Synergistic Effects of Lead on Acetic Acid-induced Colitis Via Oxidative Damage in Male Wistar Rats
Taiwo Adebayo Ajagbe *
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Serah Funke Ige
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Oluwaseun Grace Adebayo
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Adetoun Bunmi Aribatise
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Anthony Ifeoluwa Adeyefa
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Faith Eniola Adelakun
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Mathew Ayobami Fatoki
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Omotola Deborah Olatunji
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Christianah Damilola Ayeni
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
Aliyat Nafiu Olanrewaju
Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria.
*Author to whom correspondence should be addressed.
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.
Keywords: Acetic acid-induced colitis, lead acetate, oxidative stress, malondialdehyde, myeloperoxidase, tumour necrosis factor-alpha, VEGF, Caspase-3, colonic mucosal injury, Wistar rats.