Abstract:
:Recent evidence indicates that alterations in brain polyamine metabolism may be critical for nerve cell survival after a free radical initiated neurodegenerative process. It has been shown previously that A beta(1-42) and A beta(25-35) are toxic to neurons through a free radical dependent oxidative mechanism. Treatment of rat embryonic hippocampal neuronal cultures with A beta-peptides increased ornithine decarboxylase (ODC) activity and spermidine uptake, suggesting that oxidative stress upregulates the polyamine mechanism for the repair of free radical damage. Pretreatment of the cells with vitamin E prior to A beta exposure decreased ODC activity and spermidine uptake to control level. This study is the first to demonstrate that A beta treated cells show an increased polyamine metabolism in response to free radical mediated oxidative stress and that the free radical scavenger vitamin E prevents these attenuations. These results are discussed with reference to Alzheimer's disease.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Yatin SM,Yatin M,Aulick T,Ain KB,Butterfield DAdoi
10.1016/s0304-3940(99)00101-9keywords:
subject
Has Abstractpub_date
1999-03-19 00:00:00pages
17-20issue
1eissn
0304-3940issn
1872-7972pii
S0304-3940(99)00101-9journal_volume
263pub_type
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