Wei H., Bai Z.A., Xie D.M., Chen Y. and Wang M.H.. 2021. Marine Pollution Bulletin, 173:113145.

Here, we examined the 48-h acute toxicity of cadmium (Cd) in the marine copepod Tigriopus japonicus under two pCO₂ concentrations (400 and 1000 μatm). Subsequently, T. japonicus was interactively exposed to different pCO₂ (400, 1000 μatm) and Cd (control, 500 μg/L) treatments for 48 h. After exposure, biochemical and physiological responses were analyzed for the copepods. The results showed that the 48-h LC₅₀ values of Cd were calculated as 12.03 mg/L and 9.08 mg/L in T. japonicus, respectively, under 400 and 1000 μatm pCO₂ conditions. Cd exposure significantly promoted Cd exclusion/glycolysis, detoxification/stress response, and oxidative stress/apoptosis while it depressed that of antioxidant capacity. Intriguingly, CO₂-driven acidification enhanced Cd bioaccumulation and its toxicity in T. japonicus. Overall, our study provides a mechanistic understanding about the interaction between seawater acidification and Cd pollution in marine copepods.

Figure 1.Effect of seawater acidification on Cd accumulation and its toxicity. Cd exposure facilitated metal accumulation (a); Cd exposure increased the expression of abcb1, relating to Cd exclusion (b); Energy availability for Cd exclusion was increased (c); Cd exposure induced metal toxicity response including detoxification/stress response (d), oxidative stress (e), and apoptosis (f). Cd accumulation was significantly higher under increased pCO₂ plus Cd exposure versus Cd treatment (a′); Seawater acidification decreased the gene expression of abcb1 (b′); Energy availability for Cd exclusion was decreased (c′); Collectively, combined exposure of elevated pCO₂ plus Cd resulted in more metal toxicity response, i.e., detoxification/stress response (d′), oxidative stress (e′), and apoptosis (f′). For more information, please see the discussion text. Cd: cadmium.