Synergistic Effects of Lead on Acetic Acid-induced Colitis Via Oxidative Damage in Male Wistar Rats

Abstract

Background: Environmental lead exposure may contribute to gastrointestinal injury through oxidative and inflammatory mechanisms. This study investigated whether oral lead exposure aggravates acetic acid-induced colitis in male Wistar rats. Methods: Forty-eight rats were allocated to six groups of eight animals: control, colitis, lead at 30 mg/kg body weight with colitis, lead at 30 mg/kg body weight alone, lead at 60 mg/kg body weight with colitis, and lead at 60 mg/kg body weight alone. Lead acetate was administered orally for 28 days, after which colitis was induced by a single intrarectal administration of 2% acetic acid. Colonic malondialdehyde, myeloperoxidase activity, tumour necrosis factor-alpha, VEGF, Caspase-3, and histological changes were assessed. Results: The 60 mg/kg lead-plus-colitis group showed increased malondialdehyde and myeloperoxidase activity relative to the control, together with higher TNF-α and Caspase-3 levels. The reported changes were consistent with enhanced oxidative stress, inflammatory-cell infiltration, apoptotic activity, and impaired mucosal integrity. Histological examination showed dose-related mucosal inflammation, erosion, and vascular disruption, with more severe changes in the high-dose lead-plus-colitis group. Conclusion: Oral lead exposure, particularly at 60 mg/kg body weight, aggravated acetic acid-induced colonic injury in male Wistar rats. The findings support coordinated involvement of oxidative, inflammatory, vascular, and apoptotic processes, although further mechanistic studies are required.