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.
Martínez
M
M
Departamento de Anatomía Patológica, Hospital Universitario La Paz, Madrid, Spain.
Martínez
N
N
Hernández
A I
AI
Ferrándiz
M L
ML
D000111:Acetylcysteine / Q000627:therapeutic use*; D000255:Adenosine Triphosphate / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008928:Mitochondria / Q000201:enzymology; D008959:Models, Neurological; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use; D010085:Oxidative Phosphorylation; D010300:Parkinson Disease / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D017382:Reactive Oxygen Species; D013378:Substantia Nigra / Q000378:metabolism / Q000473:pathology
D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D016660:NAD(P)H Dehydrogenase (Quinone); D000111:Acetylcysteine