NDLI: 2,3,7,8-Tetrachlorodibenzo-p-dioxin causes an extensive alteration of 17 beta-estradiol metabolism in MCF-7 breast tumor cells.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin causes an extensive alteration of 17 beta-estradiol metabolism in MCF-7 breast tumor cells.

Isolation and characterization of a cDNA clone for the Cat2 gene in maize and its homology with other catalases. (Journal: Proceedings of the National Academy of Sciences of the United States of America Volume: 87 Issue: 17)

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2,3,7,8-Tetrachlorodibenzo-p-dioxin causes an extensive alteration of 17 beta-estradiol metabolism in MCF-7 breast tumor cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Spink, D. C. Dickerman, H. W. Gierthy, J. F. Lincoln, D. W.
Description	Author Affiliation: Spink DC ( Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201-0509.);
Abstract	MCF-7 breast tumor cells form multicellular foci in vitro when supplemented with 17 beta-estradiol (E2). In the presence of E2 and the aryl hydrocarbon-receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), MCF-7 cells grow to confluence but do not form foci. To investigate the role of E2 metabolism in this antiestrogenic effect of TCDD, analyses were performed by capillary GC/MS. The results revealed that pretreatment of MCF-7 cultures with TCDD (10 nM) rapidly depletes E2. In untreated cultures supplemented with 10 nM E2, the concentration of free E2 decreased to 4 nM in the first 12 hr, followed by a slower rate of decline. After 3 days most E2 in the medium was in conjugated form(s); 1.7 nM was present as free E2, and 2.9 nM was released by treatment with glucuronidase/sulfatase. In TCDD-treated cultures, E2 declined to 290 pM in 12 hr and after 2 days was not detected (less than 100 pM) either as free steroid or after treatment with glucuronidase/sulfatase. Intracellular E2 and estrone were likewise depleted by pretreatment with TCDD. Microsomes from TCDD-treated cells showed highly elevated aryl hydrocarbon-hydroxylase activity and catalyzed hydroxylations of E2 at C-2, C-4, C-15 alpha, and C-6 alpha with a combined rate of 0.85 nmol/min per nmol of cytochrome P-450 at saturating E2. These results suggest that depletion of E2 by enhanced metabolism accounts for the antiestrogenic activity of TCDD in MCF-7 cells.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	87
Language	English
Publisher	National Academy of Sciences
Publisher Date	1990-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dioxins Pharmacology Estradiol Metabolism Microsomes Aryl Hydrocarbon Hydroxylases Breast Neoplasms Cell Line Cytochrome P-450 Enzyme System Estrogens Isolation & Purification Gas Chromatography-Mass Spectrometry Hydroxylation Kinetics Drug Effects Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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