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Inhibitory Effects of Endogenous Tetrahydroisoquinolines on Mitochondrial Respiration in Mouse Brain

  • K. Suzuki
  • Y. Mizuno
  • M. Naoi
  • T. Nagatsu
  • M. Yoshida
Part of the Advances in Behavioral Biology book series (ABBI, volume 44)

Abstract

Pathogenesis of Parkinson’s disease has not been well elucidated yet. However, some hypotheses have been advocated. Mitochondrial abnormalities,1,2,3,4,5,6 and changes of iron and free radicals7,8 have been reported. The mechanism of nigrostriatal degeneration in MPTP-induced parkinsonism appears to be due to the inhibition of mitochondrial respiration by MPP+. 9,10,11,12 Chronic exposure to an unknown MPTP-like endogenous neurotoxin has been postulated as a possible etiology of Parkinson’s disease. 1,2,3,4-Tetrahydroisoquinoline (TIQ) has emerged as one of such toxins.13 We have previously reported the effects of TIQ14,15,16,17 and TIQ-related compounds18 on mitochondrial respiration. In the present study, we report the inhibitory effect of dopamine-derived endogenous tetrahydroisoquinolines against mitochondrial respiration.

Keywords

Tyrosine Hydroxylase Mouse Brain Mitochondrial Respiration Inhibitory Potency Electron Transport System 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • K. Suzuki
    • 1
    • 2
  • Y. Mizuno
    • 3
  • M. Naoi
    • 4
  • T. Nagatsu
    • 5
  • M. Yoshida
    • 2
  1. 1.Department of Internal MedicinePrefectural Tajima HospitalFukushimaJapan
  2. 2.Department of NeurologyJichi Medical SchoolTochigiJapan
  3. 3.Department of NeurologyJuntendo University School of MedicineTokyoJapan
  4. 4.Department of BiosciencesNagoya Institute of TechnologyAichiJapan
  5. 5.Department of NeurochemistryFujita Health UniversityAichiJapan

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