Salt stress-induced H2O2and Ca2+mediate K+/Na+homeostasis inPyropia haitanensis
Salt stress-induced H2O2and Ca2+mediate K+/Na+homeostasis inPyropia haitanensis
复制标题
盐胁迫诱导的 H2O2 和 Ca2 介导坛紫菜 K/Na 稳态
DOI：
10.1007/s10811-020-02284-0
复制
发表时间：
2020-10-09
影响因子：
3.3
通讯作者：
Xie, Chaotian
中科院分区：
文献类型：
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作者：
Wang, Wenlei;Xing, Lei;Xie, Chaotian
维持K +/Na（+）平衡和氧化还原平衡是磷耐受的关键。haitanensisto hypersalinity.然而，活性氧（ROS）和K +/Na（+）稳态的信号作用之间的精确联系仍然很差的特点。本研究分析了磷中过氧化氢（H2O2）的产生和通量以及H2O2对K+、Na+和Ca（2+）转运的影响。在高盐条件下的海坦尼斯暴露于高盐胁迫（110 ppm，15 min）迅速增加了P中H（2）O（2）含量和外排。haitanensiscells，这是抵消了超氧化物歧化酶活性的快速增加和激活的防御反应。NADPH氧化酶抑制剂（DPI）和活性氧清除剂（DMTU）可显著抑制盐胁迫诱导的Na+外流和Ca 2+内流。此外，Na（+）流出减少响应质膜Ca 2+渗透通道抑制剂（维拉帕米）。这表明盐胁迫下NADPH氧化酶介导的H2O2的产生可能通过Ca~（2+）依赖的Na~+/H~（+）逆向转运系统促进Na~（+）的外排。haitanensisthalli。此外，盐诱导的H2O2积累也促进了K+的流出，而外源Ca 2+可减轻这种作用。H（2）O（2）和Ca（2+）可能独立地调节P中K（+）的稳态。Haitanensis。H2O2诱导的K（+）渗漏可能会诱导细胞从正常的代谢活动转换到与适应和修复相关的代谢活动。本研究结果为阐明盐诱导的活性氧信号与潮间带海藻离子稳态之间的关系提供了新的见解。
Maintaining K+/Na(+)homeostasis and redox homeostasis is crucial for the tolerance ofP. haitanensisto hypersalinity. However, the precise link between the signaling role of reactive oxygen species (ROS) and K+/Na(+)homeostasis remains poorly characterized. In this study, we analyze hydrogen peroxide (H2O2) production and flux as well as H(2)O(2)effects on K+, Na+, and Ca(2+)transport inP. haitanensisunder hypersaline condition. An exposure to hypersaline stress (110 parts per thousand, 15 min) rapidly increased the H(2)O(2)content and efflux inP. haitanensiscells, which was counteracted by the rapid increase in superoxide dismutase activity and activation of defense responses. The enhanced Na(+)efflux and Ca(2+)influx induced by salt stress were substantially suppressed by an NADPH oxidase inhibitor (DPI) or an ROS scavenger (DMTU). Additionally, Na(+)efflux decreased in response to a plasma membrane Ca2+-permeable channel inhibitor (verapamil). This suggested that NADPH oxidase-mediated H(2)O(2)production may promote Na(+)efflux via the Ca2+-dependent Na+/H(+)antiporter system in salt-stressedP. haitanensisthalli. Moreover, salt-induced H(2)O(2)accumulation also enhanced K(+)efflux, which was alleviated by exogenous Ca2+. H(2)O(2)and Ca(2+)may independently mediate K(+)homeostasis inP. haitanensis. H2O2-induced K(+)leakage may induce cells to switch from normal metabolic activities to those associated with adaptation and repair. The present results provide new insight for clarifying the relationship between salt-induced ROS signaling and ion homeostasis in intertidal seaweed species.