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

Recent evidence indicates that alterations in brain polyamine metabolism ma y be critical for nerve cell survival after a free radical initiated neurod egenerative process. It has been shown previously that A beta(1-42) and A b eta(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 spermidi ne uptake, suggesting that oxidative stress upregulates the polyamine mecha nism for the repair of free radical damage. Pretreatment of the cells with vitamin E prior to A beta exposure decreased ODC activity and spermidine up take to control level. This study is the first to demonstrate that A beta t reated cells show an increased polyamine metabolism in response to free rad ical mediated oxidative stress and that the free radical scavenger vitamin E prevents these attenuations. These results are discussed with reference t o Alzheimer's disease. (C) 1999 Published by Elsevier Science Ireland Ltd. All rights reserved.