Quinolinic acid, the inescapable neurotoxin

被引：438

作者：

Guillemin, Gilles J. ^{[1
,2
]}

机构：

[1] Univ New S Wales, Dept Pharmacol, Sch Med Sci, Sydney, NSW 2052, Australia

[2] St Vincents Hosp, St Vincents Ctr Appl Med Res, Sydney, NSW 2010, Australia

来源：

FEBS JOURNAL | 2012年 / 279卷 / 08期

关键词：

kynurenine pathway; neurodegeneration; neuroinflammation; quinolinic acid; KYNURENINE PATHWAY ENZYMES; INHIBITS GLUTAMATE UPTAKE; RAT-BRAIN; TRYPTOPHAN-METABOLISM; INDOLEAMINE 2,3-DIOXYGENASE; ALZHEIMERS-DISEASE; HUMAN MICROGLIA; HUNTINGTONS-DISEASE; OXIDATIVE STRESS; HUMAN ASTROCYTES;

D O I：

10.1111/j.1742-4658.2012.08485.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Over the last two decades, evidence for the involvement of quinolinic acid (QUIN) in neuroinflammatory diseases has been exponentially increasing. Within the brain, QUIN is produced and released by infiltrating macrophages and activated microglia, the very cells that are prominent during neuroinflammation. QUIN acts as an agonist of the N-methyl-d-aspartate receptor and as such is considered to be a brain endogenous excitotoxin. Since the discovery of the excitotoxic activity of QUIN in the early 1980s, several other cytotoxic mechanisms have been identified. We know today that QUIN acts as a neurotoxin, gliotoxin, proinflammatory mediator, pro-oxidant molecule and can alter the integrity and cohesion of the bloodbrain barrier. This paper aims to review some of the most recent findings about the effects of QUIN and its mode of action.

引用

页码：1356 / 1365

页数：10

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