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Zinc is a micronutrient for mammalians and is essential for the normal growth, immune system, and reproduction of all mammalians including humans, and serves the fundamental role in producing hormones. Zinc as cation (Zn2+) is widely present in various tissues, with its concentration in cardiomyocytes measured at less than 1-nM. In contrast, it is approximately five-fold higher in the sarcoplasmic/endoplasmic reticulum (S(E)R) and lower than the cytosolic level in mitochondria. Zinc, although a redox-inert element, also helps to prevent the high generation of free radicals and reactive oxygen species (ROS), providing a positive effect on protein stability and the proper functioning of antioxidative enzymes. However, several studies also demonstrated that zinc also has some serious toxic effects on biological systems, which are induced through various sources, including constant exposure to polluted sites as well as consumption of overdose zinc supplements, and other natural phenomena. It can be emphasized that taking too much zinc into the body can affect health via altered functions of various organs including the cardiovascular system in mammals. Several animal and human studies have shown that zinc is associated with cellular damage and cardiac dysfunctionCardiac dysfunction. Given the numerous functions of free Zn2+ in various cellular signal transduction, both intracellular and extracellular free Zn2+ increase affect phosphorylation state and subcellular localization of proteins and kinases although its cellular concentration regulation is tightly modulated particularly by specific Zn2+ transporters. Overall, taking into consideration the molecular mechanisms of Zn2+-mediated regulation of cardiac function, including Zn2+ transporters, cellular free Zn2+ levels and Zn2+/Ca2+ signaling in the induction of cellular Zn2+-toxicity, the present chapter aims to document and bring new insights associated with specific possible Zn2+ inhibitors of the related mechanisms to understanding the Zn2+-associated molecular mechanisms of cardiovascular diseases as well as the potential drug candidates.

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Excess Labile Zinc Ion Produces Toxic Effects in Cardiac Cells Through Oxidation and/or Phosphorylation of Proteins and Kinases

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  • 发表日期：

    2025年

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  • Belma Turan

摘要

Zinc is a micronutrient for mammalians and is essential for the normal growth, immune system, and reproduction of all mammalians including humans, and serves the fundamental role in producing hormones. Zinc as cation (Zn2+) is widely present in various tissues, with its concentration in cardiomyocytes measured at less than 1-nM. In contrast, it is approximately five-fold higher in the sarcoplasmic/endoplasmic reticulum (S(E)R) and lower than the cytosolic level in mitochondria. Zinc, although a redox-inert element, also helps to prevent the high generation of free radicals and reactive oxygen species (ROS), providing a positive effect on protein stability and the proper functioning of antioxidative enzymes. However, several studies also demonstrated that zinc also has some serious toxic effects on biological systems, which are induced through various sources, including constant exposure to polluted sites as well as consumption of overdose zinc supplements, and other natural phenomena. It can be emphasized that taking too much zinc into the body can affect health via altered functions of various organs including the cardiovascular system in mammals. Several animal and human studies have shown that zinc is associated with cellular damage and cardiac dysfunctionCardiac dysfunction. Given the numerous functions of free Zn2+ in various cellular signal transduction, both intracellular and extracellular free Zn2+ increase affect phosphorylation state and subcellular localization of proteins and kinases although its cellular concentration regulation is tightly modulated particularly by specific Zn2+ transporters. Overall, taking into consideration the molecular mechanisms of Zn2+-mediated regulation of cardiac function, including Zn2+ transporters, cellular free Zn2+ levels and Zn2+/Ca2+ signaling in the induction of cellular Zn2+-toxicity, the present chapter aims to document and bring new insights associated with specific possible Zn2+ inhibitors of the related mechanisms to understanding the Zn2+-associated molecular mechanisms of cardiovascular diseases as well as the potential drug candidates.