Free radical induced increase in protein carbonyl is attenuated by low dose of adenosine in hippocampus and mid brain: implication in neurodegenerative disorders

There is strong evidence that oxidative stress participates in the etiology of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In the previous studies we have already shown that a combination of alpha-tocopherol and ascorbic acid protect neurons against tert...

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Bibliographic Details
Published inGeneral physiology and biophysics Vol. 22; no. 1; p. 29
Main Authors Parihar, M S, Pandit, M K
Format Journal Article
LanguageEnglish
Published Slovakia 01.03.2003
Subjects
Adenosine - pharmacology
Animals
Dose-Response Relationship, Drug
Free Radicals
Glutathione - analysis
Glutathione - metabolism
Hippocampus - drug effects
Hippocampus - metabolism
Male
Mesencephalon - drug effects
Mesencephalon - metabolism
Mice
Neurodegenerative Diseases - chemically induced
Neurodegenerative Diseases - metabolism
Neurons - drug effects
Neurons - metabolism
Proteins - analysis
Proteins - metabolism
tert-Butylhydroperoxide
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Summary:There is strong evidence that oxidative stress participates in the etiology of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In the previous studies we have already shown that a combination of alpha-tocopherol and ascorbic acid protect neurons against tert-butyl hydroperoxide (t-BuOOH) induced neurotoxicity in different brain regions including hippocampus and mid brain. In this work, we examined the neuroprotective effect of low dose of adenosine against protein oxidation (protein carbonyls) in parallel with the level of reduced glutathione (GSH) in hippocampus and mid brain regions of mouse brain. The t-BuOOH was injected intraperitoneally in three concentrations (50, 100, 150 mg/kg b.w.) for 10 days. Results showed dose dependent increase in protein carbonyl (PC) in hippocampus and mid brain region. This increase was accompanied by a significant (p < 0.05) decline in GSH content in both brain regions of t-BuOOH treated mice. Adenosine (1 mg/kg b.w.) protected both hippocampus and mid brain neurons against protein oxidation as evidenced by reduction in protein carbonyl content. The GSH content was significantly (p < 0.05) increased after the treatment of adenosine in both brain regions. These data show that prior treatment with low dose of adenosine attenuates the oxidative protein damage with parallel increase in the GSH level in hippocampus and mid brain of t-BuOOH induced mice.
ISSN:0231-5882