Advertisement

Superoxide Radical Release into the Cytoplasm of Heart Cells by an NADH-Driven Oxygen Activator

  • Hans Nohl
Part of the Basic Life Sciences book series (BLSC, volume 49)

Abstract

It is now unequivocally accepted, mainly on the basis of indirect evidence1–4 that heart mitochondria (RHM) release small amounts of superoxide radicals as a physiological byproduct of respiration. The existence of this process indicates not only that the oxygen radical generator is able to establish an adequate redox couple with molecular oxygen but also its interaction with the physiological electron acceptor exhibits kinetic restraints, causing electron deviation from the normal pathway to oxygen at a nonphysiological site of the respiratory chain. In isolated, normally functioning mitochondria, the latter condition was found to be closely related to energy coupling since superoxide radical formation was only observed under conditions in which, due to a lack of ADP, mitochondria were hindered from ATP-synthesis (= state 4 conditions of respiration). Although such conditions are not likely to exist in highly active energy-consuming organs, there is convincing evidence that O 2 - formation occurs in the living heart2,3.

Keywords

Heart Mitochondrion Oxygen Radical Generator Cytosolic NADH Superoxide Radical Formation External NADH 
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.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    G. Loschen, A. Azzi, B. Richter and L. Flohe, Superoxide radicals as precursors of mitochondrial hydrogen peroxide. FEBS Lett. 42: 68 (1974).PubMedCrossRefGoogle Scholar
  2. 2.
    H. Nohl and D. Hegner, Do mitochondria produce oxygen radicals in vivo? Eur. J. Biochem. 82: 563 (1978).PubMedCrossRefGoogle Scholar
  3. 3.
    E. Cadenas, A. Boveris, C.I. Ragan and A.O.M. Stoppani, Production of superoxide radicals and hydrogène peroxide by NADH-ubiquinone reductase and ubiquinol-cytochrome с reductase from beaf heart mitochondria, Arch. Biochem. Biophys. 180: 248 (1977).PubMedCrossRefGoogle Scholar
  4. 4.
    H. Nohl, The biochemical mechanism of the formation of reactive oxygen species in heart mitochondria, in: “Advances in Studies on Heart Metabolism”, B. M. Caldarera and P. Harris, eds, CLUEB, Bologna (1982).Google Scholar
  5. 5.
    H. Nohl, Demonstration of the existence of an organo-specific NADH dehydrogenase in heart mitochondria. Eur. J. Biochemо 169: 585 (1987).CrossRefGoogle Scholar
  6. 6.
    H. Nohl, Identification of the site of adriamycin activation in the heart cell. Biochem. Pharmacol. in press (1988).Google Scholar
  7. 7.
    H. Nohl and W. Jordan, The mitochondrial site of superoxide formation. Biochem. Biophys. Res. Commun. 138: 533 (1986).PubMedCrossRefGoogle Scholar
  8. 8.
    E. Bernt and H.ü. Bergmeyer, Anorganische Peroxide, in: “Methoden der enzyroatischen Analyse”, H.U. Bergmeyer, ed, Verlag Chemie, Weinheim (1974).Google Scholar

Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • Hans Nohl
    • 1
  1. 1.Institute of Pharmacology and ToxicologyVeterinary University of ViennaViennaAustria

Personalised recommendations