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Abstract Marine fish precipitate carbonates in their intestines that they subsequently excrete as part of an osmoregulatory strategy. While fish carbonates are proposed to be volumetrically significant to the global carbonate budget, no study has presented direct evidence of fish carbonates in the open ocean. Here we examine sediment trap material collected by the Oceanic Flux Program (OFP) in the North Atlantic and observe the episodic occurrence of enigmatic blue particles since 1992. The blue particles are comprised of calcite with unusually high magnesium content (up to 46 mol%) with distinctively depleted δ¹³C and enriched δ¹⁸O compared with calcite produced by common marine calcifiers. Based on the mineralogical, isotopic, and textural similarities between the blue particles and fish carbonates, we propose that the blue particles are produced by pelagic fish. Our data suggest that fish modify their intestinal fluids to create a concentrated, highly supersaturated,¹³C depleted solution capable of precipitating calcite with high magnesium content and low δ¹³C. Collectively, our data imply that fish carbonate production is an open‐ocean phenomenon, opening up the possibility that fish contribute to the production, dissolution, and export of carbonates globally. 

ABSTRACT Fish in coastal ecosystems can be exposed to acute variations in CO2 of between 0.2 and 1 kPa CO2 (2000–10,000 µatm). Coping with this environmental challenge will depend on the ability to rapidly compensate for the internal acid–base disturbance caused by sudden exposure to high environmental CO2 (blood and tissue acidosis); however, studies about the speed of acid–base regulatory responses in marine fish are scarce. We observed that upon sudden exposure to ∼1 kPa CO2, European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ∼40 min, thus restoring haemoglobin–O2 affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ∼2 h, which is one of the fastest acid–base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO3− in blood, which increased from ∼4 to ∼22 mmol l−1. While the abundance and intracellular localisation of gill Na+/K+-ATPase (NKA) and Na+/H+ exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid–base regulation was completely prevented when the same high CO2 exposure occurred in seawater with experimentally reduced HCO3− and pH, probably because reduced environmental pH inhibited gill H+ excretion via NHE3. The rapid and robust acid–base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO2 fluctuations that naturally occur in coastal environments.