L. G. Darlington

TL;DR: The kynurenine pathway is the main pathway for tryptophan metabolism and generates compounds that can modulate activity at glutamate receptors and possibly nicotinic receptors, in addition to some as-yet-unidentified sites.

TL;DR: The results suggest that quinolinic acid‐induced neuronal damage can be prevented by a receptor‐independent action of melatonin and deprenyl, agents which can act as a potent free radical scavenger and can increase the activity of endogenous antioxidant enzymes respectively.

TL;DR: The results suggest that increased tryptophan catabolism is initiated before or immediately after a stroke, and is related to the inflammatory response and oxidative stress, with a major change in 3‐hydroxyanthranilic acid levels.

TL;DR: For brain‐damaged patients, increased activation of the kynurenine pathway, oxidative stress and raised levels of inflammation continue many years after the original insult, possibly contributing to the continuing cerebral dysfunction in these patients.

TL;DR: The results demonstrate that tryptophan loading produces a highly significant increase in lipid peroxidation products in parallel with increased kynurenines, indicating oxidative stress may result from the generation of quinolinic acid, 3-hydroxykynurenine, and3-hydroxyanthranilic acid, all of which are known to have the ability to generate free radicals.