Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/66309
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dc.contributor.authorOrtiz, G.G.
dc.contributor.authorBitzer-Quintero, O.K.
dc.contributor.authorZarate, C.B.
dc.contributor.authorRodriguez-Reynoso, S.
dc.contributor.authorLarios-Arceo, F.
dc.contributor.authorVelazquez-Brizuela, I.E.
dc.contributor.authorPacheco-Moises, F.
dc.contributor.authorRosales-Corral, S.A.
dc.date.accessioned2015-11-19T18:51:12Z-
dc.date.available2015-11-19T18:51:12Z-
dc.date.issued2006
dc.identifier.urihttp://hdl.handle.net/20.500.12104/66309-
dc.description.abstractIt has been demonstrated that high concentrations of monosodium glutamate in the central nervous system induce neuronal necrosis and damage in retina and circumventricular organs. In this model, the monosodium glutamate is used to induce an epileptic state; one that requires highly concentrated doses. The purpose of this study was to evaluate the toxic effects of the monosodium glutamate in liver and kidney after an intra-peritoneal injection. For the experiment, we used 192 Wistar rats to carry out the following assessments: a) the quantification of the enzymes alanine aminotransferase and aspartate aminotransferase, b) the quantification of the lipid peroxidation products and c) the morphological evaluation of the liver and kidney. During the experiment, all of these assessments were carried out at 0, 15, 30 and 45 min after the intra-peritoneal injection. In the rats that received monosodium glutamate, we observed increments in the concentration of alanine aminotransferase and aspartate aminotransferase at 30 and 45 min. Also, an increment of the lipid peroxidation products, in kidney, was exhibited at 15, 30 and 45 min while in liver it was observed at 30 and 45 min. Degenerative changes were observed (edema-degeneration-necrosis) at 15, 30 and 45 min. © 2006 Elsevier SAS. All rights reserved.
dc.titleMonosodium glutamate-induced damage in liver and kidney: A morphological and biochemical approach
dc.typeArticle
dc.identifier.doi10.1016/j.biopha.2005.07.012
dc.relation.ispartofjournalBiomedicine and Pharmacotherapy
dc.relation.ispartofvolume60
dc.relation.ispartofissue2
dc.relation.ispartofpage86
dc.relation.ispartofpage91
dc.subject.keywordEpileptic state; Monosodium glutamate; Toxicity
dc.contributor.affiliationOrtiz, G.G., Lab. de Desarrollo-Envejecimiento, Enfermedades Neurodegenerativas, Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada No. 800, CP 44340, Guadalajara, Jalisco, Mexico; Bitzer-Quintero, O.K., Lab. de Neuroinmunomodulación, División de Neurociencias, CIBO-IMSS, Guadalajara, Jalisco, Mexico; Zárate, C.B., Lab. de Neurobiología Celular Y Molecular, División de Neurociencias, CIBO-IMSS, Guadalajara, Jalisco, Mexico; Rodríguez-Reynoso, S., División de Investigación Quirúrgica, CIBO-IMSS, Guadalajara, Jalisco, Mexico; Larios-Arceo, F., Departamento de Cirugía Pediátrica, UMAE-Pediatría, IMSS, Guadalajara, Jalisco, Mexico; Velázquez-Brizuela, I.E., Lab. de Desarrollo-Envejecimiento, Enfermedades Neurodegenerativas, Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada No. 800, CP 44340, Guadalajara, Jalisco, Mexico; Pacheco-Moisés, F., Departamento de Química, CUCEI, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Rosales-Corral, S.A., Lab. de Desarrollo-Envejecimiento, Enfermedades Neurodegenerativas, Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada No. 800, CP 44340, Guadalajara, Jalisco, Mexico
dc.relation.isReferencedByScopus
dc.relation.isReferencedByWOS
dc.identifier.urlhttp://www.scopus.com/inward/record.url?eid=2-s2.0-33644929220&partnerID=40&md5=721e43bfa98474cfc4f7dfc6ca7751d8
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