Department of Biological Sciences, California State University East Bay, Hayward, California.
Department of Animal Sciences, University of California Davis, Meyer Hall Davis, California.
J Exp Zool A Ecol Integr Physiol. 2020 Jul;333(6):421-435. doi: 10.1002/jez.2350. Epub 2020 Feb 11.
Salinity stress occurs when salt concentration in the environment changes rapidly, for example because of tidal water flow, rainstorms, drought, or evaporation from small bodies of water. However, gradual changes in salt concentration can also cause osmotic stress in aquatic habitats if levels breach thresholds that reduce the fitness of resident organisms. The latter scenario is exemplified by climate change driven salinization of estuaries and by dilution of ocean surface salinity through changes in the water cycle. In this review, we discuss how fish employ the evolutionarily conserved cellular stress response (CSR) to cope with these different forms of salinity stress. Macromolecular damage is identified as the cause of impaired physiological performance during salinity stress and serves as the signal for inducing a CSR. Basic aspects of the CSR have been observed in fish exposed to salinity stress, including repair and protection of cellular macromolecules, reallocation of energy, cell cycle arrest, and in severe cases, programmed cell death. Osmosensing and signal transduction events that regulate these aspects of the CSR provide a link between environmental salinity and adaptive physiological change required for survival. The CSR has evolved to broaden the range of salinities tolerated by certain euryhaline fish species, but is constrained in stenohaline species that are sensitive to changes in environmental salinity. Knowledge of how the CSR diverges between euryhaline and stenohaline fish enables understanding of physiological mechanisms that underlie salt tolerance and facilitates predictions as to the relative vulnerabilities of different fish species to a rapidly changing hydrosphere.
盐度胁迫发生在环境中盐浓度迅速变化时，例如由于潮汐水流、暴风雨、干旱或小水体蒸发。然而，如果盐度水平突破了降低驻留生物适应性的阈值，那么盐度的逐渐变化也会导致水生栖息地产生渗透胁迫。气候变化导致河口盐度上升和水循环变化导致海洋表面盐度稀释就是这种情况的例子。在这篇综述中，我们讨论了鱼类如何利用进化保守的细胞应激反应（CSR）来应对这些不同形式的盐度应激。大分子损伤被确定为盐度应激期间生理性能下降的原因，并作为诱导 CSR 的信号。在暴露于盐度应激的鱼类中观察到 CSR 的基本方面，包括细胞大分子的修复和保护、能量重新分配、细胞周期停滞，在严重情况下还会发生程序性细胞死亡。调节 CSR 这些方面的渗透感应和信号转导事件为环境盐度与生存所需的适应性生理变化之间提供了联系。CSR 已经进化到拓宽某些广盐性鱼类物种所能耐受的盐度范围，但在对环境盐度变化敏感的狭盐性物种中受到限制。了解 CSR 在广盐性和狭盐性鱼类之间的差异，使我们能够理解盐度耐受的生理机制，并有助于预测不同鱼类物种对快速变化的水圈的相对脆弱性。
