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Neuroprotective Strategies Against Cellular Hypoxia

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Book cover Mitochondrial Inhibitors and Neurodegenerative Disorders

Part of the book series: Contemporary Neuroscience ((CNEURO))

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Abstract

Cellular hypoxia is a crucial event in the pathophysiologic cascade of several acute (e.g., cerebral ischemia, CO intoxication) and chronic (e.g., Parkinsons’s disease, Huntington’s disease, Alzheimer’s disease) diseases of the central nervous system (CNS) (1,2). Cellular hypoxia results from insufficient oxygen or substrate supply as in ischemia or hypoglycemia. In addition, it may be caused by impairment of mitochondrial energy metabolism with chemical inhibitors of oxidative phosphorylation and/or glycolysis such as cyanide, malonate, 3-nitropropionate, iodoacetate, and a manifold of other substances. Owing to their specificity, application of these substances provides a tool to understand the role of individual mitochondrial complexes or glycolytic enzymes in cellular hypoxia. Furthermore, several substances used in clinical practice have a partially inhibiting effect on mitochondrial energy metabolism, e.g., haloperidol on mitochondrial complex I (3) and acetylsalicylic acid on coupling of oxidation and respiration (4).

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  1. Matthias W. Riepe
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Editors and Affiliations

  1. Department of Neurosurgery, and Program in Neuroscience, University of South Florida College of Medicine, Tampa, FL, USA

    Paul R. Sanberg PhD, DSc

  2. Department of Physiology, Nagoya City University Medical School, Mizuho-cho, Mizuho-ku, Nagoya, Japan

    Hitoo Nishino MD, PhD

  3. Cellular Neurophysiology, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA

    Cesario V. Borlongan PhD

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Riepe, M.W. (2000). Neuroprotective Strategies Against Cellular Hypoxia. In: Sanberg, P.R., Nishino, H., Borlongan, C.V. (eds) Mitochondrial Inhibitors and Neurodegenerative Disorders. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-692-8_17

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  • DOI: https://doi.org/10.1007/978-1-59259-692-8_17

  • Publisher Name: Humana Press, Totowa, NJ

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