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Titolo:
2,3,7,8-tetrachlorodibenzo-p-dioxin and diindolylmethanes differentially induce cytochrome P450 1A1, 1B1, and 19 in H295R human adrenocortical carcinoma cells
Autore:
Sanderson, JT; Slobbe, L; Lansbergen, GWA; Safe, S; van den Berg, M;
Indirizzi:
Univ Utrecht, Toxicol Res Inst, NL-3508 TD Utrecht, Netherlands Univ Utrecht Utrecht Netherlands NL-3508 TD 3508 TD Utrecht, Netherlands Texas A&M Univ, Dept Vet Physiol & Pharmacol, College Stn, TX 77843 USA Texas A&M Univ College Stn TX USA 77843 rmacol, College Stn, TX 77843 USA
Titolo Testata:
TOXICOLOGICAL SCIENCES
fascicolo: 1, volume: 61, anno: 2001,
pagine: 40 - 48
SICI:
1096-6080(200105)61:1<40:2ADDI>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
BREAST-CANCER CELLS; ACID REACTION-PRODUCTS; ESTROGEN METABOLISM; AROMATASE-ACTIVITY; MCF-7 CELLS; DIETARY INDOLE-3-CARBINOL; RECEPTOR AGONISTS; ESTRADIOL; RAT; 17-BETA-ESTRADIOL;
Keywords:
CYP1B1; CYP1A1; aromatase; CYP19; TCDD; diindolylmethane;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Sanderson, JT Univ Utrecht, Toxicol Res Inst, POB 80176, NL-3508 TD Utrecht, Netherlands Univ Utrecht POB 80176 Utrecht Netherlands NL-3508 TD lands
Citazione:
J.T. Sanderson et al., "2,3,7,8-tetrachlorodibenzo-p-dioxin and diindolylmethanes differentially induce cytochrome P450 1A1, 1B1, and 19 in H295R human adrenocortical carcinoma cells", TOXICOL SCI, 61(1), 2001, pp. 40-48

Abstract

Diindolylmethane (DIM) is an acid-catalyzed condensation product of indole-3-carbinol, a constituent of cruciferous vegetables, and is formed in the stomach. DIM alters estrogen metabolism and inhibits carcinogen-induced mammary tumor growth in rodents. DIM is a weak agonist for the aryl hydrocarbon (Ah) receptor acid blacks the effects of estrogens via inhibitory Ah receptor-estrogen receptor cross-talk. DIM and various structural analogs were examined in H295R cells for effects on 3 cytochrome P450 (CYP) enzymes involved in estrogen synthesis and/or metabolism: CYP1A1, CYP1B1, and CYP19 (aromatase). Aromatase activity was measured by conversion of 1 beta-H-3-androstenedione to estrone and (H2O)-H-3. H295R cells were exposed to the test chemicals dissolved in dimethyl sulfoxide for 24 h prior to analyses. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) (0-30 nM) and DIM (0-10 muM) induced ethoxyresorufin-O-deethylase (EROD) activity, as a measure of CYP1A1 and possibly 1B1 activity, with EC50 values of about 0.3 nM and 3 muM, respectively, DIM, but not TCDD, induced aromatase activity with an apparently maximal2-fold increase at 10 muM; higher concentrations of DIM and many of its analogs were cytotoxic. TCDD (30 nM) significantly increased CYP1A1 and 1B1 mRNA levels, but had no effect on mRNA for CYP19. DIM (3 muM) significantly increased mRNA levels for all three CYPs. DIM analogs with substitutions onthe 5 and 5' position (3 muM) induced aromatase and EROD activity, together with mRNA levels of CYP1A1, 1B1, and 19; analogs that were substituted onthe central carbon of the methane group showed little or no inductive activity toward the CYPs. In conclusion, DIM and several of its analogs appear to induce CYPs via multiple yet distinct pathways in H295R human adrenocortical carcinoma cells.

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Documento generato il 05/12/20 alle ore 19:53:53