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Free Radical and Iron-Mediated Injury in Lysosomes

  • I. T. Mak
  • W. B. Weglicki
Chapter
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 86)

Abstract

Considerable morphological evidence suggests that the loss of lysosomal membrane integrity occurs during experimental ischemia (1,2), however, whether the released hydrolases play an essential role prior to irreversible injury remains unclear. In recent years, increasing evidence has accumulated demonstrating that myocardial ischemia and reperfusion result in excessive production of oxygen radicals (3–5). Thus, free radical-mediated lipid peroxidation has been implicated to play a significant role in the pathogenesis of myocardial ischemic reperfusion injury. At the subcellular level, the phospholipid-rich lysosomal membrane is a potential site of free radical attack. In the present report, we summarize our recent studies of free radical reactions in lysosomes. In an effort to circumvent the technical difficulties of investigating free radical reactions in situ, we designed in vitro experiments using isolated lysosomes. The temporal relationship of the susceptibility of lysosomal membranes to oxygen radicals and the subsequent changes in lysosomal size and membrane integrity were studied.

Keywords

Lipid Peroxidation Electron Paramagnetic Resonance Free Activity Lysosomal Membrane Free Radical Reaction 
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.
    Wildenthal, K., Decker, R.S., Poole, A.R., Griffin, E.E. and Dingle, J.T. Lab. Invest. 38:656–661, 1978.PubMedGoogle Scholar
  2. 2.
    Decker, R.S., Poole, A.R., Crie, J.S., Dingle, J.T. and Wildenthal, K. Am. J. Pathol. 98:445–456, 1980.PubMedCentralPubMedGoogle Scholar
  3. 3.
    Meerson, F.Z., Kagan, V.E., Kozlov, Y.P. Belkina, L.M. and Arkhipenko, Y.V. Basic Res. Cardiol. 77:465–485, 1982.PubMedCrossRefGoogle Scholar
  4. 4.
    Bernier, M., Hearse, D.J. and Manning A.S. Cir. Res. 58:331–340, 1986.CrossRefGoogle Scholar
  5. 5.
    McCord, J.M. N. Engl. J. Med. 312:159–163, 1985.PubMedCrossRefGoogle Scholar
  6. 6.
    Aust, S.D. and White, B.C. Adv. Free Radical Biol. Med. 1:1–17, 1985.CrossRefGoogle Scholar
  7. 7.
    Beckman, J.K., Owens, K., and Weglicki, W.B. Lipids 16:796–799, 1981.PubMedCrossRefGoogle Scholar
  8. 8.
    Mak, I.T., Misra, H.P. and Weglicki, W.B. J. Biol. Chem. 258:13733–13737.Google Scholar
  9. 9.
    Ruth, R.C., Kennett, F.F. and Weglicki, W.B. J. Mol. Cell. Cardiol. 10:739–746, 1978.PubMedCrossRefGoogle Scholar
  10. 10.
    Ruth, R.C. and Weglicki, W.B. Biochem. J. 172:163–173, 1978.PubMedCentralPubMedGoogle Scholar
  11. 11.
    Singh, A. Can J. Physiol. Pharmacol. 60:1330–1345, 1982.PubMedCrossRefGoogle Scholar
  12. 12.
    McCay, P.B., Lai, E.K., Mak, I.T., Kramer, J.H., Misra, H.P. and Weglicki, W.B. Circulation 68(III):69. 1983.Google Scholar
  13. 13.
    Wills, E.D. Biochem. J. 113:315–324, 1969.PubMedCentralPubMedGoogle Scholar
  14. 14.
    Wills, E.D. Biochem. Pharmacol. 21:239–247, 1972.PubMedCrossRefGoogle Scholar
  15. 15.
    Mak, I.T. and Weglicki, W.B. J. Clin. Invest. 75:58–63, 1985.PubMedCentralPubMedCrossRefGoogle Scholar
  16. 16.
    Nienhuis, A.W. N. Engl. J. Med. 304:170–171Google Scholar
  17. 17.
    Wilson, R.L. In: Iron Metabolism: Ciba Foundation Symposium 51:331–354.Google Scholar
  18. 18.
    Kramer, J.H., Arroyo, CM., Dickens, B.F. and Weglicki, W.B. J. Free Radicals Biol. Med. (in press) 1987.Google Scholar

Copyright information

© Kluwer Academic Publishers 1988

Authors and Affiliations

  • I. T. Mak
    • 1
  • W. B. Weglicki
    • 1
  1. 1.Division of Experimental Medicine, Department of MedicineThe George Washington University Medical CenterUSA

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