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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 104024, 14 pages
http://dx.doi.org/10.1155/2013/104024
Review Article

Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

1Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, S.S.A., 14269 México, DF, Mexico
2Laboratorio de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, S.S.A., 14269 México, DF, Mexico
3Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, 04510 México, DF, Mexico

Received 14 May 2013; Revised 23 July 2013; Accepted 1 August 2013

Academic Editor: Renata Santos

Copyright © 2013 Rafael Lugo-Huitrón et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Quinolinic acid (QUIN), a neuroactive metabolite of the kynurenine pathway, is normally presented in nanomolar concentrations in human brain and cerebrospinal fluid (CSF) and is often implicated in the pathogenesis of a variety of human neurological diseases. QUIN is an agonist of N-methyl-D-aspartate (NMDA) receptor, and it has a high in vivo potency as an excitotoxin. In fact, although QUIN has an uptake system, its neuronal degradation enzyme is rapidly saturated, and the rest of extracellular QUIN can continue stimulating the NMDA receptor. However, its toxicity cannot be fully explained by its activation of NMDA receptors it is likely that additional mechanisms may also be involved. In this review we describe some of the most relevant targets of QUIN neurotoxicity which involves presynaptic receptors, energetic dysfunction, oxidative stress, transcription factors, cytoskeletal disruption, behavior alterations, and cell death.