Severe tissue damage in Atlantic cod larvae under increasing ocean acidification
Ocean acidification (OA), caused by increasing atmospheric concentrations of CO2 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...
| Published in: | Nature Climate Change |
|---|---|
| Main Authors: | , , , , , , , , |
| Format: | Article in Journal/Newspaper |
| Language: | unknown |
| Published: |
2011
|
| Subjects: | |
| Online Access: | https://epic.awi.de/id/eprint/25221/ https://hdl.handle.net/10013/epic.39300 |
| Summary: | Ocean acidification (OA), caused by increasing atmospheric concentrations of CO2 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 reproduction4,5. In teleost fishes, early life-history stages are particularly vulnerable as they lack specialized internal pH regulatory mechanisms. So far, impacts of relevant CO2 concentrations on larval fish have been found in behavior and otolith size mainly in tropical, non-commercial species. Here we show detrimental effects of OA on the development of a mass-spawning fish species of high commercial importance. We reared Atlantic cod larvae at three levels of CO2 (1) today, (2) end of next century, and (3) an extreme, coastal upwelling scenario, in a long-term (2½ 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, OA has the potential to act as an additional source of natural mortality, affecting populations of already exploited fish stocks. |
|---|