Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 37, Issue 12, Pages 1951-1962Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2004.08.021
Keywords
free radicals
Funding
- NINDS NIH HHS [R01 NS45748, R01NS39587] Funding Source: Medline
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Mitochondrial dysfunction has been implicated as a contributing factor in diverse acute and chronic neurological disorders. However, its role in the epilepsies has only recently emerged. Animal studies show that epileptic seizures result in free radical production and oxidative damage to cellular proteins, lipids, and DNA. Mitochondria contribute to the majority of seizure-induced free radical production. Seizure-induced mitochondrial superoxide production, consequent inactivation of susceptible iron-sulfur enzymes, e.g., aconitase, and resultant iron-mediated toxicity may mediate seizure-induced neuronal death. Epileptic seizures are a common feature of mitochondrial dysfunction associated with mitochondrial encephalopathies. Recent work suggests that chronic mitochondrial oxidative stress and resultant dysfunction can render the brain more susceptible to epileptic seizures. This review focuses on the emerging role of oxidative stress and mitochondrial dysfunction both as a consequence and as a cause of epileptic seizures. (C) 2004 Elsevier Inc. All rights reserved.
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