Quinolinic acid induces oxidative stress in rat brain synaptosomes

0142172 - FGU-C 20010226 RIV US eng J - Článek v odborném periodiku
Santamaria, A. - Galván-Arzate, S. - Lisý, Václav - Ali, S. F. - Duhart, H. M. - Osorio-Rico, L. - Rios, C. - Šťastný, František
Quinolinic acid induces oxidative stress in rat brain synaptosomes.
Neuroreport. Roč. 12, č. 4 (2001), s. 871-874. ISSN 0959-4965. E-ISSN 1473-558X
Grant CEP: GA ČR GA309/99/0211; GA ČR GA305/99/1317
Grant ostatní: CONACyT(MX) J28612-M; CONACyT(MX) 130.205
Výzkumný záměr: CEZ:AV0Z5011922
Klíčová slova: 2-amino-5-phosphonovaleric acid * brain regions * glutathione
Kód oboru RIV: FH - Neurologie, neurochirurgie, neurovědy
Impakt faktor: 2.374, rok: 2001

The oxidative action of quinolinic acid (QUIN), and the protective effects of glutathione (GSH), and 2-amino-5-phosphonovaleric acid (APV), were tested in rat brain synaptosomes, Reactive oxygen species (ROS) formation was quantified after the exposure of synaptosomes to increasing concentrations of QUIN (25-500 microM). The potency of QUIN to induce lipid peroxidation (LP) was tested as a regional index of thiobarbituric acid-reactive substances (TBARS) production, and the antioxidant actions of both GSH (50 microM) and APV (250 microM) on QUIN-induced LP were evaluated in synaptosomes prepared from different brain regions. QUIN induced concentration-dependent increases in ROS formation and TBARS in all regions analyzed, but increased production of fluorescent peroxidized lipids only in the striatum and the hippocampus, whereas both GSH and APV decreased this index. These results suggest that the excitotoxic action of QUIN involves regional selectivity in the oxidative status of brain synaptosomes, and may be prevented by substances exhibiting antagonism at the NMDA receptor.
Trvalý link: http://hdl.handle.net/11104/0039881