Seawater carbonate chemistry and severe tissue damage in Atlantic cod larvae under increasing ocean acidification, 2012

Ocean acidification, caused by increasing atmospheric concentrations of CO2, is one of the most critical anthropogenicthreats 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. In teleost fishes, early life-history stages are particularly vulnerable as they lack specialized internal pH regulatory mechanisms. So far, impacts of relevant CO2concentrations on larval fish have been found in behaviour and otolith size, 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 ( 2.5 1/2 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.大气二氧化碳浓度升高所引发的海洋酸化，是对海洋生物最具威胁的人为胁迫因素之一。海水碳酸盐化学组成的改变，可能干扰海洋生物的钙化作用、酸碱调节、血液循环与呼吸过程，乃至神经系统，进而导致生长速率下降、繁殖能力降低等长期效应。在硬骨鱼类（teleost fishes）中，早期生活史阶段尤为脆弱，因其缺乏特化的体内pH调节机制。迄今，相关二氧化碳浓度对仔鱼的影响已在行为与耳石（otolith）尺寸层面被观测到，相关研究对象多为热带非经济鱼类。本研究证实，海洋酸化会对一种高商业价值的集群产卵鱼类的发育产生不利影响。我们通过为期2.5个月的中型实验生态系（mesocosm）试验，将大西洋鳕仔鱼暴露于三种二氧化碳浓度环境中：(1) 当前大气二氧化碳浓度水平、(2) 下世纪末预估浓度水平、(3) 极端沿海上升流场景。暴露于高浓度二氧化碳环境会导致多数内脏器官出现严重乃至致死性的组织损伤，且损伤程度随二氧化碳浓度升高而加剧。鉴于仔鱼存活率是鱼类种群补充的瓶颈环节，海洋酸化或可成为额外的自然死亡来源，对已被开发利用的鱼类种群造成冲击。