QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by O’Dell, B. L. Search for Related Content PubMed PubMed Citation Articles by O’Dell, B. L.

---

Supplement

Role of Zinc in Plasma Membrane Function¹

Department of Biochemistry, University of Missouri, Columbia, MO 65211

The concentration of plasma zinc is the generally accepted index of zinc status. Although low plasma zinc is an essential criterion of deficiency, alone it is inadequate. To supplement this index, we sought to determine the first limiting biochemical defect in animals fed zinc-deficient diets and concluded that the limiting function is associated with a posttranslational change in plasma membrane proteins. Among the signs of zinc deficiency in rats is a bleeding tendency associated with failure of platelet aggregation, a phenomenon that correlates with impaired uptake of Ca²⁺ when stimulated. Zinc-deficient guinea pigs exhibit signs of peripheral neuropathy, and their brain synaptic vesicles exhibit impaired Ca²⁺ uptake when they are stimulated with glutamate. Red cells from zinc-deficient rats show increased osmotic fragility associated with decreased plasma membrane sulfhydryl concentration. Both phenomena are readily reversed (2 d) by dietary zinc repletion. Volume recovery is dependent on Ca-dependent K channels and the sulfhydryl redox state. Both the impaired aggregation and calcium uptake of zinc-deficient platelets are corrected by in vitro incubation of blood with glutathione. Considering the fact that plasma membranes from several cell types show impaired function that is associated with a decreased rate of calcium uptake, it is postulated that a defect in calcium channels is the first limiting biochemical defect in zinc deficiency. The calcium uptake defect and consequent impaired second-messenger function likely results from an abnormal sulfhydryl redox state in the membrane channel protein.

KEY WORDS: • zinc status • biochemical defect • sulfhydryl redox state • calcium channels • osmotic fragility • rats

This article has been cited by other articles:

				F. Kamp and C. M. Donangelo Supplementing Young Women with Both Zinc and Iron Protects Zinc-Related Antioxidant Indicators Previously Impaired by Iron Supplementation J. Nutr., November 1, 2008; 138(11): 2186 - 2189. [Abstract] [Full Text] [PDF]

				H. Shen, E. Oesterling, A. Stromberg, M. Toborek, R. MacDonald, and B. Hennig Zinc Deficiency Induces Vascular Pro-Inflammatory Parameters Associated with NF-{kappa}B and PPAR Signaling J. Am. Coll. Nutr., October 1, 2008; 27(5): 577 - 587. [Abstract] [Full Text] [PDF]

				D. A. Wiseman, S. M. Wells, M. Hubbard, J. E. Welker, and S. M. Black Alterations in zinc homeostasis underlie endothelial cell death induced by oxidative stress from acute exposure to hydrogen peroxide Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L165 - L177. [Abstract] [Full Text] [PDF]

				D. A. Wiseman, S. M. Wells, J. Wilham, M. Hubbard, J. E. Welker, and S. M. Black Endothelial response to stress from exogenous Zn2+ resembles that of NO-mediated nitrosative stress, and is protected by MT-1 overexpression Am J Physiol Cell Physiol, September 1, 2006; 291(3): C555 - C568. [Abstract] [Full Text] [PDF]

				S. Hughes and S. Samman The effect of zinc supplementation in humans on plasma lipids, antioxidant status and thrombogenesis. J. Am. Coll. Nutr., August 1, 2006; 25(4): 285 - 291. [Abstract] [Full Text] [PDF]

				S. B. Williams, L. L. Southern, and T. D. Bidner Effects of supplemental dietary phytase and pharmacological concentrations of zinc on growth performance and tissue zinc concentrations of weanling pigs J Anim Sci, February 1, 2005; 83(2): 386 - 392. [Abstract] [Full Text] [PDF]

				G. Reiterer, M. Toborek, and B. Hennig Peroxisome Proliferator Activated Receptors {alpha} and {gamma} Require Zinc for Their Anti-inflammatory Properties in Porcine Vascular Endothelial Cells J. Nutr., July 1, 2004; 134(7): 1711 - 1715. [Abstract] [Full Text]

				M. Roselli, A. Finamore, I. Garaguso, M. S. Britti, and E. Mengheri Zinc Oxide Protects Cultured Enterocytes from the Damage Induced by Escherichia coli J. Nutr., December 1, 2003; 133(12): 4077 - 4082. [Abstract] [Full Text] [PDF]

				P. Meerarani, G. Reiterer, M. Toborek, and B. Hennig Zinc Modulates PPAR{gamma} Signaling and Activation of Porcine Endothelial Cells J. Nutr., October 1, 2003; 133(10): 3058 - 3064. [Abstract] [Full Text] [PDF]

				W. Maret From the Cover: Crosstalk of the group IIa and IIb metals calcium and zinc in cellular signaling PNAS, October 23, 2001; 98(22): 12325 - 12327. [Full Text] [PDF]