Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease

Mitochondria show decreased O2 uptake -with NAD-dependent substrates- and NO production

Laura B. Valdez; Tamara Zaobornyj; Manuel J. Bandez; José María López-Cepero; Alberto Boveris; Ana Navarro


Scholarcy highlights

  • Mitochondria show decreased O2 uptake -with NAD-dependent substrates- and NO production
  • Mitochondrial complex I is highly sensitive to inactivation by oxidative reactions
  • Mitochondrial dysfunction named complex I syndrome was observed in striatum mitochondria of rotenone treated rats in an animal model of Parkinson disease
  • After 60 days of rotenone treatment, the animals showed: 6-fold increased bradykinesia and 60% decreased locomotor activity; 35-34% decreases in striatum O2 uptake and in state 3 mitochondrial respiration with malate-glutamate as substrate; 43–57% diminished striatum complex I activity with 60–71% decreased striatum mitochondrial NOS activity, determined both as biochemical activity and as functional activity; 34–40% increased rates of mitochondrial O2- and H2O2 productions and 36–46% increased contents of the products of phospholipid peroxidation and of protein oxidation; and 24% decreased striatum mitochondrial content, likely associated to decreased NO-dependent mitochondrial biogenesis
  • Rotenone-treated rats showed mitochondrial complex I syndrome associated with cellular oxidative stress in the dopaminergic brain areas of striatum and frontal cortex, a fact that describes the high sensitivity of mitochondrial complex I to inactivation by oxidative reactions
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