Disease relevance of PENTACHLORODIBENZOFURAN

• To quantify the toxicity of a mixture of three dioxin congeners, we calculated the new relative potencies (REPs) for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PeCDD), and 2,3,4,7,8- pentachlorodibenzofuran (PeCDF), focusing on their tumor promotion activity [1].

High impact information on PENTACHLORODIBENZOFURAN

• In summary, DNA microarray successfully identified dioxin-responsive genes expressed after exposure to AhR ligands (TCDD, PeCDF, PCB126) but not after exposure to the non-AhR ligand PCB153 [2].
• The aryl hydrocarbon receptor (AhR) ligands TCDD, PeCDF, and PCB126 produced very similar global gene expression profiles that were unique from the nonAhR ligand PCB153, underscoring the extensive impact of AhR activation and/or the resulting hepatic injury on global gene expression in female rat liver [2].
• Due to their anti-estrogenic capacity with benchmark-concentrations in the pM range TCDD, PCDF, and PCB126 may form a potential hazard for the reproductive success of fish species by inhibition of vitellogenesis [3].
• The slopes of the dose-responses for inhibition of ovulation generated by the individual PeCDF, PeCB, and/or their mixture with PCDDs were similar [4].
• The ovarian histology revealed that the effects of PeCDF, PeCB, and the mixture were very similar to those of PCDDs, consisting of ova in large preovulatory follicles and a lack of or reduced number of corpora lutea [4].

Chemical compound and disease context of PENTACHLORODIBENZOFURAN

• Relative toxicity and tumor-promoting ability of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PCDF), and 1,2,3,4,7,8-hexachlorodibenzofuran (HCDF) in hairless mice [5].

Biological context of PENTACHLORODIBENZOFURAN

• TCDD, PeCDF and PCB126 were administered daily to groups of rats at various doses, for 13 weeks, and biomarkers of oxidative stress, including the production of superoxide anion, lipid peroxidation and DNA-single strand breaks (SSBs), were determined in the hepatic and brain tissues at the end of the exposure period [6].

Anatomical context of PENTACHLORODIBENZOFURAN

• Exposure to TCDD, PCDF, and PCB-126 resulted in EC50 values of 0.4 to 8, 0.07 to 0.7, and 3 to 133 nM, respectively, which is in the same range as EC50 values found in primary hepatocytes of birds [7].

Gene context of PENTACHLORODIBENZOFURAN

• The 22 ng TEQ dose level (TEQ = 22) contains TCDD, PeCDF and PCB 126 at levels that correspond to 7.3, 14.5 and 73.3 ng kg(-1) day(-1), respectively, and it produced effects that correspond to ca. 50% of the maximal production of superoxide anion, lipid peroxidation and DNA SSBs in the hepatic and brain tissues of those animals [8].
• 2) In the simultaneous treatment of one of the five MSF-PCB congeners and PenCDF (3.9 ppb), TCDD (1.5 ppb) or Co-PenCB (8.8 ppb), the combination of 3-MSF-4,5,3',4'-TCB (6.8 ppb) or 4-MSF-2,5,2',3',5',6'-HCB and one of the three highly toxic chemicals significantly promoted the formation of SCEs [9].

References