Detection of catalase in rat heart mitochondria

J Biol Chem. 1991 Nov 15;266(32):22028-34.


The presence of heme-containing catalase in rat heart mitochondria (20 +/- 5 units/mg) was demonstrated by biochemical and immunocytochemical analysis. Intact rat heart mitochondria efficiently consumed exogenously added H2O2. The rate of H2O2 consumption was not influenced by succinate, glutamate/malate, or N-ethylmaleimide but was significantly inhibited by cyanide. Hydrogen peroxide decomposition by mitochondria yielded molecular oxygen in a 2:1 stoichiometry, consistent with a catalytic mechanism. Mitochondrial fractionation studies and quantitative electron microscopic immunocytochemistry revealed that most catalase was matrix-associated. Electrophoretic analysis and Western blotting of the mitochondrial matrix fraction indicated the presence of a protein with similar electrophoretic mobility to bovine and rat liver catalase and immunoreactive to anti-catalase antibody. Myocardial tissue has a lower catalase-specific activity and a greater mitochondrial H2O2 production/g of tissue than most organs. Thus catalase, representing 0.025% of heart mitochondrial protein, is important for detoxifying mitochondrial derived H2O2 and represents a key antioxidant defense mechanism for myocardial tissue.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Catalase / analysis
  • Catalase / metabolism*
  • Electron Transport Complex IV / metabolism
  • Hydrogen Peroxide / metabolism*
  • Immunohistochemistry
  • Kinetics
  • Liver / enzymology
  • Lung / enzymology
  • Lung / ultrastructure
  • Microbodies / enzymology
  • Microscopy, Immunoelectron
  • Mitochondria / enzymology
  • Mitochondria / ultrastructure
  • Mitochondria, Heart / enzymology*
  • Mitochondria, Heart / ultrastructure
  • Models, Biological
  • Molecular Weight
  • Myocardium / metabolism*
  • Oxygen Consumption
  • Rats


  • Hydrogen Peroxide
  • Catalase
  • Electron Transport Complex IV