2,3,7,8-Tetrachlorodibenzo-p-dioxin solution 10 μg/mL …
Stanton, R. J., S. Watkins, J. B. German, AND B. L. Lasley. INTERACTION OF ESTROGEN AND 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (TCDD) WITH HEPATIC FATTY ACID SYNTHESIS AND METABOLISM OF MALE CHICKENS (GALLUS DOMESTICUS). (R826298). COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY. Allen Press, Inc., Lawrence, KS, 129(2):137-150, (2001).
2,3,7,8-Tetrachlorodibenzo-p-dioxin: A Potent Inducer …
Man-Technology-Environment (MTM) Research Center, Örebro University,
The Separation Of 2,3,7,8-Substituted Polychlorinated Dibenzo-P-Dioxins And Polychlorinated Dibenzofurans Using Supercritical Fluid Chromatography.
College of Pharmacy, Yeungnam University, Kyongsan, Korea
Role of Cell Cycle Regulators in Neurotoxic Effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin
2,3,7,8-Tetrachlorodibenzo- p -dioxin inhibits ..
N2 - We have examined the molecular mechanisms for 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD)-stimulated prostaglandin synthesis in Mardin Darvey canine kidney cells (MDCK). TCDD stimulates prostaglandin synthesis in these cells, at least in part, by elevating prostaglandin endoperoxide H2 synthase-2 (PGHS-2) levels. TCDD-stimulated transcription of the PGHS-2 gene was maximal (6-fold) within 2 h and resulted in a 100-fold increase in PGHS-2 mRNA and a 25-fold increase in PGHS-2 protein levels by 4 h. Transient transfection experiments using luciferase-reporter plasmids demonstrated that control element(s) responsible for TCDD activation of the murine PGHS-2 promoter in MDCK cells are located in the first 965 nucleotides upstream from the PGHS-2 transcriptional initiation site. A canonical xenobiotic response element, similar to those that control transcription of other well-known TCDD- sensitive genes, is present at position -157, but does not appear to be sufficient for halogenated aromatic hydrocarbon (HAH) activation of the PGHS- 2 promoter. TCDD failed to stimulate transcription from the PGHS-2 promoter when reporter plasmids were transfected into Hepa 1c1c7 cells, a line which contains the functional aryl hydrocarbon receptor. It seems likely that inappropriate expression of PGHS-2 may contribute to the toxic effects of TCDD and other HAHs. In particular, PGHS-2 expression may affect those toxic reactions that involve inappropriate cellular growth, such as dermal hyperplasia and tumor formation. It is also likely that elevated synthesis of prostaglandins, which are potent regulators of immune function, could play a role in the immunotoxicity associated with HAH exposure.
2,3,7,8-Tetrachlorodibenzodioxin - mobile Wiki
N2 - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) decreased the binding of epidermal growth factor (EGF) by the human keratinocyte cell line SCC-12F. This response was concentration dependent (half-maximal effective concentration, EC50 = 1.8 nm) and stereospecific. Scatchard analysis of EGF binding indicated that treatment with TCDD resulted in a loss of high-affinity (Kd = 0.28 nm) binding sites. This loss was accompanied by a concomitant inhibition of EGF-stimulated DNA synthesis. The kinetics for the decrease of EGF binding by TCDD and benzo[a]pyrene (BP) were compared. Inhibition of EGF binding by BP was maximal by 24 hr, with 90% recovery of EGF binding apparent by 48 hr. In contrast, TCDD treatment for 72 hr was required to produce maximal inhibition, and no recovery was evident up to 10 day after removal of TCDD from the growth medium. The data indicate that modulation of EGF binding by TCDD was mediated by the Ah receptor. Subsequent cellular responses, for example, inhibition of EGF-stimulated DNA synthesis, may be important in the expression of altered differentiation patterns observed in human epidermal keratinocytes exposed to TCDD.
2,3,7,8-Tetrachlorodibenzo-p-dioxin - Alfa Chemistry
However, a good example of a non-genotoxic carcinogen for which there is a good biomarker of effect is 2,3,7,8-tetrachlorinated dibenzo- p-dioxin (TCDD).