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

Servet M. Yatin; Mustafa Yatin; Timothy Aulick; Kenneth B. Ain; D. Allan Butterfield

doi:10.1016/S0304-3940(99)00101-9

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

Servet M. Yatin, Mustafa Yatin, Timothy Aulick, Kenneth B. Ain, D. Allan Butterfield

Research output: Contribution to journal › Article › peer-review

89 Scopus citations

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 Aβ(1-42) and Aβ(25-35) are toxic to neurons through a free radical dependent oxidative mechanism. Treatment of rat embryonic hippocampal neuronal cultures with Aβ- 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 Aβ exposure decreased ODC activity and spermidine uptake to control level. This study is the first to demonstrate that Aβ 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.

Original language	English
Pages (from-to)	17-20
Number of pages	4
Journal	Neuroscience Letters
Volume	263
Issue number	1
DOIs	https://doi.org/10.1016/S0304-3940(99)00101-9
State	Published - Mar 1 1999

Bibliographical note

Funding Information:
This work was supported in part by grants NIH (AG-10836; AG-05119) (D.A.B.) and NCI (CA58935) and VA Merit Review (596-0003) (K.B.A).

Funding

This work was supported in part by grants NIH (AG-10836; AG-05119) (D.A.B.) and NCI (CA58935) and VA Merit Review (596-0003) (K.B.A).

Funders	Funder number
VA Merit Review	596-0003
National Institutes of Health (NIH)	AG-05119, AG-10836
National Institutes of Health (NIH)
National Childhood Cancer Registry – National Cancer Institute	R29CA058935
National Childhood Cancer Registry – National Cancer Institute

Keywords

Alzheimer's disease
Amyloid β-peptide
Free radicals
Ornithine decarboxylase activity
Polyamine uptake
Spermidine
Vitamin E

ASJC Scopus subject areas

General Neuroscience

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10.1016/S0304-3940(99)00101-9

Cite this

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title = "Alzheimer's amyloid β-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 Aβ(1-42) and Aβ(25-35) are toxic to neurons through a free radical dependent oxidative mechanism. Treatment of rat embryonic hippocampal neuronal cultures with Aβ- 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 Aβ exposure decreased ODC activity and spermidine uptake to control level. This study is the first to demonstrate that Aβ 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.",

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note = "Funding Information: This work was supported in part by grants NIH (AG-10836; AG-05119) (D.A.B.) and NCI (CA58935) and VA Merit Review (596-0003) (K.B.A). ",

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AU - Ain, Kenneth B.

AU - Butterfield, D. Allan

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N2 - 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 Aβ(1-42) and Aβ(25-35) are toxic to neurons through a free radical dependent oxidative mechanism. Treatment of rat embryonic hippocampal neuronal cultures with Aβ- 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 Aβ exposure decreased ODC activity and spermidine uptake to control level. This study is the first to demonstrate that Aβ 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.

AB - 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 Aβ(1-42) and Aβ(25-35) are toxic to neurons through a free radical dependent oxidative mechanism. Treatment of rat embryonic hippocampal neuronal cultures with Aβ- 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 Aβ exposure decreased ODC activity and spermidine uptake to control level. This study is the first to demonstrate that Aβ 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.

KW - Alzheimer's disease

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KW - Ornithine decarboxylase activity

KW - Polyamine uptake

KW - Spermidine

KW - Vitamin E

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

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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