Based on the finding of decreased mitochondrial complex I activity in the s
ubstantia nigra of patients with Parkinson's disease, we propose that the c
onsequent reduction of ATP synthesis and increased generation of reactive o
xygen species may be a possible cause of nigrostriatal cell death. Since su
lfhydryl groups are essential in oxidative phosphorylation, thiolic antioxi
dants may contribute to the preservation of these proteins against oxidativ
e damage. In the present paper, we hypothesize that treatment with a sulfur
-containing antioxidant such as N-acetylcysteine may provide a new neuropro
tective therapeutic strategy for Parkinson's disease.