Severe tissue damage in Atlantic cod larvae under increasing ocean acidification

Ocean acidification, caused by increasing atmospheric concentrations of CO2 (refs 1-3), is one of the most critical anthropogenic threats to marine life. Changes in seawater carbonate chemistry have the potential to disturb calcification, acid-base regulation, blood circulation and respiration, as well as the nervous system of marine organisms, leading to long-term effects such as reduced growth rates and reproduction(4,5). In teleost fishes, early life-history stages are particularly vulnerable as they lack specialized internal pH regulatory mechanisms(6,7). So far, impacts of relevant CO2 concentrations on larval fish have been found in behaviour(8,9) and otolith size(10,11), mainly in tropical, non-commercial species. Here we show detrimental effects of ocean acidification on the development of a mass-spawning fish species of high. commercial importance. We reared Atlantic cod larvae at three levels of CO2, (1) present day, (2) end of next century and (3) an extreme, coastal upwelling scenario, in a long-term (2; months) mesocosm experiment. Exposure to CO2 resulted in severe to lethal tissue damage in many internal organs, with the degree of damage increasing with CO2 concentration. As larval survival is the bottleneck to recruitment, ocean acidification has the potential to act as an additional source of natural mortality, affecting populations of already exploited fish stocks.

Organ damage in Atlantic herring larvae as a result of ocean acidification

The dissolution of anthropogenically emitted excess carbon dioxide lowers the pH of the world's ocean water. The larvae of mass spawning marine fishes may be particularly vulnerable to such ocean acidification (OA), yet the generality of earlier results is unclear. Here we show the detrimental effects of OA on the development of a commercially important fish species, the Atlantic herring (Clupea harengus). Larvae were reared at three levels of CO2: today (0.0385 kPa), end of next century (0.183 kPa), and a coastal upwelling scenario (0.426 kPa), under near-natural conditions in large outdoor tanks. Exposure to elevated CO2 levels resulted in stunted growth and development, decreased condition, and severe tissue damage in many organs, with the degree of damage increasing with CO2 concentration. This complements earlier studies of OA on Atlantic cod larvae that revealed similar organ damage but at increased growth rates and no effect on condition.

Environmental hypoxia but not minor shell damage affects scope for growth and body condition in the blue mussel Mytilus edulis (L.)

The effects of short-term (7 d) exposure to environmental hypoxia (2.11 mg O-2 L-1; control: 6.96 mg O-2 L-1) and varying degrees of shell damage (1 or 2, 1 mm diameter holes; control: no holes) on respiration rate, clearance rate, ammonia excretion rate, scope for growth (SFG) and body condition index were investigated in adult blue mussels (Mytilus edulis). There was a significant hypoxia-related reduction in SFG (>6.70 to 0.92J g(-1) h(-1)) primarily due to a reduction in energy acquisition as a result of reduced clearance rates during hypoxia. Shell damage had no significant affect on any of the physiological processes measured or the SFG calculated. Body condition was unaffected by hypoxia or shell damage. In conclusion, minor physical damage to mussels had no effect on physiological energetics but environmental hypoxia compromised growth, respiration and energy acquisition presumably by reducing feeding rates.