Exacerbating cadmium toxicity disrupts metabolism in black sea bass under marine heatwaves: insights from physiological and metabolic responses.

Marine heatwaves (MHWs) and cadmium (Cd2+) pollution are escalating threats to marine ecosystems, yet their combined effects on marine fish remain poorly understood. This study investigates the metabolic responses of juvenile black sea bass (Centropristis striata) to Cd2+ exposure and MHWs-induced heat stress, focusing on carbohydrate and lipid metabolism in the liver. Fish were exposed to Cd2+ (0, 1.83, and 6.4 mg/L) at 17 °C and 30 °C for 96 h. The results demonstrate that elevated temperature markedly increases Cd2+ bioaccumulation, with hepatic tissues showing the highest accumulation. Under combined Cd2+ and heat stress, glycolysis is initially activated (increased pk levels and LDH activity) but inhibited after 96 h (decreased pfk levels). Concurrently, upregulation of pepck and increased Glu levels indicate compensatory gluconeogenesis. Additionally, rising Cd2+ concentrations elevate liver TG, TC, and mRNA levels of fasn, scd, cpt1, and ppar-γ, while suppressing ppar-α. Co-exposure groups showed more pronounced changes than single-exposure groups. These findings suggest that black sea bass liver enhances fatty acid oxidation for energy and promotes lipid storage under stress. Oil Red O staining revealed significantly enlarged lipid droplets in the liver of the co-exposure group, confirming that heat stress exacerbates Cd2+-induced lipid accumulation. Prolonged exposure leads to energy depletion and oxidative stress. This study highlights the synergistic toxicity of Cd2+ and MHWs, underscoring the need for strategies to mitigate climate change and heavy metal impacts on marine ecosystems.