ArticleFree radical biology & medicine2011
Resveratrol and N-acetylcysteine block the cancer-initiating step in MCF-10F cells.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Resveratrol as a Promising Nutraceutical: Implications in Gut Microbiota Modulation, Inflammatory Disorders, and Colorectal Cancer.International journal of molecular sciences · 2024Review
- The 3,4-Quinones of Estrone and Estradiol Are the Initiators of Cancer whereas Resveratrol andInternational journal of molecular sciences · 2021Review
- Activity of Combinations of Antioxidants and Anthelmintic Drugs against the Adult Stage ofJournal of parasitology research · 2020Article
- Inhibition of the Formation In Vitro of Putatively Carcinogenic Metabolites Derived fromMolecules (Basel, Switzerland) · 2019Article
- The antioxidants resveratrol and N-acetylcysteine enhance anthelmintic activity of praziquantel and artesunate against Schistosoma mansoni.Parasites & vectors · 2019Article
- Combination Anthelmintic/Antioxidant Activity AgainstBiomolecules · 2019Article
- Dissecting the prevention of estrogen-dependent breast carcinogenesis through Nrf2-dependent and independent mechanisms.OncoTargets and therapy · 2019Review
- Drug Repurposing for Schistosomiasis: Combinations of Drugs or Biomolecules.Pharmaceuticals (Basel, Switzerland) · 2018Review
- A Review of Resveratrol as a Potent Chemoprotective and Synergistic Agent in Cancer Chemotherapy.Frontiers in pharmacology · 2018Review
- Etiology and prevention of prevalent types of cancer.Journal of rare diseases research & treatment · 2017Article
- Depurinating estrogen-DNA adducts, generators of cancer initiation: their minimization leads to cancer prevention.Clinical and translational medicine · 2016Review
- Associations between Dietary Intake of Fruits and Vegetables in relation to Urinary Estrogen DNA Adduct Ratio.Open journal of preventive medicine · 2014Article
- SERMs attenuate estrogen-induced malignant transformation of human mammary epithelial cells by upregulating detoxification of oxidative metabolites.Cancer prevention research (Philadelphia, Pa.) · 2014Article
- 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
- Multi-nutrient supplement improves hormone ratio associated with cancer risk.Journal of translational medicine · 2013Article
- CD44 is associated with the aggressive phenotype of nasopharyngeal carcinoma through redox regulation.International journal of molecular sciences · 2013Article
- The etiology and prevention of breast cancer.Drug discovery today. Disease mechanisms · 2012Article
- Hops (Humulus lupulus) inhibits oxidative estrogen metabolism and estrogen-induced malignant transformation in human mammary epithelial cells (MCF-10A).Cancer prevention research (Philadelphia, Pa.) · 2012Article
- Formation of dopamine quinone-DNA adducts and their potential role in the etiology of Parkinson's disease.IUBMB life · 2011Article
- Resveratrol enhances the cytotoxic profile of docetaxel and doxorubicin in solid tumour cell lines in vitro.Cell proliferation · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Substantial evidence suggests that catechol estrogen-3,4-quinones react with DNA to form predominantly the depurinating adducts 4-hydroxyestrone (estradiol)-1-N3Ade [4-OHE(1)(E(2))-1-N3Ade] and 4-OHE(1)(E(2))-1-N7Gua. Apurinic sites resulting from these adducts generate critical mutations that can initiate cancer. The paradigm of cancer initiation is based on an imbalance in estrogen metabolism between activating pathways that lead to estrogen-DNA adducts and deactivating pathways that lead to estrogen metabolites and conjugates. This imbalance can be improved to minimize formation of adducts by using antioxidants, such as resveratrol (Resv) and N-acetylcysteine (NAcCys). To compare the ability of Resv and NAcCys to block formation of estrogen-DNA adducts, we used the human breast epithelial cell line MCF-10F treated with 4-OHE(2). Resv and NAcCys directed the metabolism of 4-OHE(2) toward protective pathways. NAcCys reacted with the quinones and reduced the semiquinones to catechols. This pathway was also carried out by Resv. In addition, Resv induced the protective enzyme quinone reductase, which reduces E(1)(E(2))-3,4-quinones to 4-OHE(1)(E(2)). Resv was more effective at increasing the amount of 4-OCH(3)E(1)(E(2)) than NAcCys. Inhibition of estrogen-DNA adduct formation was similar at lower doses, but at higher doses Resv was about 50% more effective than NAcCys. Their combined effects were additive. Therefore, these two antioxidants provide an excellent combination to protect catechol estrogens from oxidation to catechol quinones.
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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.