Peroxidative damage to cardiac mitochondria: identification and purification of modified adenine nucleotide translocase

Arch Biochem Biophys. 1992 Apr;294(1):178-83. doi: 10.1016/0003-9861(92)90154-o.

Abstract

Rat myocardial membranes exposed to free radical-generating systems exhibit both lipid peroxidation and protein alterations. The most sensitive protein, a 28-kDa polypeptide, was previously shown to increase slightly in apparent molecular weight before disappearing completely from the protein profile [N. L. Parinandi, C. W. Zwizinski, and H. H. O. Schmid (1991) Arch. Biochem. Biophys. 289, 118-123]. We now report that isolated cardiac mitochondria contain a 28-kDa protein which responds in the same manner to treatment with Cu2+/t-butylhydroperoxide. The protein exhibits several characteristic properties of the mitochondrial adenine nucleotide translocase. This assignment is supported by the finding that carboxyatractyloside, a specific inhibitor of the adenine nucleotide translocase, can prevent the oxidant-induced changes in the 28-kDa protein. Efficient purification schemes for the isolation of milligram quantities of unmodified and oxidatively altered adenine nucleotide translocase from rat heart mitochondria are described.

Publication types

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

MeSH terms

  • Animals
  • Atractyloside / analogs & derivatives
  • Atractyloside / pharmacology
  • Chromatography
  • Copper / pharmacology*
  • Free Radicals
  • Lipid Peroxidation*
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / enzymology*
  • Mitochondrial ADP, ATP Translocases / chemistry
  • Mitochondrial ADP, ATP Translocases / isolation & purification
  • Mitochondrial ADP, ATP Translocases / metabolism*
  • Molecular Weight
  • Peroxides / pharmacology*
  • Rats
  • tert-Butylhydroperoxide

Substances

  • Free Radicals
  • Peroxides
  • Atractyloside
  • Copper
  • Mitochondrial ADP, ATP Translocases
  • tert-Butylhydroperoxide
  • carboxyatractyloside