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 (k
accu) 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 k
accu 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.