Modulation of Lon protease activity and aconitase turnover during aging and oxidative stress

Daniela A. Bota, Holly Van Remmen, Kelvin J.A. Davies

Research output: Contribution to journalArticle

192 Scopus citations

Abstract

We compared Lon protease expression in murine skeletal muscle of young and old, wild-type and Sod2-/+ heterozygous mice, and studied Lon involvement in the accumulation of damaged (oxidized) proteins. Lon protease protein levels were lower in old and oxidatively challenged animals, and this Lon deficiency was associated with increased levels of carbonylated proteins. We identified one of these proteins as aconitase, and another as an aconitase fragmentation product, which we can also generate in vitro by treating purified aconitase with H2O2. These results imply that aging and oxidative stress down-regulate Lon protease expression which, in turn, may be responsible for the accumulation of damaged proteins, such as aconitase, within mitochondria.

Original languageEnglish (US)
Pages (from-to)103-106
Number of pages4
JournalFEBS Letters
Volume532
Issue number1-2
DOIs
StatePublished - Dec 4 2002

Keywords

  • Aconitase
  • Aging
  • Lon protease
  • Mitochondria
  • Protein oxidation
  • Sod2

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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