Xiaorong Yang, Jinzi Wu, Siqun Jing, Michael J. Forster, Liang-Jun Yan. Mitochondrial protein sulfenation during aging in the rat brain. Biophysics Reports, 2018, 4(2): 104-113. doi: 10.1007/s41048-018-0053-3
Citation: Xiaorong Yang, Jinzi Wu, Siqun Jing, Michael J. Forster, Liang-Jun Yan. Mitochondrial protein sulfenation during aging in the rat brain. Biophysics Reports, 2018, 4(2): 104-113. doi: 10.1007/s41048-018-0053-3

Mitochondrial protein sulfenation during aging in the rat brain

doi: 10.1007/s41048-018-0053-3
Funds:  This work was supported in part by the National Institutes of Health (Grant Number R01NS079792).
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  • Corresponding author: Liang-Jun Yan
  • Received Date: 14 February 2017
  • Rev Recd Date: 28 November 2017
  • Publish Date: 30 April 2018
  • There is accumulating evidence that cysteine sulfenation (cys-SOH) in proteins plays an important role in cellular response to oxidative stress. The purpose of the present study was to identify mitochondrial proteins that undergo changes in cys-SOH during aging. Studies were conducted in rats when they were 5 or 30 months of age. Following blocking of free protein thiols with N-ethylmaleimide, protein sulfenic acids were reduced by arsenite to free thiol groups that were subsequently labeled with biotinmaleimide. Samples were then comparatively analyzed by two-dimensional Western blots, and proteins showing changes in sulfenation were selectively identified by mass spectrometry peptide sequencing. As a result, five proteins were identified. Proteins showing an age-related decrease in sulfenation include pyruvate carboxylase and pyruvate dehydrogenase; while those showing an age-related increase in sulfenation include aconitase, mitofilin, and tubulin (α-1). Results of the present study provide a general picture of mitochondrial protein sulfenation in brain oxidative stress and implicate the involvement of protein sulfenation in overall decline of mitochondrial function during brain aging.
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