Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets. (5th September 2013)

• Record Type: Journal Article
• Authors: Lugo-Huitrón, Rafael; Ugalde Muñiz, Perla; Pineda, Benjamin; Pedraza-Chaverrí, José; Ríos, Camilo; Pérez-de la Cruz, Verónica
• Other Names: Santos Renata Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2013(2013)
• Publication Date: 2013-09-05
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2013/104024
• Languages: English
• ISSNs: 1942-0900

Abstract

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.