Metabolic Brain Disease

, Volume 18, Issue 2, pp 147–154

In Vitro Effect of Homocysteine on Some Parameters of Oxidative Stress in Rat Hippocampus

Authors

  • Emilio L. Streck
    • Departamento de Bioquímica, ICBSUniversidade Federal do Rio Grande do Sul
  • Paula S. Vieira
    • Departamento de Bioquímica, ICBSUniversidade Federal do Rio Grande do Sul
  • Clóvis M. D. Wannmacher
    • Departamento de Bioquímica, ICBSUniversidade Federal do Rio Grande do Sul
  • Carlos S. Dutra-Filho
    • Departamento de Bioquímica, ICBSUniversidade Federal do Rio Grande do Sul
  • Moacir Wajner
    • Departamento de Bioquímica, ICBSUniversidade Federal do Rio Grande do Sul
  • Angela T. S. Wyse
    • Departamento de Bioquímica, ICBSUniversidade Federal do Rio Grande do Sul
Article

DOI: 10.1023/A:1023815119931

Cite this article as:
Streck, E.L., Vieira, P.S., Wannmacher, C.M.D. et al. Metab Brain Dis (2003) 18: 147. doi:10.1023/A:1023815119931

Abstract

Homocystinuria is an inherited metabolic disease characterized biochemically by increased blood and brain levels of homocysteine caused by severe deficiency of cystathionine β-synthase activity. Affected patients present mental retardation, seizures, and atherosclerosis. Oxidative stress plays an important role in the pathogenesis of many neurodegenerative and vascular diseases, such Alzheimer's disease, stroke, and atherosclerosis. However, the mechanisms underlying the neurological damage characteristic of homocystinuria are still poorly understood. To evaluate the involvement of oxidative stress on the neurological dysfunction present in homocystinuria, we measured thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, and total radical-trapping antioxidant potential (TRAP) and antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase) in rat hippocampus in the absence (controls) or in the presence of homocysteine (10–500 μM) in vitro. We demonstrated that homocysteine significantly increases TBARS and decreases TRAP, both in a dose-dependent manner, but did not change antioxidant enzymes. Our results suggest that oxidative stress is involved in the neurological dysfunction of homocystinuria. However, further studies are necessary to confirm and extend our findings to the human condition and also to determine whether antioxidant therapy may be of benefit to these patients.

Homocysteinehomocystinuriaoxidative stressTBARSTRAPantioxidant enzymes

Copyright information

© Plenum Publishing Corporation 2003