Inhibiting mitochondrial β-oxidation selectively reduces levels of nonenzymatic oxidative polyunsaturated fatty acid metabolites in the brain

  • J Cereb Blood Flow Metab. 2014 Mar;34(3):376-9. doi: 10.1038/jcbfm.2013.221.
Chuck T Chen  1 ,  Marc-Olivier Trépanier  1 ,  Kathryn E Hopperton  1 ,  Anthony F Domenichiello  1 ,  Mojgan Masoodi  2 ,  Richard P Bazinet  1
Affiliations
  • 1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
  • 2. 1] Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada [2] Nestlé Institute of Health Sciences SA, Lausanne, Switzerland.
PMID: 24326387 DOI: 10.1038/jcbfm.2013.221
Abstract

Schönfeld and Reiser recently hypothesized that fatty acid β-oxidation is a source of oxidative stress in the brain. To test this hypothesis, we inhibited brain mitochondrial β-oxidation with methyl palmoxirate (MEP) and measured oxidative polyunsaturated fatty acid (PUFA) metabolites in the rat brain. Upon MEP treatment, levels of several nonenzymatic auto-oxidative PUFA metabolites were reduced with few effects on enzymatically derived metabolites. Our finding confirms the hypothesis that reduced fatty acid β-oxidation decreases oxidative stress in the brain and β-oxidation inhibitors may be a novel therapeutic approach for brain disorders associated with oxidative stress.

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