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...
Main Authors: | , , , |
---|---|
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 |