Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/9932
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dc.contributor.authorTruongTran, A.en
dc.contributor.authorHo, L.en
dc.contributor.authorChai, F.en
dc.contributor.authorZalewski, P.en
dc.date.issued2000en
dc.identifier.citationJournal of Nutrition, 2000; 130(5):1459S-1466Sen
dc.identifier.issn0022-3166en
dc.identifier.issn1541-6100en
dc.identifier.urihttp://hdl.handle.net/2440/9932-
dc.descriptionPresented 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.abstractThe 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.statementofresponsibilityA. Q. Truong-Tran, L. H. Ho, F. Chai, and P. D. Zalewskien
dc.language.isoenen
dc.publisherAmerican Society for Nutritionen
dc.rights© 2000 The American Society for Nutritional Sciencesen
dc.source.urihttp://jn.nutrition.org.proxy.library.adelaide.edu.au/content/130/5/1459S.fullen
dc.subjectzinc; apoptosis; caspase; disease; Zinquinen
dc.titleCellular zinc fluxes and the regulation of apoptosis/gene-directed cell deathen
dc.typeJournal articleen
dc.identifier.rmid0001000156en
dc.identifier.doi10.1093/jn/130.5.1459sen
dc.identifier.pubid63909-
pubs.library.collectionMedicine publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidZalewski, P. [0000-0001-5196-2611]en
Appears in Collections:Medicine publications

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