ArticleJournal of neural transmission (Vienna, Austria : 1996)2010
No increased chromosomal damage in L-DOPA-treated patients with Parkinson's disease: a pilot study.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- Oxidative stress-related biomarkers in Parkinson's disease: A systematic review and meta-analysis.Iranian journal of neurology · 2018Review
- Evaluation of levodopa and carbidopa antioxidant activity in normal human lymphocytes in vitro: implication for oxidative stress in Parkinson's disease.Neurotoxicity research · 2015Article
- Oxidative damage to macromolecules in human Parkinson disease and the rotenone model.Free radical biology & medicine · 2013Review
- Oxidized extracellular DNA as a stress signal in human cells.Oxidative medicine and cellular longevity · 2013Review
- Chiral capillary electrophoresis-mass spectrometry of 3,4-dihydroxyphenylalanine: evidence for its enantioselective metabolism in PC-12 nerve cells.Analytical biochemistry · 2011Article
- The role of the dopamine transporter in dopamine-induced DNA damage.Brain pathology (Zurich, Switzerland) · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a neurodegenerative movement disorder affecting about 2% of the human population in old age. L-3,4-Dihydroxyphenylalanine (L-DOPA) in combination with a peripheral aromatic amino acid decarboxylase inhibition has been the most frequently prescribed drug for alleviating symptoms of PD, but a potential contribution of L-DOPA therapy to further neurodegeneration via oxidative stress is still debated. We report that the specific oxidative stress biomarker 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) level in peripheral blood lymphocyte DNA was elevated to 8.1 +/- 1.7 8-oxodG/10(6)dG in 17 chronically L-DOPA-treated PD patients, compared to 4.6 +/- 1.2 8-oxodG/10(6)dG in 12 controls. However, the total antioxidative capacity of plasma was increased to 1113 +/- 237 microM in the PD patients compared to 941 +/- 254 microM in controls. The frequency of micronuclei, a subgroup of chromosomal aberrations, in peripheral blood lymphocytes was not elevated compared to healthy age-matched individuals. In vitro, in a cell-free assay, dopamine and its precursor L-DOPA exhibited antioxidative capacity. On the other hand, the 8-oxodG concentration in cultured PC 12 cells was enhanced after dopamine treatment. This elevation may be below a threshold for manifestation as chromosomal damage.
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Registered trials
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