Metabolic Brain Disease

, Volume 24, Issue 3, pp 415–425 | Cite as

Tyrosine administration decreases glutathione and stimulates lipid and protein oxidation in rat cerebral cortex

  • Ângela M. Sgaravatti
  • Alessandra S. Magnusson
  • Amanda S. de Oliveira
  • Andréa P. Rosa
  • Caroline Paula Mescka
  • Fernanda R. Zanin
  • Carolina D. Pederzolli
  • Angela T. S. Wyse
  • Clóvis M. D. Wannmacher
  • Moacir Wajner
  • Carlos Severo Dutra-Filho
Original Paper

Abstract

Tyrosine levels are abnormally elevated in tissues and physiological fluids of patients with inborn errors of tyrosine catabolism especially in tyrosinemia type II which is caused by deficiency of tyrosine aminotransferase (TAT) and provokes eyes, skin and central nervous system disturbances. We have recently reported that tyrosine promoted oxidative stress in vitro but the exact mechanisms of brain damage in these disorder are poorly known. In the present study, we investigated the in vivo effect of L-tyrosine (500 mg/Kg) on oxidative stress indices in cerebral cortex homogenates of 14-day-old Wistar rats. A single injection of L-tyrosine decreased glutathione (GSH) and thiol-disulfide redox state (SH/SS ratio) while thiobarbituric acid-reactive substances, protein carbonyl content and glucose-6-phosphate dehydrogenase activity were enhanced. In contrast, the treatment did not affect ascorbic acid content, and the activities of superoxide dismutase, catalase and glutathione peroxidase. These results indicate that acute administration of L-tyrosine may impair antioxidant defenses and stimulate oxidative damage to lipids and proteins in cerebral cortex of young rats in vivo. This suggests that oxidative stress may represent a pathophysiological mechanism in hypetyrosinemic patients.

Keywords

Tyrosine Hypertyrosinemias Tyrosinemia type II Tyrosine administration Rat brain Oxidative stress 

Notes

Acknowledgements

This work was supported by the research grants from Programa de Núcleos de Excelência (PRONEX), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul (FAPERGS) and FINEP Rede Instituto Brasileiro de Neurociência (IBN-Net #01.06.0842-00).

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Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  • Ângela M. Sgaravatti
    • 2
  • Alessandra S. Magnusson
    • 1
  • Amanda S. de Oliveira
    • 1
  • Andréa P. Rosa
    • 1
  • Caroline Paula Mescka
    • 1
  • Fernanda R. Zanin
    • 1
  • Carolina D. Pederzolli
    • 2
  • Angela T. S. Wyse
    • 1
    • 2
  • Clóvis M. D. Wannmacher
    • 1
    • 2
  • Moacir Wajner
    • 1
    • 2
  • Carlos Severo Dutra-Filho
    • 1
    • 2
  1. 1.Departamento de Bioquímica, Instituto de Ciências Básicas da SaúdeUniversidade Federal do Rio Grande do SulPorto AlegreBrazil
  2. 2.Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da SaúdeUniversidade Federal do Rio Grande do SulPorto AlegreBrazil

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