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Article: Contribution of anion transporters to the acidosis-induced swelling and intracellular acidification of glial cells

TitleContribution of anion transporters to the acidosis-induced swelling and intracellular acidification of glial cells
Authors
Issue Date2000
Citation
Journal Of Neurochemistry, 2000, v. 75 n. 1, p. 125-132 How to Cite?
AbstractThis study examines the contribution of anion transporters to the swelling and intracellular acidification of glial cells from an extracellular lactacidosis, a condition well-known to accompany cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were exposed to lactacidosis in physiological or anion-depleted media, and different anion transport inhibitors were applied. Changes in cell volume and intracellular pH (pH(i)) were simultaneously quantified by flow cytometry. Extracellular lactacidosis (pH 6.2) led to an increase in cell volume to 125.1 ± 2.5% of baseline within 60 min, whereas the pH(i) dropped from the physiological value of 7.13 ± 0.05 to 6.32 ± 0.03. Suspension in Cl- -free or HCO3 - /CO2-free media or application of anion transport inhibitors [0.1 mM bumetanide or 0.5 mM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)] did not affect cell volume during baseline conditions but significantly reduced cell swelling from lactacidosis. In addition, the Cl- free or HCO3 -/CO2-free media and DIDS attenuated intracellular acidosis on extracellular acidification. From these findings it is concluded that besides the known activation of the Na+/H+ exchanger, activation of the Na+- independent Cl-/HCO3 - exchanger and the Na+- K+-Cl- cotransporter contributes to acidosis-induced glial swelling and the intracellular acidification. Inhibition of these processes may be of interest for future strategies in the treatment of cytotoxic brain edema from cerebral ischemia or traumatic brain injury.
Persistent Identifierhttp://hdl.handle.net/10722/149590
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRingel, Fen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorStaub, Fen_US
dc.contributor.authorBaethmann, Aen_US
dc.contributor.authorPlesnila, Nen_US
dc.date.accessioned2012-06-26T05:55:39Z-
dc.date.available2012-06-26T05:55:39Z-
dc.date.issued2000en_US
dc.identifier.citationJournal Of Neurochemistry, 2000, v. 75 n. 1, p. 125-132en_US
dc.identifier.issn0022-3042en_US
dc.identifier.urihttp://hdl.handle.net/10722/149590-
dc.description.abstractThis study examines the contribution of anion transporters to the swelling and intracellular acidification of glial cells from an extracellular lactacidosis, a condition well-known to accompany cerebral ischemia and traumatic brain injury. Suspended C6 glioma cells were exposed to lactacidosis in physiological or anion-depleted media, and different anion transport inhibitors were applied. Changes in cell volume and intracellular pH (pH(i)) were simultaneously quantified by flow cytometry. Extracellular lactacidosis (pH 6.2) led to an increase in cell volume to 125.1 ± 2.5% of baseline within 60 min, whereas the pH(i) dropped from the physiological value of 7.13 ± 0.05 to 6.32 ± 0.03. Suspension in Cl- -free or HCO3 - /CO2-free media or application of anion transport inhibitors [0.1 mM bumetanide or 0.5 mM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)] did not affect cell volume during baseline conditions but significantly reduced cell swelling from lactacidosis. In addition, the Cl- free or HCO3 -/CO2-free media and DIDS attenuated intracellular acidosis on extracellular acidification. From these findings it is concluded that besides the known activation of the Na+/H+ exchanger, activation of the Na+- independent Cl-/HCO3 - exchanger and the Na+- K+-Cl- cotransporter contributes to acidosis-induced glial swelling and the intracellular acidification. Inhibition of these processes may be of interest for future strategies in the treatment of cytotoxic brain edema from cerebral ischemia or traumatic brain injury.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Neurochemistryen_US
dc.subject.mesh4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnionsen_US
dc.subject.meshAntiporters - Physiologyen_US
dc.subject.meshBicarbonates - Administration & Dosageen_US
dc.subject.meshBumetanide - Pharmacologyen_US
dc.subject.meshCarbon Dioxide - Administration & Dosageen_US
dc.subject.meshCarrier Proteins - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshCell Size - Drug Effectsen_US
dc.subject.meshChloride-Bicarbonate Antiportersen_US
dc.subject.meshChlorides - Administration & Dosageen_US
dc.subject.meshCulture Mediaen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshGlioma - Metabolism - Pathologyen_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshLactic Aciden_US
dc.subject.meshRatsen_US
dc.subject.meshSodium-Potassium-Chloride Symportersen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleContribution of anion transporters to the acidosis-induced swelling and intracellular acidification of glial cellsen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1471-4159.2000.0750125.xen_US
dc.identifier.pmid10854255-
dc.identifier.scopuseid_2-s2.0-0034050921en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034050921&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume75en_US
dc.identifier.issue1en_US
dc.identifier.spage125en_US
dc.identifier.epage132en_US
dc.identifier.isiWOS:000087659000016-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridRingel, F=6602136569en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridStaub, F=7006611117en_US
dc.identifier.scopusauthoridBaethmann, A=7004994793en_US
dc.identifier.scopusauthoridPlesnila, N=7003609441en_US

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