Plasmodium falciparum activates endogenous Cl super(-) channels of human erythrocytes by membrane oxidation

Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection-induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole-cell patch-clamp and h...

Full description

Saved in:
Bibliographic Details
Published in:The EMBO journal 2002-01, Vol.21 (1-2), p.22-30
Main Authors: Huber, S M, Uhlemann, A, Gamper, N L, Duranton, C, Kremsner, P G, Lang, F
Format: Article
Language:English
Subjects:
Plasmodium falciparum
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 30
container_issue 1-2
container_start_page 22
container_title The EMBO journal
container_volume 21
creator Huber, S M
Uhlemann, A
Gamper, N L
Duranton, C
Kremsner, P G
Lang, F
description Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection-induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole-cell patch-clamp and hemolysis experiments were performed to define properties of the NPP. Parasitized but not control erythrocytes constitutively expressed two types of anion conductances, differing in voltage dependence and sensitivity to inhibitors. In addition, infected but not control cells hemolyzed in isosmotic sorbitol solution. Both conduct ances and hemolysis of infected cells were inhibited by reducing agents. Conversely, oxidation induced identical conductances and hemolysis in non-infected erythrocytes. In conclusion, P.falciparum activates endogenous erythrocyte channels by applying oxidative stress to the host cell membrane.
doi_str_mv 10.1093/emboj/21.1.22
format article
fullrecord <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_miscellaneous_754896209</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>754896209</sourcerecordid><originalsourceid>FETCH-LOGICAL-p639-8982cb53cde43cdfd902bf471f8dc5f4969b5b5b0bb6f8dccd6cb2c3c903d8c3</originalsourceid><addsrcrecordid>eNp9UE1PwzAMzQEkxuDIPSc-Dt3y0abJEU18SZNAgvuUOCntaJPStIj-ezLBGVl6tiz7vWcjdEHJihLF164zYb9mdEVXjB2hBWGCZjmV6gSdxrgnhBSypAv08dLq2AXbTB2udAtNr4dUahibLz26iJ234d35MEW8aXGcejdcZzcYau29ayMOFa6nTnvshnmshwDzYcvMuEsWBu0dDt-N1WMT_Bk6ThLRnf_lJXq9v3vbPGbb54enze026wVXmVSSgSk4WJcnqKwizFR5SStpoahyJZQpUhBjxKEFVoBhwEERbiXwJbr6Ze2H8Dm5OO66JoJr2-QlXbEri1wqwdKTlujy30kqGRNlIfkPqoJqGw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18226758</pqid></control><display><type>article</type><title>Plasmodium falciparum activates endogenous Cl super(-) channels of human erythrocytes by membrane oxidation</title><source>PubMed Central</source><creator>Huber, S M ; Uhlemann, A ; Gamper, N L ; Duranton, C ; Kremsner, P G ; Lang, F</creator><creatorcontrib>Huber, S M ; Uhlemann, A ; Gamper, N L ; Duranton, C ; Kremsner, P G ; Lang, F</creatorcontrib><description>Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection-induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole-cell patch-clamp and hemolysis experiments were performed to define properties of the NPP. Parasitized but not control erythrocytes constitutively expressed two types of anion conductances, differing in voltage dependence and sensitivity to inhibitors. In addition, infected but not control cells hemolyzed in isosmotic sorbitol solution. Both conduct ances and hemolysis of infected cells were inhibited by reducing agents. Conversely, oxidation induced identical conductances and hemolysis in non-infected erythrocytes. In conclusion, P.falciparum activates endogenous erythrocyte channels by applying oxidative stress to the host cell membrane.</description><identifier>ISSN: 0261-4189</identifier><identifier>DOI: 10.1093/emboj/21.1.22</identifier><language>eng</language><subject>Plasmodium falciparum</subject><ispartof>The EMBO journal, 2002-01, Vol.21 (1-2), p.22-30</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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></links><search><creatorcontrib>Huber, S M</creatorcontrib><creatorcontrib>Uhlemann, A</creatorcontrib><creatorcontrib>Gamper, N L</creatorcontrib><creatorcontrib>Duranton, C</creatorcontrib><creatorcontrib>Kremsner, P G</creatorcontrib><creatorcontrib>Lang, F</creatorcontrib><title>Plasmodium falciparum activates endogenous Cl super(-) channels of human erythrocytes by membrane oxidation</title><title>The EMBO journal</title><description>Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection-induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole-cell patch-clamp and hemolysis experiments were performed to define properties of the NPP. Parasitized but not control erythrocytes constitutively expressed two types of anion conductances, differing in voltage dependence and sensitivity to inhibitors. In addition, infected but not control cells hemolyzed in isosmotic sorbitol solution. Both conduct ances and hemolysis of infected cells were inhibited by reducing agents. Conversely, oxidation induced identical conductances and hemolysis in non-infected erythrocytes. In conclusion, P.falciparum activates endogenous erythrocyte channels by applying oxidative stress to the host cell membrane.