Tryptophan metabolism and oxidative stress in patients with Huntington's disease

• DOI: 10.1111/j.1471-4159.2005.03070.x
• Publication Date: 2005-04-13T18:47:10Z
• Authors: N. Stoy; G. M. Mackay; C. M. Forrest; J. Christofides; M. Egerton; T. W. Stone; L. G. Darlington
• Keywords: Kynurenine pathway; Kynurenic acid; Neopterin

Abstract Abnormalities in the kynurenine pathway may play a role Huntington's disease (HD). In this study, tryptophan depletion and loading were used to investigate changes blood metabolites, as well markers of inflammation oxidative stress HD patients healthy controls. Results showed that : ratio was greater than controls baseline state after depletion, indicating increased indoleamine dioxygenase activity HD. Evidence for persistent provided by elevated levels C‐reactive protein, neopterin lipid peroxidation products compared with The kynurenate suggested lower aminotransferase higher at baseline, loading, do not result any differences kynurenic acid levels, providing no supportive evidence compensatory neuroprotective acid. Quinolinic wide variations levels. data indicate high level many years onset. Levels free radical generators 3‐hydroxykynurenine 3‐hydroxyanthranilic decreased patients, hence did appear contribute stress. It is concluded exhibit abnormal handling metabolism stress, these factors could ongoing brain dysfunction.