicity. While aminoguanidine (AG) demonstrates antioxidant properties, its protective effects against arsenic-induced hepatotoxicity remain unexplored. Methods: Male mice (n = 32) were randomized into four groups (n = 8 per group): control (distilled water), arsenic (50 ppm sodium arsenite in drinking water), and two treatment groups receiving arsenic plus aminoguanidine (50 or 100 mg/kg/day, i.p.) for 28 days. Hepatic oxidative stress markers, plasma antioxidant capacity, and liver histopathology were evaluated. Results: Arsenic exposure induced significant liver histopathological changes (grade +2) and oxidative damage. AG treatment at 50 mg/kg/day showed optimal protective effects, with some samples displaying normal hepatic structure (grade 0) and others showing minimal changes (grade +1). This dose effectively reduced lipid peroxidation and protein carbonylation in liver tissue. The higher AG dose (100 mg/kg/day) demonstrated less protective effect, though it significantly improved plasma antioxidant capacity compared to the arsenic group. Conclusions: Aminoguanidine demonstrates dose-dependent hepatoprotective effects against arsenic-induced oxidative damage, with 50 mg/kg/day showing optimal efficacy. Further investigation of lower doses over extended periods is warranted to establish its therapeutic potential in arsenic toxicity.