Alzheimer's amyloid beta-peptide associated free radicals increase rat embryonic neuronal polyamine uptake and ornithine decarboxylase activity: protective effect of vitamin E.

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 Lett

journal_title

Neuroscience letters

authors

Yatin SM,Yatin M,Aulick T,Ain KB,Butterfield DA

doi

10.1016/s0304-3940(99)00101-9

keywords:

subject

Has Abstract

pub_date

1999-03-19 00:00:00

pages

17-20

issue

1

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(99)00101-9

journal_volume

263

pub_type

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