Effects of Aqueous Cadmium and Nickel Co-Exposure on Antioxidant Defense Mechanisms, Histological Changes and Metal Bioaccumulation in the Brain and Muscle of Tilapia Fish

Heavy metal contamination in aquatic ecosystems poses a severe threat to aquatic organisms, disrupting their physiological and biochemical functions.This study evaluates the impact of aqueous nickel (Ni) and cadmium (Cd) coexposure on oxidative stress, antioxidant defense mechanisms, histological alterations, and metal bioaccumulation in the brain and muscle tissues of Tilapia fish.Fish were divided into four groups: Group A (Control), Group B (Ni exposure), Group C (Cd exposure), and Group D (Ni-Cd co-exposure) and exposed to metals for a specific duration.Oxidative stress biomarkers including thiobarbituric acid reactive substances (TBARS) and reactive oxygen species (ROS), were measured alongside antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH).The findings revealed a significant increase in TBARS and ROS levels, indicating oxidative stress, while SOD, CAT, and GSH levels declined, suggesting impaired antioxidant defense.Histopathological analysis showed severe damage in both brain and muscle tissues, including neuronal degeneration, vacuolization, muscle fiber atrophy, and inflammatory responses, with the most pronounced alterations observed in the Ni-Cd coexposure group.Metal bioaccumulation analysis revealed higher Ni and Cd concentrations in the brain compared to the muscle, with the highest accumulation observed in the combined exposure group.These results highlight the toxic effects of Ni and Cd co-exposure in aquatic organisms, emphasizing the urgent need for stricter pollution control measures to protect aquatic ecosystems.