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.

在这里，我们研究了在两种p CO ₂浓度（400 和 1000 μatm）下，海洋桡足类虎斑虎鱼中镉 (Cd) 的 48 小时急性毒性。随后，T. japonicus交互暴露于不同的p CO ₂ (400, 1000 μatm) 和 Cd (对照，500 μg/L) 处理 48 小时。暴露后，分析桡足类的生化和生理反应。结果表明，在48小时的LC _50个的Cd值计算为在12.03 mg / L和9.08 mg / L的T.刺参分别，400和1000μatm下p CO ₂条件。镉暴露显着促进镉排斥/糖酵解、解毒/应激反应和氧化应激/细胞凋亡，同时抑制抗氧化能力。有趣的是，CO ₂驱动的酸化增强了粳稻中Cd 的生物积累及其毒性。总体而言，我们的研究提供了对海水酸化与海洋桡足类 Cd 污染之间相互作用的机制理解。