Abstract
Oxidative stress is involved in a number of neurological disorders, including the neurotoxic effects of ethanol. Recent studies have described a neuroprotective potential of alpha-lipoic acid (LC) in several models of neuronal cell death related to oxidative stress. We tested the hypothesis that LC could be effective in preventing ethanol-induced neurotoxicity employing the clonal hippocampa cell line HT22. A 24 h incubation with ethanol 100-600 mM caused a dose-dependent loss of cell viability and a significant increase of the overall intracellular protein oxidation. Coincubation with LC 0.1 mM resulted in a significant decrease of ethanol-related neurotoxicity and a complete prevention of the ethanol-induced intracellular protein oxidation. These results indicate that the radical scavenging properties of LC are effective to ameliorate ethanol-induced neurotoxicity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alcohol-Induced Disorders, Nervous System / drug therapy*
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Alcohol-Induced Disorders, Nervous System / metabolism
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Alcohol-Induced Disorders, Nervous System / physiopathology
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Animals
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Antioxidants / pharmacology*
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Cell Death / drug effects*
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Cell Death / physiology
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Cell Survival / drug effects
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Cell Survival / physiology
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Cells, Cultured
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Dose-Response Relationship, Drug
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Ethanol / pharmacology
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Glutathione / drug effects
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Glutathione / metabolism
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Hippocampus / drug effects
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Hippocampus / metabolism
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Mice
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Nerve Degeneration / drug therapy*
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Nerve Degeneration / metabolism
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Nerve Degeneration / physiopathology
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Nerve Tissue Proteins / drug effects*
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Nerve Tissue Proteins / metabolism
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Neurons / drug effects
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Neurons / metabolism
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Neuroprotective Agents / pharmacology
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Oxidation-Reduction / drug effects
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Oxidative Stress / drug effects*
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Oxidative Stress / physiology
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Thioctic Acid / pharmacology*
Substances
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Antioxidants
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Nerve Tissue Proteins
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Neuroprotective Agents
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Ethanol
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Thioctic Acid
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Glutathione