There is increasing interest in the effects on neuronal viability of several kynurenine metabolites of tryptophan, including the NMDA receptor agonist quinolinic acid (possibly implicated in several neurodegenerative disorders) and the glutamate antagonist kynurenic acid, a possible neuroprotectant. This study examines the ability of several other metabolites to affect neuronal viability by inducing oxidative stress. Cerebellar granule neurone cultures were prepared from 8-day neonatal Sprague-Dawley rats, and effects on neuronal viability (measured using fluorescein diacetate) of selected kynurenine pathway compounds studied, including 3-hydroxykynurenine (3-HK), 3-hydroxyanthranilic acid (3-HAA) and 5-hydroxyanthranilic acid (5-HAA), applied for 1 to 9 hours. Alterations to neurotoxicity due to variation in glucose concentration (5.5 vs. 25mM), and the presence of exogenously applied antioxidant enzymes were examined. Application of 3-HK, 3-HAA, and 5-HAA at concentrations from 10 micromolar to 1 millimolar caused dose-dependant neurotoxicity, potentiated by prolonged exposure. The remaining compounds caused neurotoxicity, intensified by increased exposure times but not dose. Tryptophan, kynurenine, anthranilic acid, quinolinic acid and picolinic acid were significantly more neurotoxic in the presence of a higher glucose concentration (p<0.05). The co-application of anthranilic acid with 3-HAA did not potentiate the neurotoxic effect of either metabolite. Catalase (200U/ml) reduced 3-HK, 3-HAA, and 5-HAA toxicity significantly (p<0.05), whereas superoxide dismutase (SOD) at 200U/ml did not. It is demonstrated that certain tryptophan metabolites cause neurotoxic effects due to oxidative stress, and that the toxicity of some metabolites can be exacerbated by increased glucose levels.