Reversal of Mitochondrial Damage Caused by Environmental Neurotoxins
Abstract
Dr G. Cohen: The original intent of the grant, as proposed by the principle investigator, Dr. 0. Cohen, was to examine the ability of monoamine oxidase- associated substrates such as dopamine and tyramine to inhibit mitochondrial respiration. The studies entailed initially characterizing the ability of the two substrates to inhibit respiration in brain mitochondria, and to subsequently identify and characterize the underlying biochemical mechanisms responsible for the inhibition. Dr. Cohen proposed the possibility that monoamine oxidase (MAO)-derived production of hydrogen peroxide could hypothetically lead to oxidative damage within the mitochondria, and induce mitochondrial dysfunction. In one publication he reported that the inhibition of mitochondrial respiration by MAO substrates was associated with significant increases in levels of glutathione-protein-mixed disulfides, and that covalent modification of protein thiols by glutathione could inactivate critical thiol-dependent proteins within the electron transport chain (Cohen and Kessler, 1999).
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2002
- Accession Number
- ADA418651
Entities
People
- Martin R. Gluck
Organizations
- Icahn School of Medicine at Mount Sinai