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individual
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date: 2026-08-24T21:51:05
publisher: vivo
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label: RDF description of Alpha-lipoic acid regulates heme oxygenase gene expression and nuclear Nrf2 activation as a mechanism of protection against arsenic exposure in HepG2 cells - http://orbis.uaslp.mx/vivo/individual/scopus2403

Consejo Nacional de Ciencia y Tecnología, CONACYT: J062448
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funding vehicle for: Alpha-lipoic acid regulates heme oxygenase gene expression and nuclear Nrf2 activation as a mechanism of protection against arsenic exposure in HepG2 cells

Article
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Environmental Toxicology and Pharmacology
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publication venue for: Alpha-lipoic acid regulates heme oxygenase gene expression and nuclear Nrf2 activation as a mechanism of protection against arsenic exposure in HepG2 cells
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Alpha-lipoic acid regulates heme oxygenase gene expression and nuclear Nrf2 activation as a mechanism of protection against arsenic exposure in HepG2 cells
type: Thing
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related by: authorship_14208
issue: 2
volume: 29
chemicalscas: arsenic, 7440-38-2; glutamate cysteine ligase, 9023-64-7; glutathione, 70-18-8; heme oxygenase, 9059-22-7; thioctic acid, 1077-29-8, 1200-22-2, 2319-84-8, 62-46-4
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estado: published
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doi: 10.1016/j.etap.2009.12.004
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related by: authorship_14210
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abstract: Oxidative stress is a known mechanism induced, among other things, by arsenic toxicity. As a response, the cell triggers the synthesis of antioxidant and stress response elements like glutathione and heme oxygenase. Alpha-lipoic acid (ALA) is a well-known antioxidant that confers protection to oxidative stress conditions. We analyzed the effect of ALA pretreatment on Nrf2-responsive gene expression of HepG2 cells exposed to As3 . Cells were treated with 5mM ALA and 8h later exposed to 50μM As3 for 24h, analyzing MTT-activity, glutathione content, Nrf2 induction and antioxidant gene expression. As3 increased glutathione (154%25), heme oxygenase, glutamate cystein ligase, modifier subunit and metallothionein (35-fold, 10-fold and 9-fold, respectively). ALA prevented the strong expression of heme oxygenase by As3 exposure (from 35- to 5-times of control cells), which correlated with the reduction of Nrf2 observed in As3 group. ALA pretreatment can down-modulate the response mediated by Nrf2 and provide protection to As3 exposed HepG2 cells. © 2010 Elsevier B.V.
has publication venue: Environmental Toxicology and Pharmacology
has funding vehicle: Consejo Nacional de Ciencia y Tecnología, CONACYT: J062448
crisid: 2404
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e iscopus: 2-s2.0-77951622584
origen: scopus
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page start: 144
date time value: article date 2404
freetext keyword: Alpha-lipoic acid; Antioxidant gene expression; Arsenic; Heme oxygenase; HepG2; Nrf2 arsenic; glutamate cysteine ligase; glutathione; heme oxygenase; metallothionein; thioctic acid; transcription factor Nrf2; antioxidant activity; article; cell protection; cell strain HepG2; controlled study; environmental exposure; enzyme activation; gene expression; human; human cell; priority journal
most specific type: Document
type: Continuant
abstract: Oxidative stress is a known mechanism induced, among other things, by arsenic toxicity. As a response, the cell triggers the synthesis of antioxidant and stress response elements like glutathione and heme oxygenase. Alpha-lipoic acid (ALA) is a well-known antioxidant that confers protection to oxidative stress conditions. We analyzed the effect of ALA pretreatment on Nrf2-responsive gene expression of HepG2 cells exposed to As3%2b. Cells were treated with 5mM ALA and 8h later exposed to 50μM As3%2b for 24h, analyzing MTT-activity, glutathione content, Nrf2 induction and antioxidant gene expression. As3%2b increased glutathione (154%25), heme oxygenase, glutamate cystein ligase, modifier subunit and metallothionein (35-fold, 10-fold and 9-fold, respectively). ALA prevented the strong expression of heme oxygenase by As3%2b exposure (from 35- to 5-times of control cells), which correlated with the reduction of Nrf2 observed in As3%2b group. ALA pretreatment can down-modulate the response mediated by Nrf2 and provide protection to As3%2b exposed HepG2 cells. © 2010 Elsevier B.V.
type: Generically Dependent Continuant
page end: 149