6-Chloro-d,l-tryptophan, 4-chloro-3-hydroxyanthranilate and dexamethasone attenuate quinolinic acid accumulation in brain and blood following systemic immune activation

Kuniaki Saito, Sanford P. Markey, Melvyn P. Heyes

研究成果: Article査読

27 被引用数 (Scopus)

抄録

Accumulations of the neurotoxin quinolinic acid (QUIN) occur in the brain and blood following immune activation and are attributed to increased metabolism of l-tryptophan through the kynurenine pathway. Systemic administration of 4-chloro-3-hydroxyanthranilate (an inhibitor of 3-hydroxyanthranilate-3,4-dioxygenase), 6-chloro-d,l-tryptophan (a substrate of the kynurenine pathway) and dexamethasone (an anti-inflammatory agent) attenuated the accumulation of QUIN in the brain and blood following systemic pokeweed mitogen administration to mice. 6-Chloro-d,l-tryptophan and dexamethasone also attenuated the increases in brain and lung indoleamine-2,3-dioxygenase activity and elevations in plasma l-kynurenine levels. We conclude that QUIN formation can be modified by drugs which act at different levels of the cascade of events that link immune stimulation to increased kynurenine pathway metabolism.

本文言語English
ページ(範囲)211-215
ページ数5
ジャーナルNeuroscience Letters
178
2
DOI
出版ステータスPublished - 12-09-1994
外部発表はい

All Science Journal Classification (ASJC) codes

  • 神経科学(全般)

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