Loading…

Homocysteine is a potent modulator of plasma membrane electron transport systems

The deregulation of homocysteine metabolism leads to hyperhomocysteinemia, a condition described as an independent cardiovascular disease risk factor. Ubiquitous plasma membrane redox systems can play a dual pro-oxidant and anti-oxidant role in defense. In this study, we test the hypothesis that hom...

Full description

Saved in:
Bibliographic Details
Published in:Journal of bioenergetics and biomembranes 2008-02, Vol.40 (1), p.45-51
Main Authors: Rodríguez-Alonso, Javier, Montañez, Raúl, Rodríguez-Caso, Luis, Medina, Miguel Ángel
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203
cites cdi_FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203
container_end_page 51
container_issue 1
container_start_page 45
container_title Journal of bioenergetics and biomembranes
container_volume 40
creator Rodríguez-Alonso, Javier
Montañez, Raúl
Rodríguez-Caso, Luis
Medina, Miguel Ángel
description The deregulation of homocysteine metabolism leads to hyperhomocysteinemia, a condition described as an independent cardiovascular disease risk factor. Ubiquitous plasma membrane redox systems can play a dual pro-oxidant and anti-oxidant role in defense. In this study, we test the hypothesis that homocysteine, as a redox active compound, could modulate the endothelial plasma membrane redox system. We show that homocysteine behaves as a very potent stimulator of this activity. Furthermore, we show that this inducing effect is also produced on tumor cells and that it can be observed at both the activity and protein levels. On the other hand, homocysteine treatment decreases the activity of the specific ectocellular tumor NADH oxidase. Taken together, these results underscore a potential antitumoral action of homocysteine.
doi_str_mv 10.1007/s10863-008-9127-0
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70270556</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1897189541</sourcerecordid><originalsourceid>FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203</originalsourceid><addsrcrecordid>eNp1kE1r3DAQhkVpaLZpf0AvRfSQm9MZWV8-hpCPQiA9JNCb0NrjssGyHEk-5N9Hyy4ECj2JQc-88_Iw9g3hAgHMz4xgddsA2KZDYRr4wDaoTNtoa_Ej2wBK1UjT_Tlln3N-hgqCgk_sFK1AqZXasN93McT-NRfazcR3mXu-xEJz4SEO6-RLTDyOfJl8Dp4HCtvkK0gT9SXFmZc65iWmwvM-JOQv7GT0U6avx_eMPd1cP17dNfcPt7-uLu-bvtVdaTqL6EVvPQoU1ui-Ra07YyWMsB009YMWtO2kF8q3XtqRjByIFKDq6iK0Z-z8kLuk-LJSLi7sck_TVOvFNTsDwoBSuoI__gGf45rm2s3V09jK1soK4QHqU8w50eiWtAs-vToEt3ftDq5dVej2rt2-wfdj8LoNNLxvHOVWQByAXL_mv5TeL_8_9Q3424lh</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>212134384</pqid></control><display><type>article</type><title>Homocysteine is a potent modulator of plasma membrane electron transport systems</title><source>Springer Nature</source><creator>Rodríguez-Alonso, Javier ; Montañez, Raúl ; Rodríguez-Caso, Luis ; Medina, Miguel Ángel</creator><creatorcontrib>Rodríguez-Alonso, Javier ; Montañez, Raúl ; Rodríguez-Caso, Luis ; Medina, Miguel Ángel</creatorcontrib><description>The deregulation of homocysteine metabolism leads to hyperhomocysteinemia, a condition described as an independent cardiovascular disease risk factor. Ubiquitous plasma membrane redox systems can play a dual pro-oxidant and anti-oxidant role in defense. In this study, we test the hypothesis that homocysteine, as a redox active compound, could modulate the endothelial plasma membrane redox system. We show that homocysteine behaves as a very potent stimulator of this activity. Furthermore, we show that this inducing effect is also produced on tumor cells and that it can be observed at both the activity and protein levels. On the other hand, homocysteine treatment decreases the activity of the specific ectocellular tumor NADH oxidase. Taken together, these results underscore a potential antitumoral action of homocysteine.</description><identifier>ISSN: 0145-479X</identifier><identifier>EISSN: 1573-6881</identifier><identifier>DOI: 10.1007/s10863-008-9127-0</identifier><identifier>PMID: 18214655</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Animals ; Antineoplastic Agents - pharmacology ; Biochemistry ; Bioenergetics ; Bioorganic Chemistry ; Cancer ; Cardiovascular diseases ; Cardiovascular Diseases - etiology ; Cardiovascular Diseases - metabolism ; Cardiovascular Diseases - pathology ; Cattle ; Cell Line, Tumor ; Cell Membrane - metabolism ; Cell Membrane - pathology ; Chemistry ; Chemistry and Materials Science ; Deregulation ; Electron Transport - drug effects ; Electrons ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Enzymes ; Health risks ; Histology ; Homocysteine ; Homocysteine - pharmacology ; Humans ; Hyperhomocysteinemia - complications ; Hyperhomocysteinemia - metabolism ; Hyperhomocysteinemia - pathology ; Membranes ; Morphology ; NADPH Oxidases - metabolism ; Neoplasm Proteins - metabolism ; Neoplasms - drug therapy ; Neoplasms - enzymology ; Organic Chemistry ; Oxidation-Reduction - drug effects ; Oxidizing agents ; Plasma ; Risk Factors</subject><ispartof>Journal of bioenergetics and biomembranes, 2008-02, Vol.40 (1), p.45-51</ispartof><rights>Springer Science+Business Media, LLC 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203</citedby><cites>FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18214655$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rodríguez-Alonso, Javier</creatorcontrib><creatorcontrib>Montañez, Raúl</creatorcontrib><creatorcontrib>Rodríguez-Caso, Luis</creatorcontrib><creatorcontrib>Medina, Miguel Ángel</creatorcontrib><title>Homocysteine is a potent modulator of plasma membrane electron transport systems</title><title>Journal of bioenergetics and biomembranes</title><addtitle>J Bioenerg Biomembr</addtitle><addtitle>J Bioenerg Biomembr</addtitle><description>The deregulation of homocysteine metabolism leads to hyperhomocysteinemia, a condition described as an independent cardiovascular disease risk factor. Ubiquitous plasma membrane redox systems can play a dual pro-oxidant and anti-oxidant role in defense. In this study, we test the hypothesis that homocysteine, as a redox active compound, could modulate the endothelial plasma membrane redox system. We show that homocysteine behaves as a very potent stimulator of this activity. Furthermore, we show that this inducing effect is also produced on tumor cells and that it can be observed at both the activity and protein levels. On the other hand, homocysteine treatment decreases the activity of the specific ectocellular tumor NADH oxidase. Taken together, these results underscore a potential antitumoral action of homocysteine.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biochemistry</subject><subject>Bioenergetics</subject><subject>Bioorganic Chemistry</subject><subject>Cancer</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular Diseases - etiology</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cardiovascular Diseases - pathology</subject><subject>Cattle</subject><subject>Cell Line, Tumor</subject><subject>Cell Membrane - metabolism</subject><subject>Cell Membrane - pathology</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Deregulation</subject><subject>Electron Transport - drug effects</subject><subject>Electrons</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Enzymes</subject><subject>Health risks</subject><subject>Histology</subject><subject>Homocysteine</subject><subject>Homocysteine - pharmacology</subject><subject>Humans</subject><subject>Hyperhomocysteinemia - complications</subject><subject>Hyperhomocysteinemia - metabolism</subject><subject>Hyperhomocysteinemia - pathology</subject><subject>Membranes</subject><subject>Morphology</subject><subject>NADPH Oxidases - metabolism</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - enzymology</subject><subject>Organic Chemistry</subject><subject>Oxidation-Reduction - drug effects</subject><subject>Oxidizing agents</subject><subject>Plasma</subject><subject>Risk Factors</subject><issn>0145-479X</issn><issn>1573-6881</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNp1kE1r3DAQhkVpaLZpf0AvRfSQm9MZWV8-hpCPQiA9JNCb0NrjssGyHEk-5N9Hyy4ECj2JQc-88_Iw9g3hAgHMz4xgddsA2KZDYRr4wDaoTNtoa_Ej2wBK1UjT_Tlln3N-hgqCgk_sFK1AqZXasN93McT-NRfazcR3mXu-xEJz4SEO6-RLTDyOfJl8Dp4HCtvkK0gT9SXFmZc65iWmwvM-JOQv7GT0U6avx_eMPd1cP17dNfcPt7-uLu-bvtVdaTqL6EVvPQoU1ui-Ra07YyWMsB009YMWtO2kF8q3XtqRjByIFKDq6iK0Z-z8kLuk-LJSLi7sck_TVOvFNTsDwoBSuoI__gGf45rm2s3V09jK1soK4QHqU8w50eiWtAs-vToEt3ftDq5dVej2rt2-wfdj8LoNNLxvHOVWQByAXL_mv5TeL_8_9Q3424lh</recordid><startdate>20080201</startdate><enddate>20080201</enddate><creator>Rodríguez-Alonso, Javier</creator><creator>Montañez, Raúl</creator><creator>Rodríguez-Caso, Luis</creator><creator>Medina, Miguel Ángel</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20080201</creationdate><title>Homocysteine is a potent modulator of plasma membrane electron transport systems</title><author>Rodríguez-Alonso, Javier ; Montañez, Raúl ; Rodríguez-Caso, Luis ; Medina, Miguel Ángel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biochemistry</topic><topic>Bioenergetics</topic><topic>Bioorganic Chemistry</topic><topic>Cancer</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular Diseases - etiology</topic><topic>Cardiovascular Diseases - metabolism</topic><topic>Cardiovascular Diseases - pathology</topic><topic>Cattle</topic><topic>Cell Line, Tumor</topic><topic>Cell Membrane - metabolism</topic><topic>Cell Membrane - pathology</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Deregulation</topic><topic>Electron