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Effects of Leukocyte-Derived Oxidants on Sarcolemmal NA,K,ATP-ASE and Calcium Transport

  • T. Matsuoka
  • T. Yanagishita
  • K. J. Kako
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 248)

Abstract

The mitochondrial electron transport chain is capable of reducing oxygen directly to water. However, 5 % of the oxygen consumption of tissues proceed by a univalent pathway in which superoxide anion, hydrogen peroxide and hydroxyl radicals are produced (for review, Thompson & Hess, 1986). Although hydroxyl radicals are very reactive, and therefore harmful, the cell is equipped with enzymes to metabolize superoxide anion and hydrogen peroxide to water, thereby bypassing the formation of hydroxyl radicals. These are superoxide dismutase, catalase and glutathione peroxidase, serving as part of physiological defense mechanisms (Thompson & Hess, 1986). Therefore, these intermediates of oxygen reduction play a pathogenic role only when their production is increased and/or when the cellular defense is reduced. Evidence has accumulated implicating oxy radical generation as an important factor in tissue injury caused by ischemia-reperfusion (Bolli, 1988; Burton, 1988; Kako et al., 1988, for reviews). Although the exact source of free radicals has not been settled, recent studies with spin resonance spectroscopy suggested it to be the endothelial cell (Zweier et al., 1988).

Keywords

ATPase Activity Calcium Uptake Lens Epithelial Cell Spin Resonance Spectroscopy Sarcolemmal Vesicle 
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. Bolli, R., 1988, Oxygen-derived free radicals and postischemic myocardial dysfunction (“stunned myocardium”). J.Am.Coll.Cardiol. 12: 239PubMedCrossRefGoogle Scholar
  2. Burton, K.P., 1988, Evidence of direct toxic effects of free radicals on the myocardium. Free Radicals Med.Biol. 4:14.Google Scholar
  3. Imlay, J.A., and Linn, S., 1988, DNA damage and oxygen radical toxicity. Science 240:1302.PubMedCrossRefGoogle Scholar
  4. Kako K.J., Kato, M., Matsuoka, T., and Mustapha, A., 1988, The depression of membrane-bound Na+ K+ ATPase activity induced by free radicals and by ischemia of the kidney. Am.J.Physiol. 254:C330.PubMedGoogle Scholar
  5. Kaminishi, T., Matsuoka, T., Yanagishita, T., and Kako, K.J., 1989, Increase versus decrease of calcium uptake by isolated heart cells by H2O2 versus HOCl. Am.J.Physiol. (in press)Google Scholar
  6. Kato, M., and Kako, K.J., 1988, Na+/Ca+ exchange of isolated sarcolemmal membrane: Effects of free radicals, insulin and insulin deficiency. Mol.Cell.Biochem. 83:15.PubMedCrossRefGoogle Scholar
  7. Shinar, E., Navok, T., and Chevion, M., 1983, The analogous mechanisms of enzymatic inactivation induced by ascorbate and superoxide in the presence of copper. J.Biol.Chem. 258: 1478. Skou,J.C, and Norby,J.G., eds., 1979, “Na, K, ATPase. Structure and Kinetics,” Academic Press,New YoGoogle Scholar
  8. Slaughter, R.S., Sutko, J.L., and Reeves, T.R., 1983, Equilibrium calcium-calcium exchange in cardiac sarcolemmal vesicles. J.Biol.Chem. 258:3183.PubMedGoogle Scholar
  9. Spector, A., Yan, G., Huang, R.C., McDermott, M.J., Gascoyne,.P.R.C., and Pigiet, V., 1988, The effect of H2O2 upon thioredoxin-enriched lens epithelial cells. J.Biol.Chem. 263:4984.PubMedGoogle Scholar
  10. ai]Thompson, J. A., and Hess M.L., 1986, The oxygen free radical system: A fundamental mechanism in the production of myocardial necrosis. Progr.Cardiovasc.Dis. 6:449.CrossRefGoogle Scholar
  11. Weiss, S.J., and Lobuglio, A.F., 1982, Phagocyte-generated oxygen metabolites and cellular injury. Lab.Invest. 47:5.PubMedGoogle Scholar
  12. Werns, S.W., and Lucchesi, B.R., 1988, Leukocytes, oxygen radicals and myocardial injury due to ischemia and reperfusion. Free Radicals Biol.Med. 4:31.CrossRefGoogle Scholar
  13. Zweier, J. L., Kuppsamy, P., and Lutty, G. A., 1988, Measurement of endothelial cell free radical generation: Evidence for a central mechanism of free radical injury in postischemic tissues. Proc.Natl.Acad.Sci.USA. 85:4046.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1989

Authors and Affiliations

  • T. Matsuoka
    • 1
  • T. Yanagishita
    • 1
  • K. J. Kako
    • 1
  1. 1.Department of PhysiologyUniversity of OttawaOttawaCanada

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