Free radicals as mediators of neuronal injury.
1. Free radicals may play an important role in several pathological conditions of the central nervous system (CNS) where they directly injure tissue and where their formation may also be a consequence of tissue injury. 2. Free radicals produce tissue damage through multiple mechanisms, including excito-toxicity, metabolic dysfunction, and disturbance of intracellular homeostasis of calcium. 3. Oxidative stress can significantly worsen acute insults, such as ischemia, as well as chronic neurodegenerative disorders including amyotrophic lateral sclerosis (ALS) and Parkinson's disease. 4. For instance, recent findings suggest a causal role for chronic oxidative stress in familial ALS, as this disease is linked to missence mutations of the copper/zinc superoxide dismutase (SOD). 5. Thus, therapeutic approaches which limit oxidative stress may be potentially beneficial in several neurological diseases.
Facchinetti
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Department of Neurology, Neuroscience and Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Dawson
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Dawson
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D000690:Amyotrophic Lateral Sclerosis / Q000503:physiopathology; D000818:Animals; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D005609:Free Radicals; D006801:Humans; D019636:Neurodegenerative Diseases / Q000503:physiopathology*; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D018384:Oxidative Stress; D010300:Parkinson Disease / Q000503:physiopathology; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000235:genetics
D005609:Free Radicals; D013482:Superoxide Dismutase