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Stabilization of Nrf2 Protein by D3T Provides Protection against Ethanol-Induced Apoptosis in PC12 Cells

Previous studies have demonstrated that maternal ethanol exposure induces a moderate increase in Nrf2 protein expression in mouse embryos. Pretreatment with the Nrf2 inducer, 3H-1, 2-dithiole-3-thione (D3T), significantly increases the Nrf2 protein levels and prevents apoptosis in ethanol-exposed em... Full description

Journal Title: PLoS One Feb 2011, Vol.6(2), p.e16845
Main Author: Dong, Jian
Other Authors: Dong, Yan , Shao-Yu, Chen
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 19326203 ; DOI: 10.1371/journal.pone.0016845
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title: Stabilization of Nrf2 Protein by D3T Provides Protection against Ethanol-Induced Apoptosis in PC12 Cells
format: Article
creator:
  • Dong, Jian
  • Dong, Yan
  • Shao-Yu, Chen
subjects:
  • United States–Us
  • North Carolina
  • Nrf2 Protein
  • Embryos
  • Defects
  • Ethanol
  • Free Radicals
  • Mutation
  • Brain Research
  • Stabilization
  • Antioxidants
  • Metabolism
  • Embryos
  • Pretreatment
  • Degradation
  • Apoptosis
  • Ethanol
  • Ethanol
  • Protein Expression
ispartof: PLoS One, Feb 2011, Vol.6(2), p.e16845
description: Previous studies have demonstrated that maternal ethanol exposure induces a moderate increase in Nrf2 protein expression in mouse embryos. Pretreatment with the Nrf2 inducer, 3H-1, 2-dithiole-3-thione (D3T), significantly increases the Nrf2 protein levels and prevents apoptosis in ethanol-exposed embryos. The present study, using PC12 cells, was designed to determine whether increased Nrf2 stability is a mechanism by which D3T enhances Nrf2 activation and subsequent antioxidant protection. Ethanol and D3T treatment resulted in a significant accumulation of Nrf2 protein in PC 12 cells. CHX chase analysis has shown that ethanol treatment delayed the degradation of Nrf2 protein in PC12 cells. A significantly greater decrease in Nrf2 protein degradation was observed in the cells treated with D3T alone or with both ethanol and D3T. In addition, D3T treatment significantly reduced ethanol-induced apoptosis. These results demonstrate that the stabilization of Nrf2 protein by D3T confers protection...
language: eng
source:
identifier: E-ISSN: 19326203 ; DOI: 10.1371/journal.pone.0016845
fulltext: fulltext_linktorsrc
issn:
  • 19326203
  • 1932-6203
url: Link


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titleStabilization of Nrf2 Protein by D3T Provides Protection against Ethanol-Induced Apoptosis in PC12 Cells
creatorDong, Jian ; Dong, Yan ; Shao-Yu, Chen
ispartofPLoS One, Feb 2011, Vol.6(2), p.e16845
identifierE-ISSN: 19326203 ; DOI: 10.1371/journal.pone.0016845
subjectUnited States–Us ; North Carolina ; Nrf2 Protein ; Embryos ; Defects ; Ethanol ; Free Radicals ; Mutation ; Brain Research ; Stabilization ; Antioxidants ; Metabolism ; Embryos ; Pretreatment ; Degradation ; Apoptosis ; Ethanol ; Ethanol ; Protein Expression
descriptionPrevious studies have demonstrated that maternal ethanol exposure induces a moderate increase in Nrf2 protein expression in mouse embryos. Pretreatment with the Nrf2 inducer, 3H-1, 2-dithiole-3-thione (D3T), significantly increases the Nrf2 protein levels and prevents apoptosis in ethanol-exposed embryos. The present study, using PC12 cells, was designed to determine whether increased Nrf2 stability is a mechanism by which D3T enhances Nrf2 activation and subsequent antioxidant protection. Ethanol and D3T treatment resulted in a significant accumulation of Nrf2 protein in PC 12 cells. CHX chase analysis has shown that ethanol treatment delayed the degradation of Nrf2 protein in PC12 cells. A significantly greater decrease in Nrf2 protein degradation was observed in the cells treated with D3T alone or with both ethanol and D3T. In addition, D3T treatment significantly reduced ethanol-induced apoptosis. These results demonstrate that the stabilization of Nrf2 protein by D3T confers protection...
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titleStabilization of Nrf2 Protein by D3T Provides Protection against Ethanol-Induced Apoptosis in PC12 Cells
descriptionPrevious studies have demonstrated that maternal ethanol exposure induces a moderate increase in Nrf2 protein expression in mouse embryos. Pretreatment with the Nrf2 inducer, 3H-1, 2-dithiole-3-thione (D3T), significantly increases the Nrf2 protein levels and prevents apoptosis in ethanol-exposed embryos. The present study, using PC12 cells, was designed to determine whether increased Nrf2 stability is a mechanism by which D3T enhances Nrf2 activation and subsequent antioxidant protection. Ethanol and D3T treatment resulted in a significant accumulation of Nrf2 protein in PC 12 cells. CHX chase analysis has shown that ethanol treatment delayed the degradation of Nrf2 protein in PC12 cells. A significantly greater decrease in Nrf2 protein degradation was observed in the cells treated with D3T alone or with both ethanol and D3T. In addition, D3T treatment significantly reduced ethanol-induced apoptosis. These results demonstrate that the stabilization of Nrf2 protein by D3T confers protection...
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titleStabilization of Nrf2 Protein by D3T Provides Protection against Ethanol-Induced Apoptosis in PC12 Cells
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abstractPrevious studies have demonstrated that maternal ethanol exposure induces a moderate increase in Nrf2 protein expression in mouse embryos. Pretreatment with the Nrf2 inducer, 3H-1, 2-dithiole-3-thione (D3T), significantly increases the Nrf2 protein levels and prevents apoptosis in ethanol-exposed embryos. The present study, using PC12 cells, was designed to determine whether increased Nrf2 stability is a mechanism by which D3T enhances Nrf2 activation and subsequent antioxidant protection. Ethanol and D3T treatment resulted in a significant accumulation of Nrf2 protein in PC 12 cells. CHX chase analysis has shown that ethanol treatment delayed the degradation of Nrf2 protein in PC12 cells. A significantly greater decrease in Nrf2 protein degradation was observed in the cells treated with D3T alone or with both ethanol and D3T. In addition, D3T treatment significantly reduced ethanol-induced apoptosis. These results demonstrate that the stabilization of Nrf2 protein by D3T confers protection...
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