Sino-US joint laboratory of Aquatic Animal Physiology, East China Sea Fisheries Research Institute, Chinese Academy of Fisheries Sciences, Shanghai, China.
Department of Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Science, University of Miami, Miami, FL, USA.
J Comp Physiol B. 2021 Jan;191(1):85-98. doi: 10.1007/s00360-020-01320-2. Epub 2020 Oct 17.
Increases in ambient salinity demand parallel increases in intestinal base secretion for maintenance of osmoregulatory status, which is likely the cause of a transient acidosis following transfer of euryhaline fish from freshwater to seawater. It was predicted that transfer of the marine Gulf toadfish (Opsanus beta) from seawater (35 ppt) to hypersaline (60 ppt) seawater (HSW) would lead to a transient acidosis that would be compensated by increases in branchial acid excretion to offset the acid-base disturbance. Toadfish exposed to HSW showed a significant decrease in blood pH and [HCO] but no increase in pCO, followed by a full recovery after 48-96 h. A similar metabolic acidosis and recovery was found when fish were exposed to 60-ppt HCO-free seawater (HEPES-buffered), which may suggest that compensation for intestinal base loss during hypersaline treatment is from gill H excretion rather than gill HCO uptake. However, we cannot rule out that reduced branchial HCO excretion contributed to an increase in net acid excretion. Since colchicine prevents full compensation, translocation of H and/or HCO transporters between cytosolic compartments and plasma membrane fractions might be involved in compensating for the hypersalinity-induced acidosis. Translocation of transporters rather than de novo synthesis may represent a faster and less energetically demanding response to rapidly fluctuating and high salinities encountered by toadfish in their natural environment.
环境盐度的增加要求肠道基础分泌相应增加，以维持渗透调节状态，这可能是洄游鱼类从淡水转移到海水后短暂酸中毒的原因。据预测，将海洋海湾蟾鱼（Opsanus beta）从海水（35 ppt）转移到高盐度（60 ppt）海水（HSW）会导致短暂的酸中毒，通过增加鳃酸排泄来补偿酸碱紊乱。暴露于 HSW 的蟾鱼血液 pH 值和 [HCO]显著下降，但 pCO 没有增加，48-96 小时后完全恢复。当鱼暴露于 60-ppt 无 HCO 的海水（HEPES 缓冲液）时，也发现了类似的代谢性酸中毒和恢复，这可能表明在高盐处理期间对肠道基础损失的补偿来自于鳃 H 排泄，而不是鳃 HCO 摄取。然而，我们不能排除减少的鳃 HCO 排泄有助于净酸排泄的增加。由于秋水仙碱不能完全补偿，H 和/或 HCO 转运蛋白可能在细胞质隔室和质膜之间的易位参与补偿高盐度诱导的酸中毒。转运蛋白的易位而不是从头合成可能代表了对蟾鱼在自然环境中遇到的快速波动和高盐度的更快、能量需求更低的反应。
