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Growth inhibition, cell-cycle arrest and apoptosis in human T-cell leukemia by the isothiocyanate sulforaphane

Growth inhibition, cell-cycle arrest and apoptosis in human T-cell leukemia by the isothiocyanate... Glucosinolates (GL) can inhibit, retard or reverse experimental multistage carcinogenesis. When brassica plant tissue is broken, GLs are hydrolyzed by the endogenous enzyme myrosinase (Myr), releasing many products including isothiocyanates (ITC). Synthetic ITCs like sulforaphane exert chemopreventive effects against chemically induced tumors in animals, modulating enzymes required for carcinogens' activation/detoxification and/or the induction of cell-cycle arrest and apoptosis in tumor cell lines. To investigate the chemopreventive potential of ITCs while reproducing the circumstances of dietary contact with sulforaphane, we studied proliferation, apoptosis induction and p53, bcl-2 and bax protein expression in Jurkat T-leukemia cells by sulforaphane, the ITC generated in situ in a quantitative manner by Myr starting from glucoraphanin (GRA). Jurkat cells were treated with different doses of GRA–Myr mixture. Effects on cell growth or survival were evaluated by counting trypan blue-excluding cells. Cell-cycle progression, apoptosis and expression of p53, bax and bcl-2 proteins were analyzed by flow cytometry. Results were analyzed by two-sided Fisher's exact test. Sulforaphane, but not GRA, caused G 2 /M-phase arrest ( P = 0.028) and increase of apoptotic cell fraction ( P < 0.0001) in a time- and dose-dependent manner. Necrosis was observed after prolonged exposure to elevated sulforaphane doses. Moreover, it markedly increased p53 and bax protein expression, and slightly affected bcl-2 expression. These findings indicate that sulforaphane but not the native GL GRA can exert both protective and toxic effects inhibiting leukemic cell growth. Sulforaphane therefore deserves study as a potential chemopreventive/chemotherapeutic antileukemic agent. Key words EB, ethidium bromide FITC, fluorescein isothiocyanate FSC, forward scatter GL, glucosinolate GRA, glucoraphanin GSH, Glutathione ITC, isothiocyanate Myr, myrosinase PI, propidium iodide SSC, side scatter. © Oxford University Press « Previous | Next Article » Table of Contents This Article Carcinogenesis (2002) 23 (4): 581-586. doi: 10.1093/carcin/23.4.581 » Abstract Free Full Text (HTML) Free Full Text (PDF) Free Classifications Molecular Epidemiology Services Article metrics Alert me when cited Alert me if corrected Find similar articles Similar articles in Web of Science Similar articles in PubMed Add to my archive Download citation Request Permissions Citing Articles Load citing article information Citing articles via CrossRef Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Fimognari, C. Articles by Hrelia, P. Search for related content PubMed PubMed citation Articles by Fimognari, C. Articles by Nüsse, M. Articles by Cesari, R. Articles by Iori, R. Articles by Cantelli-Forti, G. Articles by Hrelia, P. Related Content Load related web page information Share Email this article CiteULike Delicious Facebook Google+ Mendeley Twitter What's this? Search this journal: Advanced » Current Issue October 2015 36 (10) Alert me to new issues The Journal About this journal Rights & Permissions Dispatch date of the next issue This journal is a member of the Committee on Publication Ethics (COPE) We are mobile – find out more Journals Career Network Impact factor: 5.334 5-Yr impact factor: 5.698 Editor-in-Chief Dr Curtis C Harris, USA View full editorial board For Authors Instructions to authors Online submission Submit Now! Self archiving policy Open access options for authors - visit Oxford Open This journal enables compliance with the NIH Public Access Policy Alerting Services Email table of contents Email Advance Access CiteTrack XML RSS feed Corporate Services Advertising sales Reprints Supplements var taxonomies = ("MED00710"); Most Most Read Apoptosis in cancer Modulation of E-cadherin expression by K-Ras; involvement of DNA methyltransferase-3b Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead Tumor progression and metastasis Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability » View all Most Read articles Most Cited Oxyradicals and DNA damage Sensing and repairing DNA double-strand breaks Functional role of estrogen metabolism in target cells: review and perspectives Apoptosis in cancer Nucleotide excision repair and human syndromes » View all Most Cited articles Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department. Online ISSN 1460-2180 - Print ISSN 0143-3334 Copyright © 2015 Oxford University Press Oxford Journals Oxford University Press Site Map Privacy Policy Cookie Policy Legal Notices Frequently Asked Questions Other Oxford University Press sites: Oxford University Press Oxford Journals China Oxford Journals Japan Academic & Professional books Children's & Schools Books Dictionaries & Reference Dictionary of National Biography Digital Reference English Language Teaching Higher Education Textbooks International Education Unit Law Medicine Music Online Products & Publishing Oxford Bibliographies Online Oxford Dictionaries Online Oxford English Dictionary Oxford Language Dictionaries Online Oxford Scholarship Online Reference Rights and Permissions Resources for Retailers & Wholesalers Resources for the Healthcare Industry Very Short Introductions World's Classics function fnc_onDomLoaded() { var query_context = getQueryContext(); PF_initOIUnderbar(query_context,":QS:default","","JRN"); PF_insertOIUnderbar(0); }; if (window.addEventListener) { window.addEventListener('load', fnc_onDomLoaded, false); } else if (window.attachEvent) { window.attachEvent('onload', fnc_onDomLoaded); } var gaJsHost = (("https:" == document.location.protocol) ? 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Growth inhibition, cell-cycle arrest and apoptosis in human T-cell leukemia by the isothiocyanate sulforaphane

