Zinc in multiple sclerosis. II: Correlation with disease activity and elevated plasma membrane–bound zinc in erythrocytes from patients with multiple sclerosis

Authors

  • Dr Shih-Yieh Ho PhD,

    Corresponding author
    1. University of Connecticut Multiple Sclerosis Center, Division of Neuroimmunology, Department of Neurology, University of Connecticut Health Center, Farmington, CT 06032
    • University of Connecticut Multiple Sclerosis Center, Division of Neuroimmunology, Department of Neurology, University of Connecticut Health Center, Farmington, CT 06032
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  • Frank A. Catalanotto DMD,

    1. Department of Pediatric Dentistry, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78284
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  • Robert P. Lisak MD,

    1. Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104
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  • Paula Dore-Duffy PhD

    1. University of Connecticut Multiple Sclerosis Center, Division of Neuroimmunology, Department of Neurology, University of Connecticut Health Center, Farmington, CT 06032
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  • The first part of this paper was published in the Annals: Dore-Duffy P, Catalanotto F, Donaldson JO, et al: Zinc in multiple sclerosis. Ann Neurol 14:450–454, 1983

Abstract

Previous studies have shown that zinc levels in erythrocytes are significantly elevated in patients with multiple sclerosis (MS). To examine the correlation between erythrocyte Zn levels and disease activity, we measured erythrocyte Zn levels longitudinally. Levels were dramatically decreased during a clinically documented exacerbation of MS. To determine the localization of increased Zn levels in MS erythrocytes, we employed standard techniques for the isolation of nonhemoglobin erythrocyte membrane ghosts. Patients with MS had three times more Zn in ghost material than did controls. Chloroform–methanol extraction in erythrocyte ghosts followed by determination of Zn levels indicated that most of the membrane-bound Zn was associated with the lipid-soluble fraction. Non-lipid-associated Zn and total membrane protein concentration were similar in MS and control samples. Results suggest that mechanisms which govern cellular availability, compartmentalization of Zn, or the binding of Zn to cell surface membranes may be altered in patients with MS, and that these mechanisms vary with disease activity.

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