[Redox-dependent mechanisms of regulation of breast epithelial cell proliferation].
Identifieur interne : 000297 ( Main/Exploration ); précédent : 000296; suivant : 000298[Redox-dependent mechanisms of regulation of breast epithelial cell proliferation].
Auteurs : E A Stepovaya [Russie] ; E V Shakhristova [Russie] ; O L Nosareva [Russie] ; E V Rudikov [Russie] ; M Y Egorova [Russie] ; D Y Egorova [Russie] ; V V Novitsky [Russie]Source :
- Biomeditsinskaia khimiia [ 2310-6972 ] ; 2017.
Descripteurs français
- KwdFr :
- Agents protecteurs (pharmacologie), Antienzymes (pharmacologie), Catalase (métabolisme), Cellules épithéliales (cytologie), Cellules épithéliales (effets des médicaments et des substances chimiques), Cellules épithéliales (métabolisme), Cycle cellulaire (effets des médicaments et des substances chimiques), Cytométrie en flux (MeSH), Dithioérythritol (pharmacologie), Glandes mammaires humaines (cytologie), Glandes mammaires humaines (effets des médicaments et des substances chimiques), Glandes mammaires humaines (métabolisme), Glutarédoxines (métabolisme), Glutathion (métabolisme), Glutathione peroxidase (métabolisme), Glutathione reductase (métabolisme), Humains (MeSH), Lignée cellulaire (MeSH), N-Éthyl-maléimide (antagonistes et inhibiteurs), N-Éthyl-maléimide (pharmacologie), Oxydoréduction (MeSH), Prolifération cellulaire (effets des médicaments et des substances chimiques), Stress oxydatif (effets des médicaments et des substances chimiques), Thioredoxin-disulfide reductase (métabolisme), Thiorédoxines (métabolisme).
- MESH :
- antagonistes et inhibiteurs : N-Éthyl-maléimide.
- cytologie : Cellules épithéliales, Glandes mammaires humaines.
- effets des médicaments et des substances chimiques : Cellules épithéliales, Cycle cellulaire, Glandes mammaires humaines, Prolifération cellulaire, Stress oxydatif.
- métabolisme : Catalase, Cellules épithéliales, Glandes mammaires humaines, Glutarédoxines, Glutathion, Glutathione peroxidase, Glutathione reductase, Thioredoxin-disulfide reductase, Thiorédoxines.
- pharmacologie : Agents protecteurs, Antienzymes, Dithioérythritol, N-Éthyl-maléimide.
- Cytométrie en flux, Humains, Lignée cellulaire, Oxydoréduction.
English descriptors
- KwdEn :
- Catalase (metabolism), Cell Cycle (drug effects), Cell Line (MeSH), Cell Proliferation (drug effects), Dithioerythritol (pharmacology), Enzyme Inhibitors (pharmacology), Epithelial Cells (cytology), Epithelial Cells (drug effects), Epithelial Cells (metabolism), Ethylmaleimide (antagonists & inhibitors), Ethylmaleimide (pharmacology), Flow Cytometry (MeSH), Glutaredoxins (metabolism), Glutathione (metabolism), Glutathione Peroxidase (metabolism), Glutathione Reductase (metabolism), Humans (MeSH), Mammary Glands, Human (cytology), Mammary Glands, Human (drug effects), Mammary Glands, Human (metabolism), Oxidation-Reduction (MeSH), Oxidative Stress (drug effects), Protective Agents (pharmacology), Thioredoxin-Disulfide Reductase (metabolism), Thioredoxins (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Ethylmaleimide.
- chemical , metabolism : Catalase, Glutaredoxins, Glutathione, Glutathione Peroxidase, Glutathione Reductase, Thioredoxin-Disulfide Reductase, Thioredoxins.
- cytology : Epithelial Cells, Mammary Glands, Human.
- drug effects : Cell Cycle, Cell Proliferation, Epithelial Cells, Mammary Glands, Human, Oxidative Stress.
- metabolism : Epithelial Cells, Mammary Glands, Human.
