Human colon adenocarcinoma HT-29 cell: electrochemistry and nicotine stimulation.
Identifieur interne : 000647 ( Main/Exploration ); précédent : 000646; suivant : 000648Human colon adenocarcinoma HT-29 cell: electrochemistry and nicotine stimulation.
Auteurs : RBID : pubmed:23774106English descriptors
- KwdEn :
- Adenocarcinoma (chemistry), Adenocarcinoma (pathology), Carbon (chemistry), Cell Proliferation (drug effects), Colonic Neoplasms (chemistry), Colonic Neoplasms (pathology), Electrochemistry, Electrodes, Epinephrine (pharmacology), HT29 Cells, Humans, Nicotine (pharmacology), Oxidation-Reduction (drug effects), Tin Compounds (chemistry), Tin Compounds (therapeutic use).
- MESH :
- chemical , chemistry : Carbon, Tin Compounds.
- chemistry : Adenocarcinoma, Colonic Neoplasms.
- drug effects : Cell Proliferation, Oxidation-Reduction.
- pathology : Adenocarcinoma, Colonic Neoplasms.
- chemical , pharmacology : Epinephrine, Nicotine.
- chemical , therapeutic use : Tin Compounds.
- Electrochemistry, Electrodes, HT29 Cells, Humans.
Abstract
Recently, it was demonstrated that colorectal cancer HT-29 cells can secrete epinephrine (adrenaline) in an autocrine manner to auto-stimulate cellular growth by adrenoreceptors activation, and that this secretion is enhanced by nicotine, showing an indirect relation between colorectal cancer and tobacco. The electrochemical behaviour of human colon adenocarcinoma HT-29 cells from a colorectal adenocarcinoma cell line, the hormone and neurotransmitter epinephrine, and nicotine, were investigated by cyclic voltammetry, using indium tin oxide (ITO), glassy carbon (GC) and screen printed carbon (SPC) electrodes. The oxidation of the HT-29 cells, previously grown onto ITO or SPC surfaces, followed an irreversible oxidation process that involved the formation of a main oxidation product that undergoes irreversible reduction, as in the epinephrine oxidation mechanism. The effect of nicotine stimulation of the HT-29 cells was also investigated. Nicotine, at different concentration levels 1, 2 and 15 mM, was introduced in the culture medium and an increase with incubation time, 0 to 3h and 30 min, of the HT-29 cells oxidation and reduction peaks was observed. The interaction of nicotine with the HT-29 cells stimulated the epinephrine secretion causing an increase in epinephrine release concentration, and enabling the conclusion that epinephrine and nicotine play an important role in the colorectal tumour growth.
DOI: 10.1016/j.bioelechem.2013.05.004
PubMed: 23774106
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The electrochemical behaviour of human colon adenocarcinoma HT-29 cells from a colorectal adenocarcinoma cell line, the hormone and neurotransmitter epinephrine, and nicotine, were investigated by cyclic voltammetry, using indium tin oxide (ITO), glassy carbon (GC) and screen printed carbon (SPC) electrodes. The oxidation of the HT-29 cells, previously grown onto ITO or SPC surfaces, followed an irreversible oxidation process that involved the formation of a main oxidation product that undergoes irreversible reduction, as in the epinephrine oxidation mechanism. The effect of nicotine stimulation of the HT-29 cells was also investigated. Nicotine, at different concentration levels 1, 2 and 15 mM, was introduced in the culture medium and an increase with incubation time, 0 to 3h and 30 min, of the HT-29 cells oxidation and reduction peaks was observed. The interaction of nicotine with the HT-29 cells stimulated the epinephrine secretion causing an increase in epinephrine release concentration, and enabling the conclusion that epinephrine and nicotine play an important role in the colorectal tumour growth.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23774106</PMID><DateCreated><Year>2013</Year><Month>10</Month><Day>07</Day></DateCreated><DateCompleted><Year>2014</Year><Month>05</Month><Day>06</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-562X</ISSN><JournalIssue CitedMedium="Internet"><Volume>94</Volume><PubDate><Year>2013</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Bioelectrochemistry (Amsterdam, Netherlands)</Title><ISOAbbreviation>Bioelectrochemistry</ISOAbbreviation></Journal><ArticleTitle>Human colon adenocarcinoma HT-29 cell: electrochemistry and nicotine stimulation.