</description><subject>Plasmodium falciparum</subject><issn>0261-4189</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNp9UE1PwzAMzQEkxuDIPSc-Dt3y0abJEU18SZNAgvuUOCntaJPStIj-ezLBGVl6tiz7vWcjdEHJihLF164zYb9mdEVXjB2hBWGCZjmV6gSdxrgnhBSypAv08dLq2AXbTB2udAtNr4dUahibLz26iJ234d35MEW8aXGcejdcZzcYau29ayMOFa6nTnvshnmshwDzYcvMuEsWBu0dDt-N1WMT_Bk6ThLRnf_lJXq9v3vbPGbb54enze026wVXmVSSgSk4WJcnqKwizFR5SStpoahyJZQpUhBjxKEFVoBhwEERbiXwJbr6Ze2H8Dm5OO66JoJr2-QlXbEri1wqwdKTlujy30kqGRNlIfkPqoJqGw</recordid><startdate>20020115</startdate><enddate>20020115</enddate><creator>Huber, S M</creator><creator>Uhlemann, A</creator><creator>Gamper, N L</creator><creator>Duranton, C</creator><creator>Kremsner, P G</creator><creator>Lang, F</creator><scope>M7N</scope><scope>C1K</scope><scope>F1W</scope><scope>H95</scope><scope>H97</scope><scope>L.G</scope></search><sort><creationdate>20020115</creationdate><title>Plasmodium falciparum activates endogenous Cl super(-) channels of human erythrocytes by membrane oxidation</title><author>Huber, S M ; Uhlemann, A ; Gamper, N L ; Duranton, C ; Kremsner, P G ; Lang, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p639-8982cb53cde43cdfd902bf471f8dc5f4969b5b5b0bb6f8dccd6cb2c3c903d8c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Plasmodium falciparum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huber, S M</creatorcontrib><creatorcontrib>Uhlemann, A</creatorcontrib><creatorcontrib>Gamper, N L</creatorcontrib><creatorcontrib>Duranton, C</creatorcontrib><creatorcontrib>Kremsner, P G</creatorcontrib><creatorcontrib>Lang, F</creatorcontrib><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science &amp; Fisheries Abstracts (ASFA) 1: Biological Sciences &amp; Living Resources</collection><collection>Aquatic Science &amp; Fisheries Abstracts (ASFA) 3: Aquatic Pollution &amp; Environmental Quality</collection><collection>Aquatic Science &amp; Fisheries Abstracts (ASFA) Professional</collection><jtitle>The EMBO journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huber, S M</au><au>Uhlemann, A</au><au>Gamper, N L</au><au>Duranton, C</au><au>Kremsner, P G</au><au>Lang, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasmodium falciparum activates endogenous Cl super(-) channels of human erythrocytes by membrane oxidation</atitle><jtitle>The EMBO journal</jtitle><date>2002-01-15</date><risdate>2002</risdate><volume>21</volume><issue>1-2</issue><spage>22</spage><epage>30</epage><pages>22-30</pages><issn>0261-4189</issn><abstract>Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection-induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole-cell patch-clamp and hemolysis experiments were performed to define properties of the NPP. Parasitized but not control erythrocytes constitutively expressed two types of anion conductances, differing in voltage dependence and sensitivity to inhibitors. In addition, infected but not control cells hemolyzed in isosmotic sorbitol solution. Both conduct ances and hemolysis of infected cells were inhibited by reducing agents. Conversely, oxidation induced identical conductances and hemolysis in non-infected erythrocytes. In conclusion, P.falciparum activates endogenous erythrocyte channels by applying oxidative stress to the host cell membrane.</abstract><doi>10.1093/emboj/21.1.22</doi><tpages>9</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0261-4189
ispartof The EMBO journal, 2002-01, Vol.21 (1-2), p.22-30
issn 0261-4189
language eng
recordid cdi_proquest_miscellaneous_754896209
source PubMed Central
subjects Plasmodium falciparum
title Plasmodium falciparum activates endogenous Cl super(-) channels of human erythrocytes by membrane oxidation
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T03%3A19%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Plasmodium%20falciparum%20activates%20endogenous%20Cl%20super(-)%20channels%20of%20human%20erythrocytes%20by%20membrane%20oxidation&rft.jtitle=The%20EMBO%20journal&rft.au=Huber,%20S%20M&rft.date=2002-01-15&rft.volume=21&rft.issue=1-2&rft.spage=22&rft.epage=30&rft.pages=22-30&rft.issn=0261-4189&rft_id=info:doi/10.1093/emboj/21.1.22&rft_dat=%3Cproquest%3E754896209%3C/proquest%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-p639-8982cb53cde43cdfd902bf471f8dc5f4969b5b5b0bb6f8dccd6cb2c3c903d8c3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=18226758&rft_id=info:pmid/&rfr_iscdi=true