Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
Full metadata record
|dc.identifier.citation||Journal of Nutrition, 2000; 130(5):1459S-1466S||en|
|dc.description||Presented at the international workshop “Zinc and Health: Current Status and Future Directions,” held at the National Institutes of Health in Bethesda, MD, on November 4–5, 1998.||en|
|dc.description.abstract||The maintenance of discrete subcellular pools of zinc (Zn) is critical for the functional and structural integrity of cells. Among the important biological processes influenced by Zn is apoptosis, a process that is important in cellular homeostasis (an important cellular homeostatic process). It has also been identified as a major mechanism contributing to cell death in response to toxins and in disease, offering hope that novel therapies that target apoptotic pathways may be developed. Because Zn levels in the body can be increased in a relatively nontoxic manner, it may be possible to prevent or ameliorate degenerative disorders that are associated with high rates of apoptotic cell death. This review begins with brief introductions that address, first, the cellular biology of Zn, especially the critical labile Zn pools, and, second, the phenomenon of apoptosis. We then review the evidence relating Zn to apoptosis and address three major hypotheses: (1) that a specific pool or pools of intracellular labile Zn regulates apoptosis; (2) that systemic changes in Zn levels in the body, due to dietary factors, altered physiological states or disease, can influence cell susceptibility to apoptosis, and (3) that this altered susceptibility to apoptosis contributes to pathophysiological changes in the body. Other key issues are the identity of the molecular targets of Zn in the apoptotic cascade, the types of cells and tissues most susceptible to Zn-regulated apoptosis, the role of Zn as a coordinate regulator of mitosis and apoptosis and the apparent release of tightly bound intracellular pools of Zn during the later stages of apoptosis. This review concludes with a section highlighting areas of priority for future studies.||en|
|dc.description.statementofresponsibility||A. Q. Truong-Tran, L. H. Ho, F. Chai, and P. D. Zalewski||en|
|dc.publisher||American Society for Nutrition||en|
|dc.rights||© 2000 The American Society for Nutritional Sciences||en|
|dc.subject||zinc; apoptosis; caspase; disease; Zinquin||en|
|dc.title||Cellular zinc fluxes and the regulation of apoptosis/gene-directed cell death||en|
|dc.identifier.orcid||Zalewski, P. [0000-0001-5196-2611]||en|
|Appears in Collections:||Medicine publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.