Esbaugh Andrew J, Ern Rasmus, Nordi Wiolene M, Johnson Abbey S
J Comp Physiol B. 2016 Jan;186(1):97-109. doi: 10.1007/s00360-015-0940-6.
The changes in ocean chemistry stemming from anthropogenic CO2 release--termed ocean acidification (OA)--are predicted to have wide-ranging effects on fish and ultimately threaten global populations. The ability of fish to adapt to environmental change is currently unknown, but phenotypic plasticity has been highlighted as a crucial factor in determining species resilience. Here we show that red drum, a long-lived estuarine-dependent fish species native to the Gulf of Mexico, exhibit respiratory plasticity that increases CO2 excretion capacity when acclimated to OA conditions. Specifically, fish exposed to 14 days of 1000 µatm CO2 had a 32% reduction in branchial diffusion distance and increased expression of two putative CO2 channel proteins--rhag and rhcg1. No changes were observed in the erythrocyte CO2 transport pathways. Surprisingly, no significant changes in blood chemistry were observed between acclimated and acutely challenged animals; however, a non-significant 30 % drop in the magnitude of plasma C(CO2) elevation was observed. Reduced diffusion distance also comes with the cost of increased diffusive water loss, which would require greater osmoregulatory investment by the animal. OA exposure induced increased gill Na(+), K(+) ATPase activity and intestinal nkcc2 expression, supporting both the presumed osmotic stress and increased osmoregulatory investment. However, no differences in standard metabolic rate, maximum metabolic rate or aerobic scope were detected between control and OA acclimated individuals. Similarly, no differences in critical swim speed were detected between groups, suggesting the energetic cost related to respiratory plasticity is negligible against background metabolism. The current study demonstrated that red drum exhibit respiratory plasticity with only mild physiological trade-offs; however, this plasticity is insufficient to fully offset the OA-induced acid-base disturbance and as such is unlikely to impact species resilience.
人为释放二氧化碳导致的海洋化学变化——即海洋酸化（OA）——预计会对鱼类产生广泛影响，并最终威胁到全球鱼类种群。目前尚不清楚鱼类适应环境变化的能力，但表型可塑性已被视为决定物种恢复力的关键因素。在此，我们表明红鼓鱼，一种原产于墨西哥湾的依赖河口的长寿鱼类，具有呼吸可塑性，在适应海洋酸化条件时会增加二氧化碳排泄能力。具体而言，暴露于1000微大气压二氧化碳环境14天的鱼类，鳃扩散距离减少了32%，并且两种假定的二氧化碳通道蛋白——Rhag和Rhcg1的表达增加。红细胞二氧化碳运输途径未观察到变化。令人惊讶的是，在适应环境和急性应激的动物之间，血液化学指标未观察到显著变化；然而，血浆C(CO2)升高幅度出现了30%的非显著下降。扩散距离的缩短也伴随着扩散性水分流失增加的代价，这将需要动物进行更大的渗透调节投入。暴露于海洋酸化环境会导致鳃Na(+)、K(+) ATP酶活性增加以及肠道nkcc2表达增加，这既支持了假定的渗透应激，也表明渗透调节投入增加。然而，在对照组和适应海洋酸化的个体之间，未检测到标准代谢率、最大代谢率或有氧代谢范围的差异。同样，在不同组之间未检测到临界游泳速度的差异，这表明与呼吸可塑性相关的能量消耗相对于基础代谢来说可以忽略不计。当前研究表明，红鼓鱼表现出呼吸可塑性，且仅伴随着轻微的生理权衡；然而，这种可塑性不足以完全抵消海洋酸化引起的酸碱紊乱，因此不太可能影响物种恢复力。
