Journal of Bioenergetics and Biomembranes

, Volume 41, Issue 6, pp 517-521

First online:

Brain mitochondrial dysfunction and oxidative damage in Parkinson’s disease

  • Ana NavarroAffiliated withDepartment of Biochemistry and Molecular Biology, School of Medicine, University of Cádiz Email author 
  • , Alberto BoverisAffiliated withSchool of Pharmacy and Biochemistry, University of Buenos Aires

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Complex factors contribute to the appearance of Parkinson’s disease (PD), but with a constant mitochondrial involvement. There are two interdependent conditions in PD: brain mitochondrial dysfunction and brain mitochondrial oxidative damage. Mitochondrial dysfunction and reduced complex I activity are recognized in substantia nigra and in frontal cortex in PD patients. The molecular mechanism involved in the inactivation of complex I is likely accounted by the sum of ONOO mediated reactions, reactions with free radical intermediates of the lipid peroxidation process and amine-aldehyde adduction reactions. The inhibitory effects on complex I lead synergistically to denaturation of the protein structure and to further increases of O 2 and ONOO production at the vicinity of complex I. An adaptive response in PD patients has been described with increases in mtNOS activity, mitochondrial mass and mitochondrial biogenesis. Mitochondrial dysfunction in the human frontal cortex is to be considered a factor contributing to impaired cognition in PD.


Complex I Frontal cortex mitochondria Brain mitochondria in PD mtNOS