Exposure to Nickel-Cadmium Contamination of Drinking Water Culminates in Liver Cirrhosis, Renal Azotemia, and Metabolic Stress in Rats.

Drinking water polluted by heavy metals has the potential to expose delicate biological systems to a range of health issues. This study embraced the health risks that may arise from subchronic exposure of thirty-four male Wistar rats to nickel (Ni)-cadmium (Cd)-contaminated water. It was done by using the Box-Behnken design (BBD) with three treatment factors (Ni and Cd doses at 50-150 mg/L and exposure at 14-21-28 days) at a single alpha level, resulting in seventeen experimental combinations. Responses such as serum creatinine (CREA) level, blood urea nitrogen (BUN) level, BUN/CREA ratio (BCR), aspartate and alanine aminotransferases (AST and ALT) activities, and the De Ritis ratio (DRR), as well as malondialdehyde (MDA) level, catalase (CAT), and superoxide dismutase (SOD) activities, were evaluated. The results revealed that these pollutants jointly caused hepatocellular damage by raising AST and ALT activities and renal dysfunction by increasing CREA and BUN levels in Wistar rats' sera (p < 0.05). These outcomes were further supported by BCR and DRR values beyond 1. In rats' hepatocytes and renal tissues, synergistic interactions of these metals resulted in higher MDA levels and significant impairments of CAT and SOD activities (p < 0.05). In order to accurately forecast the effects on the responses, the study generated seven acceptable regression models (p < 0.05) with r-squared values of > 80% at no discernible lack of fit (p > 0.05). The findings hereby demonstrated that Wistar rats exposed to these pollutants at varied doses had increased risks of developing liver cirrhosis and azotemia marked by metabolic stress.

Exposure of African Catfish (Clarias gariepinus) to Lead and Zinc Modulates Membrane-Bound Transport Protein: A Plausible Effect on Na+/K+-ATPase Activity.

The contamination of the aquatic ecosystem beyond tolerable limits may pose serious health challenges to its components. This study evaluated the toxic effects of a binary mixture of lead (Pb) and zinc (Zn) compounds on the activity of Na+/K+-ATPase in tissues of Clarias gariepinus in a controlled aquatic system. The study employed Box-Behnken Design (BBD) with 17 runs in which Pb and Zn concentrations were considered process variables in a time-dependent fashion. Metal exposure levels consisted of 0, 10 and 20% of 96 h-LC50 of Pb (55.12 mg/L) and Zn (32.15 mg/L) for three weeks. Thereafter, membrane-bound Na+/K+-ATPase activity was assessed in gill, hepatic and renal tissues, and data generated from the BBD were used for the development of models. Three regression models were obtained, for gill, hepatic and renal Na+/K+-ATPase activities with exposure to metals differ significantly (p < 0.05) at R2 > 90%, and no significant lack of fit (p > 0.05) was observed in each case. Congruent to the synergistic interactions observed between Pb and Zn in the study, the gill and hepatic Na+/K+-ATPase activities were significantly inhibited, whereas renal Na+/K+-ATPase activity was significantly stimulated (p < 0.05). The optimized models were considered reliable, as they were confirmed in the laboratory through accurate prediction of hepatic, renal and gill Na+/K+-ATPase activities with equivalences of 1.22 ± 0.17, 1.66 ± 0.07 and 3.50 ± 0.33 µmol pi/min/mg protein (p < 0.05) respectively. It is hereby concluded that the synergistic interaction between Pb and Zn truncated the physiological function of Na+/K+-ATPase activity in the respective tissues except for renal tissue of exposed C. gariepinus.