- chemical , pharmacology : Dithioerythritol, Enzyme Inhibitors, Ethylmaleimide, Protective Agents.
- Cell Line, Flow Cytometry, Humans, Oxidation-Reduction.
Abstract
Activation of free radical oxidation in different cell types, including breast epithelial cells, may result in damage to macromolecules, in particular, proteins taking part in regulation of cell proliferation and apoptosis. The glutathione, glutaredoxin and thioredoxin systems play an essential role in maintaining intracellular redox homeostasis. Due to this fact, modulation of cellular redox status under the effect of an SH group inhibitor and an SH group protector may be used as a model for studying the role of redox proteins and glutathione in regulating cell proliferation in different pathological processes. In this study we have evaluated the state of the thioredoxin, glutaredoxin and glutathione systems as well as their role in regulating proliferation of HBL-100 breast epithelial cells under redox status modulation with N-ethylmaleimide (NEM) and 1,4-dithioerythriol (DTE). Modulating the redox status of breast epithelial cells under the effect of NEM and DTE influences the functional activity of glutathione-dependent enzymes, glutaredoxin, thioredoxin, and thioredoxin reductase through changes in the GSH and GSSG concentrations. In HBL-100 cells under redox-status modulation, we have found an increase in the number of cells in the S-phase of the cell cycle and a decrease in the number of cells in the G0/G1 and G2/М phases, as opposed to the values in the intact culture. The proposed model of proliferative activity of cells under redox status modulation may be used for development of new therapeutic approaches for treatment of diseases accompanied by oxidative stress generation.
DOI: 10.18097/PBMC20176302159
PubMed: 28414288
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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last="Stepovaya">E A Stepovaya</name><affiliation wicri:level="1"><nlm:affiliation>Siberian State Medical University, Tomsk, Russia.</nlm:affiliation><country xml:lang="fr">Russie</country><wicri:regionArea>Siberian State Medical University, Tomsk</wicri:regionArea><wicri:noRegion>Tomsk</wicri:noRegion></affiliation></author><author><name sortKey="Shakhristova, E V" sort="Shakhristova, E V" uniqKey="Shakhristova E" first="E V" last="Shakhristova">E V Shakhristova</name><affiliation wicri:level="1"><nlm:affiliation>Siberian State Medical University, Tomsk, Russia.</nlm:affiliation><country xml:lang="fr">Russie</country><wicri:regionArea>Siberian State Medical University, Tomsk</wicri:regionArea><wicri:noRegion>Tomsk</wicri:noRegion></affiliation></author><author><name sortKey="Nosareva, O L" sort="Nosareva, O L" uniqKey="Nosareva O" first="O L" last="Nosareva">O L Nosareva</name><affiliation wicri:level="1"><nlm:affiliation>Siberian State Medical University, Tomsk, 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type="ISSN">2310-6972</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Catalase (metabolism)</term><term>Cell Cycle (drug effects)</term><term>Cell Line (MeSH)</term><term>Cell Proliferation (drug effects)</term><term>Dithioerythritol (pharmacology)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Epithelial Cells (cytology)</term><term>Epithelial Cells (drug effects)</term><term>Epithelial Cells (metabolism)</term><term>Ethylmaleimide (antagonists & inhibitors)</term><term>Ethylmaleimide (pharmacology)</term><term>Flow Cytometry (MeSH)</term><term>Glutaredoxins (metabolism)</term><term>Glutathione (metabolism)</term><term>Glutathione Peroxidase (metabolism)</term><term>Glutathione Reductase (metabolism)</term><term>Humans (MeSH)</term><term>Mammary Glands, Human (cytology)</term><term>Mammary Glands, Human (drug effects)</term><term>Mammary Glands, Human (metabolism)</term><term>Oxidation-Reduction (MeSH)</term><term>Oxidative Stress (drug effects)</term><term>Protective Agents (pharmacology)</term><term>Thioredoxin-Disulfide Reductase (metabolism)</term><term>Thioredoxins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Agents protecteurs (pharmacologie)</term><term>Antienzymes (pharmacologie)</term><term>Catalase (métabolisme)</term><term>Cellules épithéliales (cytologie)</term><term>Cellules épithéliales (effets des médicaments et des substances chimiques)</term><term>Cellules épithéliales (métabolisme)</term><term>Cycle