Abstract

Previously, we found that ocean acidification (OA) mitigates mercury (Hg) toxicity to marine copepod Tigriopus japonicus under multigenerational exposure (four generations, F0-F3). To determine the response mechanisms of T. japonicus against long-term exposure to OA and Hg pollution, we investigated the proteome of F3 copepods after multigenerational exposure to four conditions: pCO2 400 μatm + control; pCO2 1000 μatm + control; pCO2 400 μatm +1.0 μg/L Hg; and pCO2 1000 μatm +1.0 μg/L Hg. Functional enrichment analysis indicated that OA enhanced the copepod's energy production mainly by increasing protein assimilation and proteolysis as a compensatory strategy, which explained its physiological resilience to reduced pH. Conversely, Hg treatment decreased many critical processes, including ferric iron binding, antioxidant activity, cellular homeostasis, and glutathione metabolism, and these toxic events could translate into higher-level responses, i.e., restrained reproduction in copepods. Importantly, the mediation of Hg toxicity in T. japonicus by OA could be explained by the enhanced lysosome-autophagy pathway proteomes that are responsible for repairing and removing damaged proteins and enzymes under stress. Overall, this study provided molecular insights into the response of T. japonicus to long-term exposure of OA and Hg, with a particular emphasis on the mitigating impact of the CO2-driven acidification on Hg toxicity.

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