Is quinolinic acid an endogenous excitotoxin in alcohol withdrawal?

Levels of tryptophan in brain are increased by the action of chronic ethanol, particularly in the event of compromised hepatic function. This is likely to result in elevated brain levels of the potent excitotoxin quinolinic acid (quinolinate) since levels of this tryptophan metabolite can be elevated considerably by tryptophan loading. Ethanol may also selectively increase the activity of enzymes important in the synthesis of quinolinic acid such as tryptophan oxygenase. It is concluded that ethanol may generate significant levels of the NMDA receptor agonist, quinolinic acid, possibly even toxic levels in localized brain areas, especially during ethanol withdrawal and when associated with acute or chronic hepatotoxicity.