Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 85, Issue 15, Pages 3407-3415Publisher
WILEY
DOI: 10.1002/jnr.21498
Keywords
PARP-1; nitric oxide; calcium; apoptosis; mitochondrial permeability transition
Categories
Funding
- NICHD NIH HHS [HD16596, P01 HD016596, P01 HD016596-240013] Funding Source: Medline
- NINDS NIH HHS [NS07375, T32 NS007375, R21 NS050653, NS050653, NS34152, R01 NS034152, R01 NS034152-12] Funding Source: Medline
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Altered mitochondrial energy metabolism contributes to the pathophysiology of acute brain injury caused by ischemia, trauma, and neurotoxins and by chronic neurodegenerative disorders such as Parkinson's and Huntington's diseases. Although much evidence supports that the electron transport chain dysfunction in these metabolic abnormalities has both genetic and intracellular environmental causes, alternative mechanisms are being explored. These include direct, reversible inhibition of cytochrome oxidase by nitric oxide, release of mitochondrial cytochrome c, oxidative inhibition of mitochondrial matrix dehydrogenases and adenine nucleotide transport, the availability of NAD for dehydrogenase reactions, respiratory uncoupling by activities such as that of the permeability transition pore, and altered mitochondrial structure and intracellular trafficking. This review focuses on the catabolism of neuronal NAD and the release of neuronal mitochondrial NAD as important contributors to metabolic dysfunction. In addition, the relationship between apoptotic signaling cascades and disruption of mitochondrial energy metabolism is considered in light of the fine balance between apoptotic and necrotic neural cell death. (c) 2007 Wiley-Liss, Inc.
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