</ArticleTitle><Pagination><MedlinePgn>30-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bioelechem.2013.05.004</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1567-5394(13)00055-8</ELocationID><Abstract><AbstractText>Recently, it was demonstrated that colorectal cancer HT-29 cells can secrete epinephrine (adrenaline) in an autocrine manner to auto-stimulate cellular growth by adrenoreceptors activation, and that this secretion is enhanced by nicotine, showing an indirect relation between colorectal cancer and tobacco. The electrochemical behaviour of human colon adenocarcinoma HT-29 cells from a colorectal adenocarcinoma cell line, the hormone and neurotransmitter epinephrine, and nicotine, were investigated by cyclic voltammetry, using indium tin oxide (ITO), glassy carbon (GC) and screen printed carbon (SPC) electrodes. The oxidation of the HT-29 cells, previously grown onto ITO or SPC surfaces, followed an irreversible oxidation process that involved the formation of a main oxidation product that undergoes irreversible reduction, as in the epinephrine oxidation mechanism. The effect of nicotine stimulation of the HT-29 cells was also investigated. Nicotine, at different concentration levels 1, 2 and 15 mM, was introduced in the culture medium and an increase with incubation time, 0 to 3h and 30 min, of the HT-29 cells oxidation and reduction peaks was observed. The interaction of nicotine with the HT-29 cells stimulated the epinephrine secretion causing an increase in epinephrine release concentration, and enabling the conclusion that epinephrine and nicotine play an important role in the colorectal tumour growth.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Oliveira</LastName><ForeName>S C B</ForeName><Initials>SC</Initials><Affiliation>Departamento de Química, Faculdade de Ciências e Tecnologia, Universidade de Coimbra, 3004-535 Coimbra, Portugal.</Affiliation></Author><Author ValidYN="Y"><LastName>Santarino</LastName><ForeName>I B</ForeName><Initials>IB</Initials></Author><Author ValidYN="Y"><LastName>Enache</LastName><ForeName>T A</ForeName><Initials>TA</Initials></Author><Author ValidYN="Y"><LastName>Nunes</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Laranjinha</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Barbosa</LastName><ForeName>R M</ForeName><Initials>RM</Initials></Author><Author ValidYN="Y"><LastName>Oliveira-Brett</LastName><ForeName>A M</ForeName><Initials>AM</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType>Journal Article</PublicationType><PublicationType>Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>05</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Bioelectrochemistry</MedlineTA><NlmUniqueID>100953583</NlmUniqueID><ISSNLinking>1567-5394</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance>Tin Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>54-11-5</RegistryNumber><NameOfSubstance>Nicotine</NameOfSubstance></Chemical><Chemical><RegistryNumber>71243-84-0</RegistryNumber><NameOfSubstance>indium tin oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>7440-44-0</RegistryNumber><NameOfSubstance>Carbon</NameOfSubstance></Chemical><Chemical><RegistryNumber>YKH834O4BH</RegistryNumber><NameOfSubstance>Epinephrine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N">Adenocarcinoma</DescriptorName><QualifierName MajorTopicYN="Y">chemistry</QualifierName><QualifierName MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Carbon</DescriptorName><QualifierName MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Colonic Neoplasms</DescriptorName><QualifierName MajorTopicYN="Y">chemistry</QualifierName><QualifierName MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Electrochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Electrodes</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Epinephrine</DescriptorName><QualifierName MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">HT29 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Nicotine</DescriptorName><QualifierName MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Oxidation-Reduction</DescriptorName><QualifierName MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Tin Compounds</DescriptorName><QualifierName MajorTopicYN="N">chemistry</QualifierName><QualifierName MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Carbon electrodes</Keyword><Keyword MajorTopicYN="N">Colon cancer HT-29 cells</Keyword><Keyword MajorTopicYN="N">Epinephrine</Keyword><Keyword MajorTopicYN="N">ITO electrodes</Keyword><Keyword MajorTopicYN="N">Nicotine</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>3</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>5</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>5</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2013</Year><Month>5</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>6</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>6</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>5</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23774106</ArticleId><ArticleId IdType="pii">S1567-5394(13)00055-8</ArticleId><ArticleId IdType="doi">10.1016/j.bioelechem.2013.05.004</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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