Promotion of oxidative stress by L-tryptophan in cerebral cortex of rats.

Abstract

Despite the significant brain abnormalities, the neurotoxic mechanisms of brain injury in hypertryptophanemia are virtually unknown. In this work, it was investigated the in vitro effect of l-tryptophan on various parameters of oxidative stress, namely spontaneous chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR) and glutathione (GSH) levels in cerebral cortex from 30-day-old rats. Tryptophan significantly increased chemiluminescence and TBA-RS measurements indicating that this amino acid induced lipid peroxidation in vitro. We also observed that tryptophan significantly decreased the brain antioxidant defenses by reducing the values of TRAP, TAR and GSH, reflecting that the overall content of antioxidants was reduced by tryptophan. Furthermore, the tryptophan-induced increase of TBA-RS was fully prevented by GSH and by combination of catalase plus superoxide dismutase, but not by the inhibitor of nitric oxide synthase N(omega)-nitro-L-arginine methyl ester (L-NAME). In case these findings also occur in human hypertryptophanemia or in other neurodegenerative diseases in which tryptophan accumulates, it is feasible that oxidative stress may be involved in the mechanism leading to the brain injury observed in patients affected by these disorders.

• Authors: Luciane Rosa Feksa, Alexandra Latini, Virgínia Cielo Rech, Moacir Wajner, Carlos Severo Dutra-Filho, Angela Terezinha de Souza Wyse, Clovis Milton Duval Wannmacher
• Journal: Neurochemistry international (Neurochem Int) Vol. 49 Issue 1 Pg. 87-93 (Jul 2006) ISSN: 0197-0186 [Print] England
• PMID: 16497412 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antioxidants
• Enzyme Inhibitors
• Free Radicals
• Thiobarbituric Acid Reactive Substances
• Tryptophan
• Catalase
• Nitric Oxide Synthase Type I
• Superoxide Dismutase
• Glutathione
• NG-Nitroarginine Methyl Ester

Topics

• Amino Acid Metabolism, Inborn Errors (metabolism, physiopathology)
• Animals
• Antioxidants (metabolism)
• Catalase (metabolism, pharmacology)
• Cerebral Cortex (drug effects, metabolism, physiopathology)
• Disease Models, Animal
• Down-Regulation (drug effects, physiology)
• Enzyme Inhibitors (pharmacology)
• Free Radicals (metabolism)
• Glutathione (metabolism, pharmacology)
• Lipid Peroxidation (drug effects, physiology)
• Luminescence
• Male
• NG-Nitroarginine Methyl Ester (pharmacology)
• Nerve Degeneration (chemically induced, metabolism, physiopathology)
• Nitric Oxide Synthase Type I (antagonists & inhibitors, metabolism)
• Oxidative Stress (drug effects, physiology)
• Rats
• Rats, Wistar
• Superoxide Dismutase (metabolism, pharmacology)
• Thiobarbituric Acid Reactive Substances (analysis, metabolism)
• Tryptophan (metabolism, toxicity)