Disease relevance of NCI-C56611

• TCDD and 2,3,7,8-tetrachlorodibenzofuran (TCDBF) showed the same toxicity to B6 thymuses with a 50% inhibition of lymphoid development (EC50) at 10(-10) M concentration [1].
• Insulin stimulated proliferation of MCF-7 human breast cancer cells in serum-free medium, whereas 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 2,3,7,8-tetrachlorodibenzofuran (TCDF) did not affect cell growth [2].
• Treatment of pregnant C57BL/6N mice with 2,3,7,8-tetrachlorodibenzofuran (TCDF) (0, 250, 500, and 1000 micrograms/kg on gestation day 10 or 0, 10, 30, 50, and 100 micrograms/kg on gestation days 10-13) results in dose-related increases in isolated cleft palates and hydronephrotic kidneys in the offspring [3].
• 2,3,7,8-Tetrachlorodibenzofuran (TCDBF) was administered in single doses (0.1-0.8 mg/kg body weight) intraperitoneally to pregnant C57BL mice on d 10, 11, 12, or 13 of gestation [4].

High impact information on NCI-C56611

• Binding of [3H]TCDD to the 9S component was competitively inhibited by incubation in the presence of 2,3,7,8-tetrachlorodibenzofuran, dibenz(a,h)anthracene, and nonradioactive TCDD, all known to be potent agonists for Ah-receptor-mediated induction of aryl hydrocarbon hydroxylase [5].
• The binding of estramustine to diluted prostatic cytosol was shown to be competitively inhibited by 2,3,7,8-tetrachlorodibenzofuran [6].
• Polychlorinated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzofuran (TCDF) have been shown to induce transcription of the cytochrome P-450IA1 gene by activating an intracellular receptor protein (the Ah- or dioxin receptor) to bind to specific DNA sequences, termed xenobiotic response elements (XREs) [7].
• Culture conditions allowing for cytochrome P-450IA1 induction by 2,3,7,8-tetrachlorodibenzofuran (TCDF) in normal human keratinocytes (HK) were investigated [8].
• The IC50 value for receptor binding of indolo[3,2-b]carbazole as well as for 2,3,7,8-tetrachlorodibenzofuran was 3.6 nM, whereas that of 5,6-benzoflavone was 26 nM [9].

Biological context of NCI-C56611

• Physiological model for the pharmacokinetics of 2,3,7,8-tetrachlorodibenzofuran in several species [10].
• The lack of correlation of 2,3,7,8-tetrachlorodibenzofuran and 3,3',4,4'-tetrachlorobiphenyl (PCB77) to CYP1A gene expression is likely due to the rapid metabolism of these two congeners [11].
• Dietary 2,3,7,8-tetrachlorodibenzofuran in rainbow trout: accumulation, disposition, and hepatic mixed-function oxidase enzyme induction [12].
• 2,3,7,8-Tetrachlorodibenzofuran tissue distribution and excretion in guinea pig [13].
• The comparison between measured and estimated values showed that the present modeling approach represented the background levels of congeners in the environment, daily intake, and body burden reasonably well, except for in the case of 2,3,7,8-TCDF [14].

Anatomical context of NCI-C56611

• Characterization of 2,3,7,8-tetrachlorodibenzofuran-dependent suppression and AH receptor pathway gene expression in the developing mouse mammary gland [15].
• 2,3,7,8-Tetrachlorodibenzofuran (TCDF) induced CYP1A1 mRNA, protein, and activity in SC fish in all tissues examined (liver, heart, gut, gill, kidney, spleen, and gonad) [16].
• 0. The binding capacity for 1.5 nM [3H]TCDD in the leukocyte cytosol was completely saturated by incubation in the presence of 150 nM unlabelled 2,3,7,8-tetrachlorodibenzofuran [17].
• 2,3,7,8-Tetrachlorodibenzofuran (TCDBF) and 3,3',4,4'-tetrachloroazoxybenzene (TCAOB) were added together to the thymus organ culture, each at a concentration that caused about 25-50% lymphoid development inhibition [18].
• The effect of exposure time on the induction of 7-ethoxyresorufin O-deethylase (EROD) by 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7,8-tetrachlorodibenzofuran (TCDF), and 3,3',4, 4'-tetrachlorobiphenyl (PCB 77) was examined in two liver cell lines: rainbow trout RTL-W1 and rat H4IIE [19].

Associations of NCI-C56611 with other chemical compounds

• 2,3,7,8-Tetrachlorodibenzofuran (2,3,7,8-TCDF), 1,2,3,7,8-pentachlorodibenzofuran (1,2,3,7,8-PCDF) and 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PCDF) showed the highest AHH inducing activity among the PCDF isomers tested [20].
• Scup were injected ip with 3,3',4,4'-tetrachlorobiphenyl (TCB) at 1 mg/kg, or with 2,3,7,8-tetrachlorodibenzofuran (TCDF) at 3 micrograms/kg [21].
• Studies were performed to investigate the effects of 2,3,7,8-tetrachlorodibenzofuran (TCDF) on immune function in adult Hartley guinea pigs [22].
• PCB 153, 138, 118 and 101 were the dominant congeners observed in fish product samples studied, while 1,2,3,7,8-pentachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran contributed the most to total PCDD and PCDF loadings [23].

Gene context of NCI-C56611

• Dioxin-labeled PSP was then incubated with rat liver cytosol in the presence or absence of a 200-fold excess of nonradioactive competitor, 2,3,7,8-tetrachlorodibenzofuran [24].
• Following administration of [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin or unlabelled 2,3,7,8-tetrachlorodibenzofuran to C57 BL/6 mice or Sprague-Dawley rats these compounds were bound to lipoproteins which subsequently underwent rapid and pronounced degradative processing, possibly catalysed by lipoprotein lipase, to heavier entities [25].
• In an effort to determine whether environmental chemicals at the two sites might contribute to altered P-gp expression, depurated fish were exposed either to sediment collected from SC or 2,3,7,8-tetrachlorodibenzofuran, a contaminant found at the NBH site and a model aryl hydrocarbon receptor agonist [26].

Analytical, diagnostic and therapeutic context of NCI-C56611

• Radioimmunoassay for quantitation of 2,3,7,8-tetrachlorodibenzofuran [27].
• The amounts of PCDD and PCDF congeners in rats on day 5 administered dioxin mixtures were lower in the 0.01% chlorophyll group than in the control group, ranging from 3.5 to 50.0% for PCDD congeners and from 3.7 to 41.7% lower for PCDF congeners, except for 2,3,7,8-tetrachlorodibenzofuran [28].

References