Effects of Consumption of Potash (Akanwu) on Oxidative Stress, Antioxidant Status and Liver Enzymes in Male Wistar Rats

Background: Oxidative stress results from an imbalance between oxidant production and antioxidant defenses, leading to cellular damage. Potash (Akanwu), commonly consumed in some regions, has been implicated in oxidative toxicity. This study investigated the effects of chronic potash consumption on oxidative stress, antioxidant status, and liver enzyme activity in male Wistar rats.
Methods: Thirty-five male Wistar rats were divided into five groups (n=7). Group A served as control, while Groups B–E orally received potash at 250, 500, 750, and 1000 mg/kg daily for 60 days. Serum biomarkers including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), total antioxidant capacity (TAC), reactive oxygen species (ROS), hydrogen peroxide (H₂O₂), and nitric oxide (NO) were measured using spectrophotometric assays. Liver enzymes (ALT, AST, ALP) were assayed with commercial kits, and histological evaluation of liver tissue was performed. 
Results: Potash administration produced a biphasic antioxidant response. At lower doses (250–500 mg/kg), SOD, CAT, TAC, and NO were elevated, while at higher doses (750–1000 mg/kg), these antioxidants declined significantly, while ROS and H₂O₂ increased, indicating oxidative stress. ALT and AST remained unchanged, but ALP was significantly reduced across treatment groups. Histological analysis revealed normal hepatocytes with mild vascular congestion at 750 mg/kg. 
Conclusion: Regular consumption of potash disrupts redox balance in male Wistar rats, elevates ROS and H₂O₂ while suppressing antioxidant defenses at higher doses. The biphasic response of SOD, CAT, TAC, and NO suggests initial adaptation followed by exhaustion of antioxidant systems. Although overt hepatocellular injury was absent, reduced ALP activity and altered oxidative markers highlight potash’s toxicological potential.