Investigating the hepato-nephroprotective effects of deferoxamine in lead-induced toxicity of rats

Lead is a well-known toxic heavy metal with detrimental effects on various tissues and organs. Chelation therapy remains the principal therapeutic strategy for reducing lead toxicity through enhancement of metal elimination from blood and tissues. Deferoxamine (DFO), an iron chelator, has demonstrated protective effects against multiple heavy metals. This study evaluates the hepatoprotective and nephroprotective effects of DFO following lead-induced toxicity in Wistar rats. Six groups were studied: a control group receiving 2 mL/kg of normal saline, and five lead-exposed groups (40 mg/kg lead acetate for one week) treated with saline, DFO (200 mg/kg), DFO (400 mg/kg), EDTA (50 mg/kg), or a combination of DFO (400 mg/kg) and EDTA (50 mg/kg) for one-week post-poisoning. Oxidative stress markers, cell viability, DNA damage, and histopathological changes in liver, kidney, and blood samples were assessed. The results demonstrated that DFO alone or in combination with EDTA significantly reduced oxidative stress, improved antioxidant enzyme levels (glutathione, catalase, and superoxide dismutase), decreased malondialdehyde levels, minimized DNA damage, and enhanced cell viability compared to untreated lead-poisoned rats. Histological analysis corroborated these findings, showing marked tissue protection. DFO at 400 mg/kg, alone or combined with EDTA, showed the strongest protection against lead-induced hepatotoxicity and nephrotoxicity.