The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Resveratrol inhibits TCDD-induced expression of CYP1A1 and CYP1B1 and catechol estrogen-mediated oxidative DNA damage in cultured human mammary epithelial cells
Open accessAbstract
Resveratrol (3,5,4'-trihydroxystilbene), a naturally occurring phytoalexin present in grapes and other foods, has been reported to possess chemopreventive effects as revealed by its striking inhibition of diverse cellular events associated with tumor initiation, promotion and progression. In our present study, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), when treated with the cultured human mammary epithelial (MCF-10A) cells, induced the expression of cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) that are responsible for the oxidation of 17beta-estradiol to produce catechol estrogens. Resveratrol strongly inhibited the TCDD-induced aryl hydrocarbon receptor (AhR) DNA binding activity, the expression of CYP1A1 and CYP1B1 and their catalytic activities in MCF-10A cells. It also reduced the formation of 2-hydroxyestradiol and 4-hydroxyestradiol from 17beta-estradiol by recombinant human CYP1A1 and CYP1B1, respectively. Furthermore, resveratrol significantly attenuated the intracellular reactive oxygen species (ROS) formation and oxidative DNA damage as well as the cytotoxicity induced by the catechol estrogens. Our data suggest that CYP1A1- and CYP1B1-catalyzed catechol estrogen formation might play a key role in TCDD-induced oxidative damage, and resveratrol can act as a potential chemopreventive against dioxin-induced human mammary carcinogenesis by blocking the metabolic formation of the catechol estrogens and scavenging the ROS generated during their redox cycling.
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Cites
Cancer chemopreventive activity of resveratrol, a natural product derived from grapes
Jang, M., Cai, L., Udeani, G. O., Slowing, K. V., Thomas, C. F., Beecher, C. W. W., Fong, H. H. S., Farnsworth, N. R., Kinghorn, A. D., Mehta, R. G., et al. (1997) · Science · doi:10.1126/science.275.5297.218 · Cited by 4,935
Cancer chemoprevention with dietary phytochemicals
Surh, Y.-J. (2003) · Nature reviews. Cancer · doi:10.1038/nrc1189 · Cited by 2,955
I NHIBITION OF C ARCINOGENESIS BY D IETARY P OLYPHENOLIC C OMPOUNDS
Yang, C. S., Landau, J. M., Huang, M.-T., & Newmark, H. L. (2001) · Annual Review of Nutrition · doi:10.1146/annurev.nutr.21.1.381 · Cited by 1,260
Inhibition of cancer growth by resveratrol is related to its low bioavailability
Asensi, M., Medina, I., Ortega, A., Carretero, J., Baño, M. C., Obrador, E., & Estrela, J. M. (2002) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(02)00911-5 · Cited by 388
Afaq, F., Adhami, V. M., & Ahmad, N. (2003) · Toxicology and Applied Pharmacology · doi:10.1016/s0041-008x(02)00014-5 · Cited by 262
Cited by
Surh, Y.-J., Kundu, J. K., Na, H.-K., & Lee, J.-S. (2005) · The Journal of Nutrition · doi:10.1093/jn/135.12.2993s · Cited by 363
Antioxidant Effects of Resveratrol in Cardiovascular, Cerebral and Metabolic Diseases
Carrizzo, A., Forte, M., Damato, A., Trimarco, V., Salzano, F., Bartolo, M., Maciag, A., Puca, A. A., & Vecchione, C. (2013) · Food and Chemical Toxicology · doi:10.1016/j.fct.2013.07.021 · Cited by 203
Dull, A.-M., Moga, M. A., Dimienescu, O. G., Sechel, G., Burtea, V., & Anastasiu, C. V. (2019) · Molecules · doi:10.3390/molecules24040667 · Cited by 141
Metadata
- Authors
- Chen, Z.-H.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-06-03
- Volume
- 25
- Issue
- 10
- Pages
- 2005-2013
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W2136175619
- Cited by
- 175
- References
- 5
- FWCI
- 7.46
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Chen, Z.-H. (2004). Resveratrol inhibits TCDD-induced expression of CYP1A1 and CYP1B1 and catechol estrogen-mediated oxidative DNA damage in cultured human mammary epithelial cells. Carcinogenesis. https://doi.org/10.1093/carcin/bgh183
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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