Mitochondrial Inhibitors and Neurodegenerative Disorders

1. Front Matter

   Pages i-xvii

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2. Mitochondrial Toxins

   1. Front Matter

      Pages 1-1

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   2. Clinical Manifestations and Mechanisms of Action of Environmental Mitochondrial Toxins

      • Mohammad I. Sabri, Peter S. Spencer, Safia Baggia, Albert C. Ludolph

      Pages 3-19

   3. History of 3-Nitropropionic Acid

      • Bradley F. Hamilton, Daniel H. Gould, David L. Gustine

      Pages 21-33

   4. The Neurochemistry of 3-Nitropropionic Acid

      • Norman C. Reynolds Jr., Wen Lin

      Pages 35-49

3. Mitochondrial Dysfunctions

   1. Front Matter

      Pages 51-51

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   2. In Vitro Studies of 3-Nitropropionic Acid

      • Gail D. Zeevalk

      Pages 53-72

   3. Cognitive and Motor Deficits Produced by Acute and Chronic Administration of 3-Nitropropionic Acid in Rats

      • Gary L. Dunbar, Deborah A. Shear, Jie Dong, Kristi L. Haik-Creguer

      Pages 73-92

   4. Comparative Study on 3-Nitropropionic Acid Neurotoxicity

      • Cesario V. Borlongan, Toru Shimizu, Paul R. Sanberg

      Pages 93-106

   5. Mechanisms of 3-Nitropropionic Acid Neurotoxicity

      • James W. Geddes, Vimala Bondada, Zhen Pang

      Pages 107-120

   6. Gender-Related Difference of the Effect of 3-Nitropropionic Acid on Striatal Artery

      • Keiya Nakajima, Yasunobu Shimano, Kunio Torii, Hitoo Nishino

      Pages 121-127

   7. Variable Susceptibility to Neurotoxicity of Systemic 3-Nitropropionic Acid

      • Tajrena Alexi, Richard L. M. Faull, Paul E. Hughes

      Pages 129-140

   8. The 3-Nitropropionic Acid Model of Huntington’s Disease

      • Keith J. Page, Alicia Meldrum, Stephen B. Dunnett

      Pages 141-156

   9. Mechanisms of Action of 3-Nitropropionic Acid

      • Michiko Kumazaki, Chucharin Ungsuparkorn, Shripad B. Deshpande, Atsuo Fukuda, Hitoo Nishino

      Pages 157-165

   10. Mitochondrial Inhibition and Neuronal Death in Huntington’s Disease

       • María Isabel Behrens

       Pages 167-176

   11. Effects of Brain Mitochondrial Metabolism, Aging, and Caloric Restriction on Membrane Lipids and Proteins

       • S. Prasad Gabbita, John M. Carney, Allan Butterfield

       Pages 177-200

   12. Malonate

       • Alicia Meldrum, Keith J. Page, Barry J. Everitt, Stephen B. Dunnett

       Pages 201-217

   13. Malonic Acid and the Chronic Administration Model of Excitotoxicity

       • Terence J. Bazzett, Roger L. Albin, Jill B. Becker

       Pages 219-231

   14. Sodium Azide-Induced Neurotoxicity

       • Yun Wang, Cesario V. Borlongan

       Pages 233-242

4. Treatment Interventions for Mitochondrial-Induced Neurotoxicity

   1. Front Matter

      Pages 243-243

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Mitochondria have long been the Rodney Dangerfield of cellular organelles. Believed to be the remnants of bacterial infection of eukaryotic cells eons ago, the mitochondrion evolved a symbiotic relationship in which it dutifully served as the efficient source of A TP for cell function. The extraordinary dependence of cells on the energy provided by mito­ chondrial oxidative metabolism of glucose, especially through critical organs such as the heart and brain, is underlined by the fatal consequences of toxins that interfere with the mitochondrial electron transport system. Consistent with their ancestry, the mitochondria have their own DNA that encodes many but not all of their proteins. The mitochon­ dria and their genes come from the mother via the ovum since sperm do not possess mitochondria. This extranuclear form of inheritance derived exclusively from the female side has proven to be a powerful tool for tracing the evolution by the number of base substitutions in mtDNA. That mitochondrial gene mutations might be a source of human dis­ ease became evident a decade ago with the characterization of a group of multisystem disorders, typically involving the nervous system, which are transmitted from mother to child. Specific point mutations in mtDNA have been associated with the different syndromes.

• Nervous System
• Parkinson
• brain
• central nervous system
• chemistry
• death
• dopamine
• hypoxia
• metabolism
• mitochondria
• neurochemistry
• neurodegenerative disorders
• protein

"...is a concise summary of the present state of research in the area of mitochondrial toxins and their role in animal models of neurodegenerative disease."-J Neuropsychiatry Clin Neurosci

• Department of Neurosurgery, and Program in Neuroscience, University of South Florida College of Medicine, Tampa, USA

  Paul R. Sanberg

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

  Hitoo Nishino

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

  Cesario V. Borlongan

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