No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease.
Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. Serum concentrations of two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.
Ahlskog
J E
JE
Department of Neurology, Mayo Clinic Rochester, Minnesota 55905, USA.
Uitti
R J
RJ
Low
P A
PA
Tyce
G M
GM
Nickander
K K
KK
Petersen
R C
RC
Kokmen
E
E
D000368:Aged; D000544:Alzheimer Disease / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D000978:Antiparkinson Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001921:Brain / Q000378:metabolism*; D000077465:Cabergoline; D002230:Carbidopa / Q000008:administration & dosage / Q000627:therapeutic use; D003920:Diabetes Mellitus / Q000097:blood / Q000378:metabolism; D004873:Ergolines / Q000008:administration & dosage / Q000627:therapeutic use; D005260:Female; D005609:Free Radicals; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage / Q000627:therapeutic use; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D018384:Oxidative Stress; D010300:Parkinson Disease / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D012642:Selegiline / Q000008:administration & dosage / Q000627:therapeutic use; D014810:Vitamin E / Q000008:administration & dosage / Q000627:therapeutic use
D000978:Antiparkinson Agents; D004873:Ergolines; D005609:Free Radicals; D014810:Vitamin E; D012642:Selegiline; D007980:Levodopa; D008315:Malondialdehyde; D000077465:Cabergoline; D002230:Carbidopa