Tryptophan administration induces oxidative stress in brain cortex of rats.

Metabolic Brain Disease
Luciane Rosa FeksaClovis Milton Duval Wannmacher

Abstract

Despite the significant brain abnormalities, the neurotoxic mechanisms of brain injury in hypertryptophanemia are virtually unknown. In this work, we determined the thiobarbituric acid-reactive substances, 2',7'-dihydrodichlorofluorescein oxidation, reduced glutathione and the activities of catalase, superoxide dismutase and glutathione peroxidase in cerebral cortex from rats loaded with L-tryptophan. High L-tryptophan concentrations, similar to those found in hypertryptophanemic patients were induced by three subcutaneous injections of saline-buffered tryptophan (2 micromol/g body weight) to 30-day-old Wistar rats. The parameters were assessed 1 h after the last injection. It was observed that tryptophan significantly increased thiobarbituric acid-reactive substances, 2',7'-dihydrodichlorofluorescein oxidation and reduced glutathione, whereas it reduced catalase activity. Pre-treatment with taurine (1.6 micromol/g of body weight), or alpha-tocopherol plus ascorbic acid (40 and 100 microg/g body weight, respectively) prevented those effects of tryptophan, reinforcing the hypothesis that tryptophan induces oxidative stress in brain cortex of the rats. Therefore, these findings also occur in human hypertryptophanemia or in other ...Continue Reading

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Citations

Nov 15, 2011·Molecular and Cellular Biochemistry·Vivian Strassburger AndradeClóvis Milton Duval Wannmacher
Apr 3, 2014·Oxidative Medicine and Cellular Longevity·Jazmin Reyes OcampoVerónica Pérez de la Cruz
Jan 13, 2012·Neurochemical Research·Denise Bertin RojasClóvis Milton Duval Wannmacher
Nov 19, 2009·Neurotoxicity Research·Yiquan ChenGilles J Guillemin

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