This review considers the molecular mechanisms involved in the redox regulation of the Na,K-ATPase. The enzyme creates a transmembrane gradient of sodium and potassium ions, which is necessary for the vital activity of all animal cells, and acts as a receptor of cardiotonic steroids (CTSs), which regulate cell proliferation and apoptosis. The function of the Na,K-ATPase depends on the cell’s redox status. Although oxidative stress was initially found to inhibit the enzyme, it is clear now that the redox regulation of the Na,K-ATPase activity is a complex process that cannot be explained only by oxidative damage to the protein. Na,K-ATPase activity is maximal at physiological oxygen concentrations and decreases by both hypoxia and hyperoxia, as well as due to decrease or increase of intracellular glutathione concentrations. Thus, a specific range of redox conditions provides maximal activity of the Na,K-ATPase. Now it is obvious that a disturbance of the Na,K-ATPase activity in a number of pathologies such as hypoxia, ischemia, diabetes, Alzheimer’s disease is associated with a change in redox status in the cells. The receptor function of the Na,K-ATPase also depends on the cell redox status and it isshould be taken into account when studying the effects of cardiotonic steroids on cells and tissues. The very special point of this review is the redox modifications of thiol groups in Na,K-ATPase subunits and the regulatory processes in which they are involved in normal and pathological conditions. Insight into the molecular mechanisms of redox regulation provides a better understanding of what is necessary for preventing Na,K-ATPase dysfunction in pathological conditions and thus reducing cell damage.

这篇评论考虑了Na，K-ATPase的氧化还原调节的分子机制。该酶产生钠和钾离子的跨膜梯度，这对于所有动物细胞的生命活动都是必不可少的，并且充当调节细胞增殖和凋亡的强心类固醇（CTS）的受体。Na，K-ATPase的功能取决于细胞的氧化还原状态。尽管最初发现氧化应激会抑制该酶，但现在很清楚，Na，K-ATPase活性的氧化还原调节是一个复杂的过程，不能仅通过对蛋白质的氧化损伤来解释。Na，K-ATPase活性在生理氧浓度下最大，并因缺氧和高氧而降低，也归因于细胞内谷胱甘肽浓度的降低或增加。从而，特定范围的氧化还原条件可提供Na，K-ATPase的最大活性。现在很明显，在许多病理如缺氧，缺血，糖尿病，阿尔茨海默氏病中，Na，K-ATP酶活性的紊乱与细胞中氧化还原状态的改变有关。Na，K-ATPase的受体功能还取决于细胞的氧化还原状态，在研究强心类固醇对细胞和组织的影响时应考虑到这一点。这篇综述的特别之处在于Na，K-ATPase亚基中巯基的氧化还原修饰以及它们参与正常和病理状况的调节过程。深入了解氧化还原调节的分子机制可更好地了解预防Na的必要条件，