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 3 − ] but no increase in pCO 2 , 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 3 − -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 3 − uptake. However, we cannot rule out that reduced branchial HCO 3 − excretion contributed to an increase in net acid excretion. Since colchicine prevents full compensation, translocation of H + and/or HCO 3 − 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.

中文翻译：

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海洋硬骨鱼 Opsanus beta 通过 H+ 排泄或减少 HCO3− 排泄而不是 HCO3− 摄取来补偿高盐度水中的酸中毒

环境盐度的增加需要同时增加肠道基础分泌物以维持渗透压调节状态，这可能是广盐性鱼类从淡水转移到海水后暂时性酸中毒的原因。据预测，海洋海湾蟾鱼 ( Opsanus beta ) 从海水 (35 ppt) 转移到高盐度 (60 ppt) 海水 (HSW) 将导致暂时性酸中毒，可通过增加鳃酸排泄来抵消酸– 基础干扰。暴露于 HSW 的蟾鱼显示血液 pH 值和 [HCO 3 - ] 显着降低，但 pCO 2 没有增加，随后在 48-96 小时后完全恢复。当鱼暴露于 60 ppt HCO 3 − 游离海水（HEPES 缓冲）时，发现了类似的代谢性酸中毒和恢复，这可能表明高盐处理期间肠道碱损失的补偿来自鳃H + 排泄而不是鳃HCO 3 - 吸收。然而，我们不能排除鳃HCO 3 - 排泄减少导致净酸排泄增加。由于秋水仙碱阻止完全补偿，H + 和/或 HCO 3 - 转运蛋白在细胞质区室和质膜部分之间的易位可能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对蟾鱼在其自然环境中遇到的快速波动和高盐度的更快且能量要求较低的反应。我们不能排除鳃HCO 3 - 排泄减少导致净酸排泄增加。由于秋水仙碱阻止完全补偿，H + 和/或 HCO 3 - 转运蛋白在细胞质区室和质膜部分之间的易位可能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对蟾鱼在其自然环境中遇到的快速波动和高盐度的更快且能量要求较低的反应。我们不能排除鳃HCO 3 - 排泄减少导致净酸排泄增加。由于秋水仙碱阻止完全补偿，H + 和/或 HCO 3 - 转运蛋白在细胞质区室和质膜部分之间的易位可能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对蟾鱼在其自然环境中遇到的快速波动和高盐度的更快且能量要求较低的反应。