LAUSR

Coastal systems experience diel fluctuation of pCO2 and cadmium (Cd) pollution; nevertheless, the effect of fluctuating pCO2 on Cd biotoxicity is poorly known. In this study, we initially performed the isotopically enriched organism bioassay to label Tigriopus japonicus with 113Cd (5 μg/L) to determine the Cd accumulation rate constant (kaccu) under ambient (400 μatm) and steadily (1000 μatm) and fluctuatingly elevated (1000 ± 600 μatm) pCO2 conditions for 48 h. Next, T. japonicus was interactively subjected to the above pCO2 exposures at Cd (control, 5, and 500 μg/L) treatments for 7 d. Biochemical and physiological responses for copepods were analyzed. The results showed that steadily increased pCO2 facilitated Cd bioaccumulation compared to ambient pCO2, and it was more under fluctuating acidification conditions. Despite compensatory reactions (e.g., increased energy production), Cd ultimately induced oxidative damage and apoptosis. Meanwhile, combined treatment exhibited higher toxicity (e.g., increased apoptosis) relative to Cd exposure, and even more if fluctuating acidification was considered. Intriguingly, fluctuating acidification inhibited Cd exclusion in Cd-treated copepods compared to steady acidification, linking to higher Cd kaccu and bioaccumulation. Collectively, CO2-driven acidification could aggravate Cd toxicity, providing a mechanistic understanding of the interaction between seawater acidification and Cd pollution in marine copepods.