cellulaire (effets des médicaments et des substances chimiques)</term><term>Cytométrie en flux (MeSH)</term><term>Dithioérythritol (pharmacologie)</term><term>Glandes mammaires humaines (cytologie)</term><term>Glandes mammaires humaines (effets des médicaments et des substances chimiques)</term><term>Glandes mammaires humaines (métabolisme)</term><term>Glutarédoxines (métabolisme)</term><term>Glutathion (métabolisme)</term><term>Glutathione peroxidase (métabolisme)</term><term>Glutathione reductase (métabolisme)</term><term>Humains (MeSH)</term><term>Lignée cellulaire (MeSH)</term><term>N-Éthyl-maléimide (antagonistes et inhibiteurs)</term><term>N-Éthyl-maléimide (pharmacologie)</term><term>Oxydoréduction (MeSH)</term><term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Thioredoxin-disulfide reductase (métabolisme)</term><term>Thiorédoxines (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Ethylmaleimide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catalase</term><term>Glutaredoxins</term><term>Glutathione</term><term>Glutathione Peroxidase</term><term>Glutathione Reductase</term><term>Thioredoxin-Disulfide Reductase</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>N-Éthyl-maléimide</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Glandes mammaires humaines</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Epithelial Cells</term><term>Mammary Glands, Human</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Cycle</term><term>Cell Proliferation</term><term>Epithelial Cells</term><term>Mammary Glands, Human</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cellules épithéliales</term><term>Cycle cellulaire</term><term>Glandes mammaires humaines</term><term>Prolifération cellulaire</term><term>Stress oxydatif</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Mammary Glands, Human</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Catalase</term><term>Cellules épithéliales</term><term>Glandes mammaires humaines</term><term>Glutarédoxines</term><term>Glutathion</term><term>Glutathione peroxidase</term><term>Glutathione reductase</term><term>Thioredoxin-disulfide reductase</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agents protecteurs</term><term>Antienzymes</term><term>Dithioérythritol</term><term>N-Éthyl-maléimide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dithioerythritol</term><term>Enzyme Inhibitors</term><term>Ethylmaleimide</term><term>Protective Agents</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Flow Cytometry</term><term>Humans</term><term>Oxidation-Reduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cytométrie en flux</term><term>Humains</term><term>Lignée cellulaire</term><term>Oxydoréduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Activation of free radical oxidation in different cell types, including breast epithelial cells, may result in damage to macromolecules, in particular, proteins taking part in regulation of cell proliferation and apoptosis. The glutathione, glutaredoxin and thioredoxin systems play an essential role in maintaining intracellular redox homeostasis. Due to this fact, modulation of cellular redox status under the effect of an SH group inhibitor and an SH group protector may be used as a model for studying the role of redox proteins and glutathione in regulating cell proliferation in different pathological processes. In this study we have evaluated the state of the thioredoxin, glutaredoxin and glutathione systems as well as their role in regulating proliferation of HBL-100 breast epithelial cells under redox status modulation with N-ethylmaleimide (NEM) and 1,4-dithioerythriol (DTE). Modulating the redox status of breast epithelial cells under the effect of NEM and DTE influences the functional activity of glutathione-dependent enzymes, glutaredoxin, thioredoxin, and thioredoxin reductase through changes in the GSH and GSSG concentrations. In HBL-100 cells under redox-status modulation, we have found an increase in the number of cells in the S-phase of the cell cycle and a decrease in the number of cells in the G0/G1 and G2/М phases, as opposed to the values in the intact culture. The proposed model of proliferative activity of cells under redox status modulation may be used for development of new therapeutic approaches for treatment of diseases accompanied by oxidative stress generation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28414288</PMID><DateCompleted><Year>2017</Year><Month>09</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>10</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">2310-6972</ISSN><JournalIssue CitedMedium="Print"><Volume>63</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Biomeditsinskaia khimiia</Title><ISOAbbreviation>Biomed Khim</ISOAbbreviation></Journal><ArticleTitle>[Redox-dependent mechanisms of regulation of breast epithelial cell proliferation].