Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress

Ethanol withdrawal is linked to elevated oxidative damage to neurons. Here we report our findings on the contribution of phenolic antioxidants (17β-estradiol, p-octyl-phenol and 2,6-di-tert-butyl-4-methylphenol) to counterbalance sudden ethanol withdrawal-initiated oxidative events in hippocampus-de...

Full description

Bibliographic Details
Main Authors: Marianna E. Jung, James W. Simpkins, Laszlo Prokai, Katalin Prokai-Tatrai
Format: Article
Language:English
Published: MDPI AG 2009-04-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:http://www.mdpi.com/1422-0067/10/4/1773/
id doaj-0135c480ee9544e18e9f10180e0c6aab
record_format Article
spelling doaj-0135c480ee9544e18e9f10180e0c6aab2020-11-24T21:21:30ZengMDPI AGInternational Journal of Molecular Sciences1422-00672009-04-011041773178710.3390/ijms10041773Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative StressMarianna E. JungJames W. SimpkinsLaszlo ProkaiKatalin Prokai-TatraiEthanol withdrawal is linked to elevated oxidative damage to neurons. Here we report our findings on the contribution of phenolic antioxidants (17β-estradiol, p-octyl-phenol and 2,6-di-tert-butyl-4-methylphenol) to counterbalance sudden ethanol withdrawal-initiated oxidative events in hippocampus-derived cultured HT-22 cells. We showed that ethanol withdrawal for 4 h after 24-h ethanol treatment provoked greater levels of oxidative damage than the preceding ethanol exposure. Phenolic antioxidant treatment either during ethanol exposure or ethanol withdrawal only, however, dose-dependently reversed cellular oxidative damage, as demonstrated by the significantly enhanced cell viability, reduced malondialdehyde production and protein carbonylation, compared to untreated cells. Interestingly, the antioxidant treatment schedule had no significant impact on the observed neuroprotection. In addition, the efficacy of the three phenolic compounds was practically equipotent in protecting HT-22 cells in spite of predictions based on an in silico study and a cell free assay of lipid peroxidation. This finding implies that free-radical scavenging may not be the sole factor responsible for the observed neuroprotection and warrants further studies to establish, whether the HT-22 line is indeed a suitable model for in vitro screening of antioxidants against EW-related neuronal damage. http://www.mdpi.com/1422-0067/10/4/1773/Ethanol withdrawalLipid peroxidationOxidative stressPhenolic antioxidantProtein carbonylation
collection DOAJ
language English
format Article
sources DOAJ
author Marianna E. Jung
James W. Simpkins
Laszlo Prokai
Katalin Prokai-Tatrai
spellingShingle Marianna E. Jung
James W. Simpkins
Laszlo Prokai
Katalin Prokai-Tatrai
Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
International Journal of Molecular Sciences
Ethanol withdrawal
Lipid peroxidation
Oxidative stress
Phenolic antioxidant
Protein carbonylation
author_facet Marianna E. Jung
James W. Simpkins
Laszlo Prokai
Katalin Prokai-Tatrai
author_sort Marianna E. Jung
title Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
title_short Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
title_full Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
title_fullStr Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
title_full_unstemmed Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
title_sort phenolic compounds protect cultured hippocampal neurons against ethanol-withdrawal induced oxidative stress
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2009-04-01
description Ethanol withdrawal is linked to elevated oxidative damage to neurons. Here we report our findings on the contribution of phenolic antioxidants (17β-estradiol, p-octyl-phenol and 2,6-di-tert-butyl-4-methylphenol) to counterbalance sudden ethanol withdrawal-initiated oxidative events in hippocampus-derived cultured HT-22 cells. We showed that ethanol withdrawal for 4 h after 24-h ethanol treatment provoked greater levels of oxidative damage than the preceding ethanol exposure. Phenolic antioxidant treatment either during ethanol exposure or ethanol withdrawal only, however, dose-dependently reversed cellular oxidative damage, as demonstrated by the significantly enhanced cell viability, reduced malondialdehyde production and protein carbonylation, compared to untreated cells. Interestingly, the antioxidant treatment schedule had no significant impact on the observed neuroprotection. In addition, the efficacy of the three phenolic compounds was practically equipotent in protecting HT-22 cells in spite of predictions based on an in silico study and a cell free assay of lipid peroxidation. This finding implies that free-radical scavenging may not be the sole factor responsible for the observed neuroprotection and warrants further studies to establish, whether the HT-22 line is indeed a suitable model for in vitro screening of antioxidants against EW-related neuronal damage.
topic Ethanol withdrawal
Lipid peroxidation
Oxidative stress
Phenolic antioxidant
Protein carbonylation
url http://www.mdpi.com/1422-0067/10/4/1773/
work_keys_str_mv AT mariannaejung phenoliccompoundsprotectculturedhippocampalneuronsagainstethanolwithdrawalinducedoxidativestress
AT jameswsimpkins phenoliccompoundsprotectculturedhippocampalneuronsagainstethanolwithdrawalinducedoxidativestress
AT laszloprokai phenoliccompoundsprotectculturedhippocampalneuronsagainstethanolwithdrawalinducedoxidativestress
AT katalinprokaitatrai phenoliccompoundsprotectculturedhippocampalneuronsagainstethanolwithdrawalinducedoxidativestress
_version_ 1725999655730282496