Deficiency of subunits in heart mitochondrial NADH-ubiquinone oxidoreductase of a patient with mitochondrial encephalomyopathy and cardiomyopathy

Biochem Biophys Res Commun. 1986 Oct 15;140(1):88-93. doi: 10.1016/0006-291x(86)91061-2.

Abstract

The heart mitochondria isolated from a patient with hypertrophic cardiomyopathy associated with mitochondrial encephalomyopathy were analyzed by immunoblotting using specific antibody against each of the purified mitochondrial energy transducing complexes from beef heart. Subunits of NADH-ubiquinone oxidoreductase (Complex I) were markedly decreased and those of cytochrome c oxidase (Complex IV) were decreased to some extent, but the deficiency of any of these subunits was only partial. On the other hand, the contents of subunits of ubiquinol-cytochrome c oxidoreductase (Complex III) were normal. These results suggest that the decreased levels of some of the Complex I subunits might be the primary cause of disorder in this patient.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Brain Diseases, Metabolic / enzymology*
  • Cardiomyopathy, Hypertrophic / enzymology*
  • Cytochrome-c Oxidase Deficiency
  • Female
  • Humans
  • Mitochondria, Heart / enzymology*
  • Muscular Diseases / enzymology*
  • NAD(P)H Dehydrogenase (Quinone)
  • Quinone Reductases / deficiency*
  • Quinone Reductases / immunology

Substances

  • NAD(P)H Dehydrogenase (Quinone)
  • Quinone Reductases