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Publisher
Oxford University Press
Copyright
Copyright © 2015 Oxford University Press
ISSN
0143-3334
eISSN
1460-2180
DOI
10.1093/carcin/23.4.581
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Abstract

Glucosinolates (GL) can inhibit, retard or reverse experimental multistage carcinogenesis. When brassica plant tissue is broken, GLs are hydrolyzed by the endogenous enzyme myrosinase (Myr), releasing many products including isothiocyanates (ITC). Synthetic ITCs like sulforaphane exert chemopreventive effects against chemically induced tumors in animals, modulating enzymes required for carcinogens' activation/detoxification and/or the induction of cell-cycle arrest and apoptosis in tumor cell lines. To investigate the chemopreventive potential of ITCs while reproducing the circumstances of dietary contact with sulforaphane, we studied proliferation, apoptosis induction and p53, bcl-2 and bax protein expression in Jurkat T-leukemia cells by sulforaphane, the ITC generated in situ in a quantitative manner by Myr starting from glucoraphanin (GRA). Jurkat cells were treated with different doses of GRA–Myr mixture. Effects on cell growth or survival were evaluated by counting trypan blue-excluding cells. Cell-cycle progression, apoptosis and expression of p53, bax and bcl-2 proteins were analyzed by flow cytometry. Results were analyzed by two-sided Fisher's exact test. Sulforaphane, but not GRA, caused G 2 /M-phase arrest ( P = 0.028) and increase of apoptotic cell fraction ( P < 0.0001) in a time- and dose-dependent manner. Necrosis was observed after prolonged exposure to elevated sulforaphane doses. Moreover, it markedly increased p53 and bax protein expression, and slightly affected bcl-2 expression. These findings indicate that sulforaphane but not the native GL GRA can exert both protective and toxic effects inhibiting leukemic cell growth. Sulforaphane therefore deserves study as a potential chemopreventive/chemotherapeutic antileukemic agent. Key words EB, ethidium bromide FITC, fluorescein isothiocyanate FSC, forward scatter GL, glucosinolate GRA, glucoraphanin GSH, Glutathione ITC, isothiocyanate Myr, myrosinase PI, propidium iodide SSC, side scatter. © Oxford University Press « Previous | Next Article » Table of Contents This Article Carcinogenesis (2002) 23 (4): 581-586. doi: 10.1093/carcin/23.4.581 » Abstract Free Full Text (HTML) Free Full Text (PDF) Free Classifications Molecular Epidemiology Services Article metrics Alert me when cited Alert me if corrected Find similar articles Similar articles in Web of Science Similar articles in PubMed Add to my archive Download citation Request Permissions Citing Articles Load citing article information Citing articles via CrossRef Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Fimognari, C. Articles by Hrelia, P. Search for related content PubMed PubMed citation Articles by Fimognari, C. Articles by Nüsse, M. Articles by Cesari, R. Articles by Iori, R. Articles by Cantelli-Forti, G. Articles by Hrelia, P. Related Content Load related web page information Share Email this article CiteULike Delicious Facebook Google+ Mendeley Twitter What's this? Search this journal: Advanced » Current Issue October 2015 36 (10) Alert me to new issues The Journal About this journal Rights & Permissions Dispatch date of the next issue This journal is a member of the Committee on Publication Ethics (COPE) We are mobile – find out more Journals Career Network Impact factor: 5.334 5-Yr impact factor: 5.698 Editor-in-Chief Dr Curtis C Harris, USA View full editorial board For Authors Instructions to authors Online submission Submit Now! Self archiving policy Open access options for authors - visit Oxford Open This journal enables compliance with the NIH Public Access Policy Alerting Services Email table of contents Email Advance Access CiteTrack XML RSS feed Corporate Services Advertising sales Reprints Supplements var taxonomies = ("MED00710"); Most Most Read Apoptosis in cancer Modulation of E-cadherin expression by K-Ras; involvement of DNA methyltransferase-3b Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead Tumor progression and metastasis Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability » View all Most Read articles Most Cited Oxyradicals and DNA damage Sensing and repairing DNA double-strand breaks Functional role of estrogen metabolism in target cells: review and perspectives Apoptosis in cancer Nucleotide excision repair and human syndromes » View all Most Cited articles Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department. Online ISSN 1460-2180 - Print ISSN 0143-3334 Copyright © 2015 Oxford University Press Oxford Journals Oxford University Press Site Map Privacy Policy Cookie Policy Legal Notices Frequently Asked Questions Other Oxford University Press sites: Oxford University Press Oxford Journals China Oxford Journals Japan Academic & Professional books Children's & Schools Books Dictionaries & Reference Dictionary of National Biography Digital Reference English Language Teaching Higher Education Textbooks International Education Unit Law Medicine Music Online Products & Publishing Oxford Bibliographies Online Oxford Dictionaries Online Oxford English Dictionary Oxford Language Dictionaries Online Oxford Scholarship Online Reference Rights and Permissions Resources for Retailers & Wholesalers Resources for the Healthcare Industry Very Short Introductions World's Classics function fnc_onDomLoaded() { var query_context = getQueryContext(); PF_initOIUnderbar(query_context,":QS:default","","JRN"); PF_insertOIUnderbar(0); }; if (window.addEventListener) { window.addEventListener('load', fnc_onDomLoaded, false); } else if (window.attachEvent) { window.attachEvent('onload', fnc_onDomLoaded); } var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); try { var pageTracker = _gat._getTracker("UA-189672-16"); pageTracker._setDomainName(".oxfordjournals.org"); pageTracker._trackPageview(); } catch(err) {}

Journal

Carcinogenesis – Oxford University Press

Published: Apr 1, 2002

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