</ArticleTitle><Pagination><MedlinePgn>159-164</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.18097/PBMC20176302159</ELocationID><Abstract><AbstractText>Activation of free radical oxidation in different cell types, including breast epithelial cells, may result in damage to macromolecules, in particular, proteins taking part in regulation of cell proliferation and apoptosis. The glutathione, glutaredoxin and thioredoxin systems play an essential role in maintaining intracellular redox homeostasis. Due to this fact, modulation of cellular redox status under the effect of an SH group inhibitor and an SH group protector may be used as a model for studying the role of redox proteins and glutathione in regulating cell proliferation in different pathological processes. In this study we have evaluated the state of the thioredoxin, glutaredoxin and glutathione systems as well as their role in regulating proliferation of HBL-100 breast epithelial cells under redox status modulation with N-ethylmaleimide (NEM) and 1,4-dithioerythriol (DTE). Modulating the redox status of breast epithelial cells under the effect of NEM and DTE influences the functional activity of glutathione-dependent enzymes, glutaredoxin, thioredoxin, and thioredoxin reductase through changes in the GSH and GSSG concentrations. In HBL-100 cells under redox-status modulation, we have found an increase in the number of cells in the S-phase of the cell cycle and a decrease in the number of cells in the G0/G1 and G2/М phases, as opposed to the values in the intact culture. The proposed model of proliferative activity of cells under redox status modulation may be used for development of new therapeutic approaches for treatment of diseases accompanied by oxidative stress generation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Stepovaya</LastName><ForeName>E A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shakhristova</LastName><ForeName>E V</ForeName><Initials>EV</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nosareva</LastName><ForeName>O L</ForeName><Initials>OL</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rudikov</LastName><ForeName>E V</ForeName><Initials>EV</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Egorova</LastName><ForeName>M Y</ForeName><Initials>MY</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Egorova</LastName><ForeName>D Y</ForeName><Initials>DY</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Novitsky</LastName><ForeName>V V</ForeName><Initials>VV</Initials><AffiliationInfo><Affiliation>Siberian State Medical University, Tomsk, Russia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>rus</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Redoks-zavisimye mekhanizmy reguliatsii proliferatsii kletok épiteliia molochnoĭ zhelezy.</VernacularTitle></Article><MedlineJournalInfo><Country>Russia (Federation)</Country><MedlineTA>Biomed Khim</MedlineTA><NlmUniqueID>101196966</NlmUniqueID><ISSNLinking>2310-6905</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516005">GLRX protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020011">Protective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491203">TXN protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>52500-60-4</RegistryNumber><NameOfSubstance UI="D013879">Thioredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>6892-68-8</RegistryNumber><NameOfSubstance UI="D004226">Dithioerythritol</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.9</RegistryNumber><NameOfSubstance UI="D005979">Glutathione Peroxidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.1.7</RegistryNumber><NameOfSubstance UI="D005980">Glutathione Reductase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.8.1.9</RegistryNumber><NameOfSubstance UI="D013880">Thioredoxin-Disulfide Reductase</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>O3C74ACM9V</RegistryNumber><NameOfSubstance