Marine Science Institute, University of Texas at Austin, Port Aransas, TX 78373, USA; Department of Environmental Conservation, University of Massachusetts Amherst, Amherst, MA 01003, USA; Fisheries Resources Division, Southwest Fisheries Science Center, National Marine Fisheries Service (NMFS), National Oceanic and Atmospheric Administration (NOAA), La Jolla, CA 92037, USA.
Marine Science Institute, University of Texas at Austin, Port Aransas, TX 78373, USA.
Comp Biochem Physiol A Mol Integr Physiol. 2020 Dec;250:110779. doi: 10.1016/j.cbpa.2020.110779. Epub 2020 Aug 5.
Respiratory acidosis and subsequent metabolic compensation are well-studied processes in fish exposed to elevated CO (hypercapnia). Yet, such exposures in the marine environment are invariably accompanied by a return of environmental CO to atmospheric baselines. This understudied phenomenon has the potential to cause a respiratory alkalosis that would necessitate base excretion. Here we sought to explore this question and the associated physiological mechanisms that may accompany base excretions using the red drum (Sciaenops ocellatus). As expected, when high pCO (15,000 μatm CO) acclimated red drum were transferred to normal pCO, their net H excretion shifted from positive (0.157 ± 0.044 μmol g h) to negative (-0.606 ± 0.116 μmol g h) in the 2 h post-transfer period. Net H excretion returned to control rates during the 3 to 24 h flux period. Gene expression and enzyme activity assays demonstrated that while the acidosis resulted in significant changes in several relevant transporters, no significant changes accompanied the alkalosis phase. Confocal microscopy was used to assess alkalosis-stimulated translocation of V-type H ATPase to the basolateral membrane previously seen in other marine species; however, no apparent translocation was observed. Overall, these data demonstrate that fluctuations in environmental CO result in both acidic and alkalotic respiratory disturbances; however, red drum maintain sufficient regulatory capacity to accommodate base excretion. Furthermore, this work does not support a role for basolateral VHA translocation in metabolic compensation from a systemic alkalosis in teleosts.
呼吸性酸中毒和随后的代谢代偿在暴露于高二氧化碳（高碳酸血症）的鱼类中是研究得很好的过程。然而，海洋环境中的这种暴露总是伴随着环境二氧化碳回到大气基线。这种研究不足的现象有可能导致呼吸性碱中毒，从而需要排泄碱基。在这里，我们使用红鼓鱼（Sciaenops ocellatus）来探索这个问题以及可能伴随碱基排泄的相关生理机制。正如预期的那样，当高 pCO（15,000 μatm CO）驯化的红鼓鱼被转移到正常的 pCO 时，它们的净 H 排泄在转移后的 2 小时内从正（0.157±0.044 μmol g h）变为负（-0.606±0.116 μmol g h）。在 3 到 24 小时的通量期间，净 H 排泄恢复到对照速率。基因表达和酶活性测定表明，尽管酸中毒导致了几个相关转运蛋白的显著变化，但碱中毒阶段没有明显的变化。共聚焦显微镜用于评估先前在其他海洋物种中观察到的 V 型 H ATP 酶在碱中毒刺激下向基底外侧膜的易位；然而，没有观察到明显的易位。总的来说，这些数据表明，环境二氧化碳的波动会导致呼吸性酸中毒和碱中毒的干扰；然而，红鼓鱼具有足够的调节能力来适应碱基排泄。此外，这项工作不支持基底外侧 VHA 易位在鱼类全身性碱中毒的代谢代偿中的作用。
