Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2002-7-10
pubmed:abstractText
Previous studies have shown that acute systemic administration of ethanol induced ascorbic acid release in the striatum. However, the pharmacological implications of ethanol-induced striatal ascorbic acid release are unclear. In the present study, ethanol-induced extracellular changes of ascorbic acid and hydroxyl radical levels were detected in rat striatum by using brain microdialysis coupled to high-performance liquid chromatography with electrochemical detection. It was found that both in male and female rats, ethanol (3.0 g/kg, i.p.) increased striatal ascorbic acid release in the first 60 min after ethanol administration. Meanwhile, the extracellular hydroxyl radical levels, detected as 2,3- and 2,5-DHBA, were significantly decreased. However, when the ascorbic acid levels returned to the baseline, hydroxyl radical levels rebounded. Administration of DL-fenfluramine (20 mg/kg, i.p.) had no effect on the basal levels of ascorbic acid and hydroxyl radical, but significantly blocked ethanol-induced ascorbic acid release and increased hydroxyl radical levels significantly. Exogenous administration of ascorbic acid (20 mg/kg, s.c.) increased the extracellular levels of ascorbic acid in the striatum, and inhibited the increase of 2,3- and 2,5-DHBA in DL-fenfluramine plus ethanol group. These results provide first evidence that release of endogenous ascorbic acid in the striatum plays an important role in preventing oxidative stress by trapping hydroxyl radical in the central nervous system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
944
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
90-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12106669-Alcohol-Induced Disorders, Nervous System, pubmed-meshheading:12106669-Animals, pubmed-meshheading:12106669-Ascorbic Acid, pubmed-meshheading:12106669-Drug Interactions, pubmed-meshheading:12106669-Ethanol, pubmed-meshheading:12106669-Extracellular Space, pubmed-meshheading:12106669-Female, pubmed-meshheading:12106669-Fenfluramine, pubmed-meshheading:12106669-Hydroxybenzoic Acids, pubmed-meshheading:12106669-Hydroxyl Radical, pubmed-meshheading:12106669-Male, pubmed-meshheading:12106669-Microdialysis, pubmed-meshheading:12106669-Neostriatum, pubmed-meshheading:12106669-Nerve Degeneration, pubmed-meshheading:12106669-Neurons, pubmed-meshheading:12106669-Oxidative Stress, pubmed-meshheading:12106669-Rats, pubmed-meshheading:12106669-Serotonin Uptake Inhibitors, pubmed-meshheading:12106669-Sex Characteristics
pubmed:year
2002
pubmed:articleTitle
Endogenous released ascorbic acid suppresses ethanol-induced hydroxyl radical production in rat striatum.
pubmed:affiliation
Department of Pharmacology, Shenyang Pharmaceutical University, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't