Title : Cadmium-induced disruption of Na?/K?-ATPase activity in Clarias batrachus: Implications for aquatic toxicology
Abstract:
Heavy metal contamination of aquatic ecosystems is a major global environmental concern and a central issue in aquatic pollution and toxicology due to the persistence, mobility, and high toxicity of these pollutants. Heavy metals such as cadmium (Cd), readily bioaccumulate and biomagnify, posing serious risks to aquatic organisms and human health. Cadmium, in particular, is a widespread heavy metal pollutant and a potent agent of heavy metal toxicity that is directly absorbed by fish through the gills, gastrointestinal tract, and skin, where it disrupts key physiological and biochemical processes. Fish are widely recognized as sensitive bioindicators of heavy metal toxicity and aquatic pollution, reflecting the health status of contaminated aquatic environments. The present study investigated the effects of cadmium exposure in fresh water and higher salinity on Na?/K?-ATPase activity in the gills and kidneys of the catfish, Clarias batrachus as a model species in aquatic toxicology. Na?/K?-ATPase is a vital membrane-bound enzyme involved in ion transport, osmoregulation, and maintenance of cellular homeostasis. Fish were transferred from tap water (TW) to cadmium-exposed tap water (Cd+TW) and cadmium-exposed 30% seawater (Cd+30% SW), and enzyme activity was quantified in key osmoregulatory tissues (gills and kidneys). Gill Na?/K?-ATPase activity showed a highly significant reduction in both cadmium-treated groups (except on day 6 in 30% SW) compared with controls (TW), with strong statistical significance (**P < 0.01 to ****P < 0.0001), indicating severe disruption of branchial ion transport and enhanced heavy metal toxicity and suggesting that cadmium-induced oxidative stress and energy reallocation reduced osmoregulatory capacity. Kidney Na?/K?-ATPase activity was also significantly reduced in the Cd+TW group (**P < 0.01 to ****P < 0.0001), confirming renal sensitivity to cadmium toxicity. In contrast, no significant suppression was observed in the Cd+30% SW group, indicating that increased salinity prevented or attenuated cadmium-induced inhibition of renal Na?/K?-ATPase. Overall, these findings demonstrate that cadmium-driven heavy metal toxicity significantly impairs osmoregulatory enzyme function in Clarias batrachus, and that environmental salinity is an important modulatory factor in aquatic pollution and toxicology. The study further supports the use of fish as effective bioindicators for monitoring heavy metal contamination in aquaculture and natural aquatic systems.

