| pubmed-article:9593899 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0235032 | lld:lifeskim |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0017817 | lld:lifeskim |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0220839 | lld:lifeskim |
| pubmed-article:9593899 | lifeskim:mentions | umls-concept:C0333668 | lld:lifeskim |
| pubmed-article:9593899 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:9593899 | pubmed:dateCreated | 1998-7-7 | lld:pubmed |
| pubmed-article:9593899 | pubmed:abstractText | The role of mitochondrial energy metabolism in glutamate mediated neurotoxicity was studied in rat neurones in primary culture. A brief (15 min) exposure of the neurones to glutamate caused a dose-dependent (0.01-1 mM) increase in cyclic GMP levels together with delayed (24 h) neurotoxicity and ATP depletion. These effects were prevented by either the nitric oxide (.NO) synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (NAME; 1 mM) or by the N-methyl-D-aspartate (NMDA) glutamate-subtype receptor antagonist D-(-)-2-amino-5-phosphonopentanoate (APV; 0.1 mM). Glutamate exposure (0.1 mM and 1 mM) followed by 24 h of incubation caused the inhibition of succinate-cytochrome c reductase (20-25%) and cytochrome c oxidase (31%) activities in the surviving neurones, without affecting NADH-coenzyme-Q1 reductase activity. The rate of oxygen consumption was impaired in neurones exposed to 1 mM glutamate, either with glucose (by 26%) or succinate (by 39%) as substrates. These effects on the mitochondrial respiratory chain and neuronal respiration, together with the observed glutathione depletion (20%) by glutamate exposure were completely prevented by NAME or APV. Our results suggest that mitochondrial dysfunction and impairment of antioxidant status may account for glutamate-mediated neurotoxicity via a mechanism involving .NO biosynthesis. | lld:pubmed |
| pubmed-article:9593899 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9593899 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9593899 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9593899 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9593899 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9593899 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9593899 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9593899 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9593899 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9593899 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9593899 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9593899 | pubmed:issn | 0006-8993 | lld:pubmed |
| pubmed-article:9593899 | pubmed:author | pubmed-author:MedinaJ MJM | lld:pubmed |
| pubmed-article:9593899 | pubmed:author | pubmed-author:HealesS JSJ | lld:pubmed |
| pubmed-article:9593899 | pubmed:author | pubmed-author:AlmeidaAA | lld:pubmed |
| pubmed-article:9593899 | pubmed:author | pubmed-author:BolañosJ PJP | lld:pubmed |
| pubmed-article:9593899 | pubmed:copyrightInfo | Copyright 1998 Elsevier Science B.V. | lld:pubmed |
| pubmed-article:9593899 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9593899 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:9593899 | pubmed:volume | 790 | lld:pubmed |
| pubmed-article:9593899 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9593899 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9593899 | pubmed:pagination | 209-16 | lld:pubmed |
| pubmed-article:9593899 | pubmed:dateRevised | 2009-9-29 | lld:pubmed |
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| pubmed-article:9593899 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9593899 | pubmed:articleTitle | Glutamate neurotoxicity is associated with nitric oxide-mediated mitochondrial dysfunction and glutathione depletion. | lld:pubmed |
| pubmed-article:9593899 | pubmed:affiliation | Departamento de Bioquímica y Biología Molecular, Universidad de Salamanca, Salamanca, Spain. | lld:pubmed |
| pubmed-article:9593899 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9593899 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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