ArticleIUBMB life2011
Formation of dopamine quinone-DNA adducts and their potential role in the etiology of Parkinson's disease.
Article in IUBMB life, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 42 citations in OpenAlex.
- Aminochrome-Induced Disruption of Autophagosome-Lysosome Fusion: Implications for Protein Aggregation in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Synthesis and Characterization of Chemically Stable N7-dG Estrone and Catechol Adducts.Molecules (Basel, Switzerland) · 2026Article
- Neuroprotective Properties of Quinone Reductase 2 Inhibitor M-11, a 2-Mercaptobenzimidazole Derivative.International journal of molecular sciences · 2021Article
- Calcium, Bioenergetics, and Parkinson's Disease.Cells · 2020Review
- Chemical Reactivities ofInternational journal of molecular sciences · 2020Review
- Formation and Biological Targets of Quinones: Cytotoxic versus Cytoprotective Effects.Chemical research in toxicology · 2017Article
- Oxidative and nitrative stress in neurodegeneration.Neurobiology of disease · 2015Review
- Induction of NQO1 and Neuroprotection by a Novel Compound KMS04014 in Parkinson's Disease Models.Journal of molecular neuroscience : MN · 2015Article
- Plant-derived neuroprotective agents in Parkinson's disease.American journal of translational research · 2015Review
- The vesicular monoamine transporter 2: an underexplored pharmacological target.Neurochemistry international · 2014Review
- The molecular etiology and prevention of estrogen-initiated cancers: Ockham's Razor: Pluralitas non est ponenda sine necessitate. Plurality should not be posited without necessity.Molecular aspects of medicine · 2014Review
- Vesicular integrity in Parkinson's disease.Current neurology and neuroscience reports · 2013Review
- Imbalanced estrogen metabolism in the brain: possible relevance to the etiology of Parkinson's disease.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2011Article
- Unbalanced metabolism of endogenous estrogens in the etiology and prevention of human cancer.The Journal of steroid biochemistry and molecular biology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The neurotransmitter dopamine is oxidized to its quinone (DA-Q), which at neutral pH undergoes intramolecular cyclization by 1,4-Michael addition, followed by oxidation to form leukochrome, then aminochrome, and finally neuromelanin. At lower pH, the amino group of DA is partially protonated, allowing the competitive intermolecular 1,4-Michael addition with nucleophiles in DNA to form the depurinating adducts, DA-6-N3Ade and DA-6-N7Gua. Catechol estrogen-3,4-quinones react by 1,4-Michael addition to form the depurinating 4-hydroxyestrone(estradiol)-1-N3Ade [4-OHE1(E2)-1-N3Ade] and 4-OHE1(E2)-1-N7Gua adducts, which are implicated in the initiation of breast and other human cancers. The effect of pH was studied by reacting tyrosinase-activated DA with DNA and measuring the formation of depurinating adducts. The most adducts were formed at pH 4, 5, and 6, and their level was nominal at pH 7 and 8. The N3Ade adduct depurinated instantaneously, but N7Gua had a half-life of 3 H. The slow loss of the N7Gua adduct is analogous to that observed in previous studies of natural and synthetic estrogens. The antioxidants N-acetylcysteine and resveratrol efficiently blocked formation of the DA-DNA adducts. Thus, slightly acidic conditions render competitive the reaction of DA-Q with DNA to form depurinating adducts. We hypothesize that formation of these adducts could lead to mutations that initiate Parkinson's disease. If so, use of N-acetylcysteine and resveratrol as dietary supplements may prevent initiation of this disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.