Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis.

Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Research Abstract Details 

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Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Abstract Text:

Xiaoping Qi,Alfred S Lewin,Liang Sun,William W Hauswirth,John Guy,

The mechanisms of axonal and neuronal degeneration causing visual and neurologic disability in multiple sclerosis are poorly understood. Here we explored the contribution of mitochondria to neurodegeneration in the experimental autoimmune encephalomyelitis animal model of multiple sclerosis. Oxidative injury to the murine mitochondrion preceded the infiltration of inflammatory cells, classically heralded as the mediators of demyelination and axonal injury by transection. Nitration of mitochondrial proteins affected key subunits of complexes I and IV of the respiratory chain and a chaperone critical to the stabilization and translocation of proteins into the organelle. Oxidative products were associated with loss of mitochondrial membrane potential and apoptotic cell death. Reductions in the rate of synthesis of adenosine triphosphate were severe and even greater than those associated with disorders caused by mutated mitochondrial DNA. Mitochondrial vacuolization, swelling, and dissolution of cristae occurred in axons as early as 3 days after sensitization for experimental autoimmune encephalomyelitis. Our findings implicate mitochondrial dysfunction induced by protein inactivation and mediated by oxidative stress initiates a cascade of molecular events leading to apoptosis and neurodegeneration in experimental autoimmune encephalomyelitis that is not mediated by inflammatory cells.

Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Publishing Authors By Initials

X Qi,AS Lewin,L Sun,WW Hauswirth,J Guy,

For similar inorganic chemicals: free radicals: reactive oxygen species research abstracts see: inorganic chemicals: free radicals: reactive oxygen species research

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Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of biological chemistry

VOLUME: 281

Page Numbers: 31950-62

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 18

MONTH: 08

YEAR: 2006

Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985121

Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Keywords Mesh Terms:

KEYWORDS: Reactive Oxygen Species

MESH TERMS: chemistry

Chemical & Substance for Abstract: Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis. Information

Substance Name: Nitric Oxide Synthase

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Mitochondrial protein nitration primes neurodegeneration in experimental autoimmune encephalomyelitis.

AFFILIATION: Department of Ophthalmology, the University of Florida College of Medicine, Gainesville, Florida 32610-0284, USA.

Country: United States

AGENCY: United States NEI

GRANT: EY12355

ACRONYM: EY

MEDLINETA: J Biol Chem

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