Neurochemical Research

, Volume 20, Issue 1, pp 31–38

Deoletion of brain glutathione is accompanied by impaired micochondrial function and decreased N-acetyl aspartate concentration

  • R. Heales
  • S. E. C. Davies
  • T. E. Bates
  • J. B. Clark
Original Articles

DOI: 10.1007/BF00995149

Cite this article as:
Heales, R., Davies, S.E.C., Bates, T.E. et al. Neurochem Res (1995) 20: 31. doi:10.1007/BF00995149

Abstract

The effect of depletion of reduced glutathione (GSH) on brain mitochondrial function and N-acetyl aspartate concentration has been investigated. Using pre-weanling rats, GSH was depleted by L-buthionine sulfoximine administration for up to 10 days. In both whole brain homogenates and purified mitochondrial preparations complex IV (cytochrome c oxidase) activity was decreased, by up to 27%, as a result of this treatment. In addition, after 10 days of GSH depletion, citrate synthase activity was significantly reduced, by 18%, in the purified mitochondrial preparations, but not in whole brain homogenates, suggesting increased leakiness of the mitochondrial membrane. The whole brain N-acetyl aspartate concentration was also significantly depleted at this time point, by 11%. It is concluded that brain GSH is important for the maintenance of optimum mitochondrial function and that prolonged depletion leads also to loss of neuronal integrity. The relevance of these findings to Parkinson's disease and the inborn errors of glutathione mtabolism are also discussed.

Key Words

Glutathione mitochondria N-acetyl aspartate oxidative stress 

Copyright information

© Plenum Publishing Corporation 1995

Authors and Affiliations

  • R. Heales
    • 1
  • S. E. C. Davies
    • 1
  • T. E. Bates
    • 1
  • J. B. Clark
    • 1
  1. 1.Department of Neurochemistry, Institute of NeurologyUniversity of LondonLondonEngland

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