UI="D005033">Ethylmaleimide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002453" MajorTopicYN="N">Cell Cycle</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004226" MajorTopicYN="N">Dithioerythritol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005033" MajorTopicYN="N">Ethylmaleimide</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005979" MajorTopicYN="N">Glutathione Peroxidase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005980" MajorTopicYN="N">Glutathione Reductase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042361" MajorTopicYN="N">Mammary Glands, Human</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020011" MajorTopicYN="N">Protective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013880" MajorTopicYN="N">Thioredoxin-Disulfide Reductase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="rus"><AbstractText>Aktivatsiia svobodnoradikal'nogo okisleniia v razlichnykh tipakh kletok, v tom chisle kletkakh épiteliia molochnoĭ zhelezy, sposobna privodit' k povrezhdeniiu makromolekul, v chastnosti belkov, uchastvuiushchikh v reguliatsii proliferatsii i programmirovannoĭ kletochnoĭ gibeli. V podderzhanii vnutrikletochnogo redoks-gomeostaza vazhnuiu rol' igraiut sistemy glutationa, tioredoksina i glutaredoksina. V sviazi s étim moduliatsiia redoks-statusa kletok pri deĭstvii blokatora i protektora SH-grupp belkov mozhet byt' ispol'zovana v kachestve modeli dlia izucheniia roli redoks-belkov i glutationa v reguliatsii proliferatsii kletok pri razvitii razlichnykh patologicheskikh protsessov. V dannoĭ rabote issledovali sostoianie sistem tioredoksina, glutaredoksina, glutationa i ikh rol' v reguliatsii proliferatsii kletok épiteliia molochnoĭ zhelezy linii HBL-100 pri moduliatsii redoks-statusa s pomoshch'iu N-étilmaleimida i 1,4-ditioéritritola. Moduliatsiia redoks-statusa kletok épiteliia molochnoĭ zhelezy pri deĭstvii blokatora (N-étilmaleimida) i protektora (1,4-ditioéritritola) tiolovykh grupp belkov i peptidov, sposobstvuet izmeneniiu funktsional'noĭ aktivnosti glutationzavisimykh fermentov, glutaredoksina, tioredoksina i tioredoksinreduktazy posredstvom izmeneniia kontsentratsii GSH i GSSG. V kletkakh linii HBL-100 pri moduliatsii redoks-statusa obnaruzheno uvelichenie kolichestva kletok v S faze kletochnogo tsikla i snizhenie – v G0/G1 i G2/M fazakh po sravneniiu so znacheniiami pokazateleĭ v intaktnoĭ kul'ture. Predlozhennyĭ sposob otsenki proliferativnoĭ aktivnosti kletok pri moduliatsii ikh redoks-sostoianiia mozhet byt' ispol'zovan pri razrabotke novykh terapevticheskikh podkhodov dlia lecheniia zabolevaniĭ, soprovozhdaiushchikhsia razvitiem okislitel'nogo stressa.</AbstractText></OtherAbstract><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">breast epithelial cells</Keyword><Keyword MajorTopicYN="N">glutaredoxin</Keyword><Keyword MajorTopicYN="N">glutathione</Keyword><Keyword MajorTopicYN="N">oxidative stress</Keyword><Keyword MajorTopicYN="N">proliferation</Keyword><Keyword MajorTopicYN="N">thioredoxin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>4</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>4</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>9</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28414288</ArticleId><ArticleId IdType="doi">10.18097/PBMC20176302159</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Russie</li></country></list><tree><country name="Russie"><noRegion><name sortKey="Stepovaya, E A" sort="Stepovaya, E A" uniqKey="Stepovaya E" first="E A" last="Stepovaya">E A Stepovaya</name></noRegion><name sortKey="Egorova, D Y" sort="Egorova, D Y" uniqKey="Egorova D" first="D Y" last="Egorova">D Y Egorova</name><name sortKey="Egorova, M Y" sort="Egorova, M Y" uniqKey="Egorova M" first="M Y" last="Egorova">M Y Egorova</name><name sortKey="Nosareva, O L" sort="Nosareva, O L" uniqKey="Nosareva O" first="O L" last="Nosareva">O L Nosareva</name><name sortKey="Novitsky, V V" sort="Novitsky, V V" uniqKey="Novitsky V" first="V V" last="Novitsky">V V Novitsky</name><name sortKey="Rudikov, E V" sort="Rudikov, E V" uniqKey="Rudikov E" first="E V" last="Rudikov">E V Rudikov</name><name sortKey="Shakhristova, E V" sort="Shakhristova, E V" uniqKey="Shakhristova E" first="E V" last="Shakhristova">E V Shakhristova</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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