Ocean acidification dampens warming and contamination effects on the physiological stress response of a commercially important fish

Abstract. Increases in carbon dioxide (CO₂) and other greenhouse gases emissions are leading to changes in ocean temperature and carbonate chemistry, the so-called ocean warming and acidification phenomena, respectively. Methylmercury (MeHg) is the most abundant form of mercury (Hg), well-known for its toxic effects on biota and environmental persistency. Despite more than likely co-occurrence in future oceans, the interactive effects of these stressors are largely unknown. Here we assessed organ-dependent Hg accumulation (gills, liver and muscle) within a warming (ΔT = 4 ºC) and acidification (ΔpCO₂ = 1100 µatm) context, and the respective phenotypic responses of molecular chaperone and antioxidant enzymatic machineries, in a commercially important fish (the meagre Argyrosomus regius). After 30 days of exposure, although no mortalities were observed in any treatments, Hg concentration was significantly enhanced under warming conditions, significantly more so in the liver. On the other hand, increased CO₂ decreased Hg accumulation and, despite negative effects prompted as a sole stressor, consistently elicited an antagonistic effect with temperature and contamination on oxidative stress (catalase, superoxide dismutase and glutathione-S-tranferase activities) and heat shock (Hsp70 levels) responses. We argue that the mechanistic interactions are grounded on simultaneous increase in excessive hydrogen (H⁺) and reactive oxygen species (e.g. O₂⁻) free radicals, and subsequent chemical reaction equilibrium balancing. Additional multi-stressor experiments are needed to understand such biochemical mechanism and further disentangle interactive (additive, synergistic or antagonistic) stressor effects on fish ecophysiology in the oceans of tomorrow.