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Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol

[Image: see text] Arsenic trioxide (As(2)O(3)) is an environmental carcinogen and a putative endocrine disruptor. Resveratrol has been shown to reverse As(2)O(3)-induced oxidative damage. In immortalized but nontransformed estrogen receptor α-negative human breast cells (MCF10A), we observed that 25...

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Autores principales: Mondal, Bodhisattwa, Chen, Hongxia, Wen, Weihua, Cavalieri, Ercole L., Rogan, Eleanor G., Zahid, Muhammad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Chemical Society 2018
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5981766/
https://www.ncbi.nlm.nih.gov/pubmed/29876539
http://dx.doi.org/10.1021/acsomega.7b01727
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author Mondal, Bodhisattwa
Chen, Hongxia
Wen, Weihua
Cavalieri, Ercole L.
Rogan, Eleanor G.
Zahid, Muhammad
author_facet Mondal, Bodhisattwa
Chen, Hongxia
Wen, Weihua
Cavalieri, Ercole L.
Rogan, Eleanor G.
Zahid, Muhammad
author_sort Mondal, Bodhisattwa
collection PubMed
description [Image: see text] Arsenic trioxide (As(2)O(3)) is an environmental carcinogen and a putative endocrine disruptor. Resveratrol has been shown to reverse As(2)O(3)-induced oxidative damage. In immortalized but nontransformed estrogen receptor α-negative human breast cells (MCF10A), we observed that 25 μM resveratrol ameliorated As(2)O(3)-induced cytotoxicity. As(2)O(3), in the presence or absence of 25 μM resveratrol, induced quinone reductase (NAD(P)H quinone dehydrogenase 1), via the induction of NFE2-related factor 2. As(2)O(3) caused a repression of cytochrome P450 (CYP)1B1, but the addition of 25 μM resveratrol rescued the expression of cytochrome P450 1B1 and kept it at a constant level. Therefore, 25 μM resveratrol can modulate the effects of As(2)O(3) on enzymes involved in estrogen metabolism.
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spelling pubmed-59817662018-06-04 Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol Mondal, Bodhisattwa Chen, Hongxia Wen, Weihua Cavalieri, Ercole L. Rogan, Eleanor G. Zahid, Muhammad ACS Omega [Image: see text] Arsenic trioxide (As(2)O(3)) is an environmental carcinogen and a putative endocrine disruptor. Resveratrol has been shown to reverse As(2)O(3)-induced oxidative damage. In immortalized but nontransformed estrogen receptor α-negative human breast cells (MCF10A), we observed that 25 μM resveratrol ameliorated As(2)O(3)-induced cytotoxicity. As(2)O(3), in the presence or absence of 25 μM resveratrol, induced quinone reductase (NAD(P)H quinone dehydrogenase 1), via the induction of NFE2-related factor 2. As(2)O(3) caused a repression of cytochrome P450 (CYP)1B1, but the addition of 25 μM resveratrol rescued the expression of cytochrome P450 1B1 and kept it at a constant level. Therefore, 25 μM resveratrol can modulate the effects of As(2)O(3) on enzymes involved in estrogen metabolism. American Chemical Society 2018-05-21 /pmc/articles/PMC5981766/ /pubmed/29876539 http://dx.doi.org/10.1021/acsomega.7b01727 Text en Copyright © 2018 American Chemical Society This is an open access article published under an ACS AuthorChoice License (http://pubs.acs.org/page/policy/authorchoice_termsofuse.html) , which permits copying and redistribution of the article or any adaptations for non-commercial purposes.
spellingShingle Mondal, Bodhisattwa
Chen, Hongxia
Wen, Weihua
Cavalieri, Ercole L.
Rogan, Eleanor G.
Zahid, Muhammad
Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol
title Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol
title_full Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol
title_fullStr Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol
title_full_unstemmed Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol
title_short Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol
title_sort modulation of cellular response to arsenic trioxide toxicity by resveratrol
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5981766/
https://www.ncbi.nlm.nih.gov/pubmed/29876539
http://dx.doi.org/10.1021/acsomega.7b01727
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