Transport - drug effects</topic><topic>Electrons</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Enzymes</topic><topic>Health risks</topic><topic>Histology</topic><topic>Homocysteine</topic><topic>Homocysteine - pharmacology</topic><topic>Humans</topic><topic>Hyperhomocysteinemia - complications</topic><topic>Hyperhomocysteinemia - metabolism</topic><topic>Hyperhomocysteinemia - pathology</topic><topic>Membranes</topic><topic>Morphology</topic><topic>NADPH Oxidases - metabolism</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - enzymology</topic><topic>Organic Chemistry</topic><topic>Oxidation-Reduction - drug effects</topic><topic>Oxidizing agents</topic><topic>Plasma</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rodríguez-Alonso, Javier</creatorcontrib><creatorcontrib>Montañez, Raúl</creatorcontrib><creatorcontrib>Rodríguez-Caso, Luis</creatorcontrib><creatorcontrib>Medina, Miguel Ángel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest_Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science &amp; Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Materials science collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bioenergetics and biomembranes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rodríguez-Alonso, Javier</au><au>Montañez, Raúl</au><au>Rodríguez-Caso, Luis</au><au>Medina, Miguel Ángel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Homocysteine is a potent modulator of plasma membrane electron transport systems</atitle><jtitle>Journal of bioenergetics and biomembranes</jtitle><stitle>J Bioenerg Biomembr</stitle><addtitle>J Bioenerg Biomembr</addtitle><date>2008-02-01</date><risdate>2008</risdate><volume>40</volume><issue>1</issue><spage>45</spage><epage>51</epage><pages>45-51</pages><issn>0145-479X</issn><eissn>1573-6881</eissn><abstract>The deregulation of homocysteine metabolism leads to hyperhomocysteinemia, a condition described as an independent cardiovascular disease risk factor. Ubiquitous plasma membrane redox systems can play a dual pro-oxidant and anti-oxidant role in defense. In this study, we test the hypothesis that homocysteine, as a redox active compound, could modulate the endothelial plasma membrane redox system. We show that homocysteine behaves as a very potent stimulator of this activity. Furthermore, we show that this inducing effect is also produced on tumor cells and that it can be observed at both the activity and protein levels. On the other hand, homocysteine treatment decreases the activity of the specific ectocellular tumor NADH oxidase. Taken together, these results underscore a potential antitumoral action of homocysteine.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>18214655</pmid><doi>10.1007/s10863-008-9127-0</doi><tpages>7</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0145-479X
ispartof Journal of bioenergetics and biomembranes, 2008-02, Vol.40 (1), p.45-51
issn 0145-479X
1573-6881
language eng
recordid cdi_proquest_miscellaneous_70270556
source Springer Nature
subjects Animal Anatomy
Animal Biochemistry
Animals
Antineoplastic Agents - pharmacology
Biochemistry
Bioenergetics
Bioorganic Chemistry
Cancer
Cardiovascular diseases
Cardiovascular Diseases - etiology
Cardiovascular Diseases - metabolism
Cardiovascular Diseases - pathology
Cattle
Cell Line, Tumor
Cell Membrane - metabolism
Cell Membrane - pathology
Chemistry
Chemistry and Materials Science
Deregulation
Electron Transport - drug effects
Electrons
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Enzymes
Health risks
Histology
Homocysteine
Homocysteine - pharmacology
Humans
Hyperhomocysteinemia - complications
Hyperhomocysteinemia - metabolism
Hyperhomocysteinemia - pathology
Membranes
Morphology
NADPH Oxidases - metabolism
Neoplasm Proteins - metabolism
Neoplasms - drug therapy
Neoplasms - enzymology
Organic Chemistry
Oxidation-Reduction - drug effects
Oxidizing agents
Plasma
Risk Factors
title Homocysteine is a potent modulator of plasma membrane electron transport systems
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T08%3A18%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Homocysteine%20is%20a%20potent%20modulator%20of%20plasma%20membrane%20electron%20transport%20systems&rft.jtitle=Journal%20of%20bioenergetics%20and%20biomembranes&rft.au=Rodr%C3%ADguez-Alonso,%20Javier&rft.date=2008-02-01&rft.volume=40&rft.issue=1&rft.spage=45&rft.epage=51&rft.pages=45-51&rft.issn=0145-479X&rft.eissn=1573-6881&rft_id=info:doi/10.1007/s10863-008-9127-0&rft_dat=%3Cproquest_cross%3E1897189541%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c369t-9811a2c8a1212876c316697840f0bd6ecd62eb94a25a3a48fe74dee501591a203%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=212134384&rft_id=info:pmid/18214655&rfr_iscdi=true