0000000000483076
AUTHOR
Natividad Martı́nez
Hypothesis: can N-acetylcysteine be beneficial in Parkinson's disease?
Based on the finding of decreased mitochondrial complex I activity in the substantia nigra of patients with Parkinson's disease, we propose that the consequent reduction of ATP synthesis and increased generation of reactive oxygen species may be a possible cause of nigrostriatal cell death. Since sulfhydryl groups are essential in oxidative phosphorylation, thiolic antioxidants may contribute to the preservation of these proteins against oxidative damage. In the present paper, we hypothesize that treatment with a sulfur-containing antioxidant such as N-acetylcysteine may provide a new neuroprotective therapeutic strategy for Parkinson's disease.
N-acetylcysteine protects against age-related increase in oxidized proteins in mouse synaptic mitochondria.
Since it has been proposed that oxidized protein accumulation plays a critical role in brain aging, we have investigated the effect of a thiolic antioxidant on protein carbonyl content in synaptic mitochondria from female OF-1 mice. At 48 weeks of age, a control group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of N-acetylcysteine. A 24-week treatment resulted in a significant decrease in protein carbonyl content in synaptic mitochondria of the N-acetylcysteine-treated animals as compared to age-matched controls.