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Article: Effect of α-Trinositol on Swelling and Damage of Glial Cells by Lactacidosis and Glutamate

TitleEffect of α-Trinositol on Swelling and Damage of Glial Cells by Lactacidosis and Glutamate
Authors
Issue Date1997
Citation
Acta Neurochirurgica, Supplement, 1997, v. 1997 n. 70, p. 179-181 How to Cite?
AbstractThe therapeutic efficacy of α-trinositol (D-myo-inositol-1,2,6-trisphosphate), an isomer of the intracellular messenger IP3, was analized for cytotoxic swelling and damage of glial cells in vitro from lactacidosis or glutamate. Lactacidosis and the interstitial accumulation of glutamate are prominent sequelae in ischemic or traumatic brain tissue. C6 glioma cells harvested from culture and suspended in a physiological medium were either exposed to pH 5.0 by administration of lactic acid, or to 1 mM glutamate at normal pH. Cell swelling and viability were quantified by blood flow cytometry. Addition of α-trinositol (3 mM) under control conditions at pH 7.4 resulted in transient cell shrinking to 96.5 ± 1.3% of control within 3 min (p < 0.05). Lactacidosis of pH 5.0 led to an increase in cell volume to 139.7 ± 1.3% within 20 min, whereas α-trinositol reduced the swelling response by approximately 25% (p < 0.01). In addition, cell viability was severely affected at pH 5.0 amounting to only 53.8 ± 3.1% after 60 min. α-Trinositol was found to markedly improve cell viability; at 60 min 70.2 ± 1.6% of the cells were still viable (p < 0.01). Addition of glutamate (1 mM) led to a steady increase in cell size, reaching 110% of control after 120 min, irrespective of wether α-trinositol was present or not. The attenuation of cell swelling may be attributed to an interference with pH-regulatory mechanisms, such as the Na+/H+-antiporter, while protection of cell viability might be caused be effects of α-trinositol on Ca2+-overload. On the other hand, the increase in cell volume by glutamate associated with its intracellular uptake was not influenced by α-trinositol.
Persistent Identifierhttp://hdl.handle.net/10722/149565
ISSN
2015 SCImago Journal Rankings: 0.379
References

 

DC FieldValueLanguage
dc.contributor.authorStaub, Fen_US
dc.contributor.authorPeters, Jen_US
dc.contributor.authorPlesnila, Nen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorBaethmann, Aen_US
dc.date.accessioned2012-06-26T05:55:21Z-
dc.date.available2012-06-26T05:55:21Z-
dc.date.issued1997en_US
dc.identifier.citationActa Neurochirurgica, Supplement, 1997, v. 1997 n. 70, p. 179-181en_US
dc.identifier.issn0065-1419en_US
dc.identifier.urihttp://hdl.handle.net/10722/149565-
dc.description.abstractThe therapeutic efficacy of α-trinositol (D-myo-inositol-1,2,6-trisphosphate), an isomer of the intracellular messenger IP3, was analized for cytotoxic swelling and damage of glial cells in vitro from lactacidosis or glutamate. Lactacidosis and the interstitial accumulation of glutamate are prominent sequelae in ischemic or traumatic brain tissue. C6 glioma cells harvested from culture and suspended in a physiological medium were either exposed to pH 5.0 by administration of lactic acid, or to 1 mM glutamate at normal pH. Cell swelling and viability were quantified by blood flow cytometry. Addition of α-trinositol (3 mM) under control conditions at pH 7.4 resulted in transient cell shrinking to 96.5 ± 1.3% of control within 3 min (p < 0.05). Lactacidosis of pH 5.0 led to an increase in cell volume to 139.7 ± 1.3% within 20 min, whereas α-trinositol reduced the swelling response by approximately 25% (p < 0.01). In addition, cell viability was severely affected at pH 5.0 amounting to only 53.8 ± 3.1% after 60 min. α-Trinositol was found to markedly improve cell viability; at 60 min 70.2 ± 1.6% of the cells were still viable (p < 0.01). Addition of glutamate (1 mM) led to a steady increase in cell size, reaching 110% of control after 120 min, irrespective of wether α-trinositol was present or not. The attenuation of cell swelling may be attributed to an interference with pH-regulatory mechanisms, such as the Na+/H+-antiporter, while protection of cell viability might be caused be effects of α-trinositol on Ca2+-overload. On the other hand, the increase in cell volume by glutamate associated with its intracellular uptake was not influenced by α-trinositol.en_US
dc.languageengen_US
dc.relation.ispartofActa Neurochirurgica, Supplementen_US
dc.subject.meshAcidosis, Lactic - Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Therapeutic Useen_US
dc.subject.meshBrain Edema - Drug Therapy - Pathologyen_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshGlutamic Acid - Toxicityen_US
dc.subject.meshInositol Phosphates - Therapeutic Useen_US
dc.subject.meshNeuroglia - Drug Effects - Pathologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleEffect of α-Trinositol on Swelling and Damage of Glial Cells by Lactacidosis and Glutamateen_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.pmid9416315en_US
dc.identifier.scopuseid_2-s2.0-0031300027en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031300027&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1997en_US
dc.identifier.issue70en_US
dc.identifier.spage179en_US
dc.identifier.epage181en_US
dc.publisher.placeAustriaen_US
dc.identifier.scopusauthoridStaub, F=7006611117en_US
dc.identifier.scopusauthoridPeters, J=7404191248en_US
dc.identifier.scopusauthoridPlesnila, N=7003609441en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridBaethmann, A=7004994793en_US

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