Abstract
Sodium azide (20mg/kgsc), given for a maximum of 3 days to rats, significantly decreased the alpha-tocopherol concentrations in the cortex on day 2 and in the striatum on day 3. In these brain regions the oxidized glutathione values showed 30 to 36% (statistically not significant) elevation on day 3. Reduced glutathione levels were not altered. The observations suggest an important role for alpha-tocopherol in the defense against azide induced free radicals probably including NO and lipid peroxide radicals.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cerebral Cortex / drug effects*
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Cerebral Cortex / metabolism
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Cerebral Cortex / physiopathology
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Electron Transport / drug effects
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Electron Transport / physiology
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Energy Metabolism / drug effects
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Energy Metabolism / physiology
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Enzyme Inhibitors / pharmacology*
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Free Radicals / metabolism*
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Glutamic Acid / metabolism
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Glutathione / biosynthesis
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Glutathione / drug effects
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Lipid Peroxidation / drug effects
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Lipid Peroxidation / physiology
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Male
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Neostriatum / drug effects*
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Neostriatum / metabolism
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Neostriatum / physiopathology
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Neurodegenerative Diseases / drug therapy
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Neurodegenerative Diseases / metabolism
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Neurodegenerative Diseases / physiopathology
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Nitric Oxide / biosynthesis
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Oxidative Stress / drug effects*
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Oxidative Stress / physiology
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate / drug effects
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Receptors, N-Methyl-D-Aspartate / metabolism
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Sodium Azide / pharmacology*
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Subcellular Fractions / drug effects
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Subcellular Fractions / metabolism
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Vitamin E / biosynthesis*
Substances
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Enzyme Inhibitors
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Free Radicals
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Receptors, N-Methyl-D-Aspartate
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Vitamin E
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Nitric Oxide
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Glutamic Acid
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Sodium Azide
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Glutathione