Impaired Zinc and Copper Status and Altered Fatty Acid Cell Membrane Composition in Essential Hypertension

  • C. Russo
  • O. Olivieri
  • D. Girelli
  • M. Azzini
  • P. Guarini
  • A. M. Stanzial
  • S. Friso
  • R. Pasqualini
  • R. Corrocher

Abstract

The apparent antagonism between Zinc (Zn) and Copper (Cu) is a well-known phenomenon and has been documented in various chronic diseases. An impairment in Zn and Cu status has been shown in hypertensive animals (1), suggesting a possible relationship with the pathogenesis of hypertension. Zn and Cu are involved in lipid metabolism, and several studies indicated that a major aspect of Zn-Cu interaction may be related to the opposing effects on essential fatty acids (EFA) metabolism or by differential stimulation of the synthesis of prostaglandins (PGs), whose influence on blood pressure (BP) regulation has been widely documented (2). The conversion of C-18 polyunsaturated fatty acids (PUFA) into the longerchain metabolites proceeds through desaturation and elongation steps; desaturation processes are catalyzed by the Δ4-Δ5-Δ6 desaturases, which are the rate-limiting enzymes in the pathway, and whose activities specifically require Zn and Cu (2). Thus, Zn and Cu availability may modulate the balance of PGs precursors. Also, since C-20 and C-22 are the major PUFA found in phospholipids, most of the cellular functions (fluidity, permeability or the ion transport systems activity) are in some way related to their metabolism (3).

Keywords

Desaturase Activity Flame Atomic Absorption Spectrometry Copper Status Essential Hypertensive Patient Essential Hypertensive 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    G.D. Allen and L.M. Klevay, Current Opinion in Lipidology 5, 22–28. (1994).CrossRefGoogle Scholar
  2. 2.
    S.C. Cunnane, Prog. Lipid Res. 21, 73–90 (1982).CrossRefGoogle Scholar
  3. 3.
    D.F. Horrobin, Semin. Thromb. Hemostasis 19, 129–137 (1993).CrossRefGoogle Scholar
  4. 4.
    M. Narce, P. Asdrubal, M.C. Delachambre, E. Vericel, M. Lagarde, J.P. Poisson, Mol. Cell Biochem. 141, 9–13(1994).CrossRefGoogle Scholar
  5. 5.
    O. Olivieri, D. Girelli, A.M. Stanzial et al, Am. J. Clin. Nutr. 60, 510–517 (1994).Google Scholar
  6. 6.
    D. Girelli, M. Azzini, O. Olivieri et al, Clin. Chim. Acta 211, 155–166 (1992).CrossRefGoogle Scholar
  7. 7.
    A. Misra and P. Fridovich, J. Biol. Chem. 247, 3170–3175 (1972).Google Scholar
  8. 8.
    M. Canessa, N. Adragna H. Solomon, T.M. Connolly and D.C. Tosteson, N. Engl. J. Med. 302, 772–778 (1980).CrossRefGoogle Scholar
  9. 9.
    R.P. Garay, G. Dagher, M.G. Pernollet and M.A. Devynck, Nature 284, 281–283 (1980).CrossRefGoogle Scholar
  10. 10.
    G. Bianchi, P. Ferrari, D. Trizio et al, Hypertension 7, 319–325 (1985).Google Scholar
  11. 11.
    S.C. Cunnane, Prog. Food Nutr. Sci. 12, 151–188 (1988).Google Scholar
  12. 12.
    J.J. Strain, Proc. Nutr. Soc. 53, 583–598 (1994).CrossRefGoogle Scholar
  13. 13.
    A.F. Dominiczak, Y. McLaren, J.R. Kusel et al, Am. J. Hypertens. 6, 1003–1008 (1993).Google Scholar
  14. 14.
    A.J. Naftilan, V.Y. Dzau, J. Loscalzo, Hypertension 8 (suppl II), S19–S24 (1986).Google Scholar
  15. 15.
    J.D. Ollerenshaw, A.M. Heagerty, R.F. Bing and J.D. Swales, J. Human Hypertens. 1,9–12(1987).Google Scholar

Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • C. Russo
    • 1
  • O. Olivieri
    • 1
  • D. Girelli
    • 1
  • M. Azzini
    • 1
  • P. Guarini
    • 1
  • A. M. Stanzial
    • 1
  • S. Friso
    • 1
  • R. Pasqualini
    • 1
  • R. Corrocher
    • 1
  1. 1.Institute of Internal MedicineUniversity of VeronaVeronaItaly

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