Toxicological effects of cobalt on common carp: oxidative stress, ionic imbalance, fatty acid disruption, and gill histopathology.

Cobalt (Co) is an essential element to fish and other organisms that become toxic at high concentrations. This element is emerging as a concerning pollutant in water bodies, potentially endangering the health of marine biota. The aim of this study was to investigate the short-term subcellular toxicity of cobalt in the common carp Cyprinus carpio (0, 1.13, 11.34, 22.68 and 45.37 µg/L of Co²⁺ for 72 h), with emphasis on oxidative balance (enzymatic and non-enzymatic antioxidants), fatty acid composition, Na⁺K⁺/Mg²⁺ATPases activities and histopathological changes. Co exposure increased the levels of the ferric reducing antioxidant power, hydrogen peroxide, malondialdehyde and protein carbonyl along with enzymatic and non-enzymatic antioxidant-related markers. The observed prooxidant-antioxidant imbalance in exposed fish was solidified by histological sections confirming alterations in the histomorphological structure of C. carpio gills. Results showed that increases in Co²⁺ exposure of fish altered the ATPases activities revealing changes in osmoregulation. Additionally, the analysis of fatty acids (FA) underscored shifts in the fish's fatty acid profile, which is indicative of Co²⁺ impact on C. carpio overall metabolism and immune response. Significant changes occurred in some major FA which were associated with lipid peroxidation increase and the inhibition of Na⁺K⁺ and Mg²⁺ ATPases activities. Overall, the current results suggest that the mechanism of Co²⁺ toxicity involves oxidative damage, disruption of ionic balance, cellular homeostasis and the normal physiological function of the fish gills.