2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related congeners affect the immune system, causing immunosuppression and thymic atrophy in a variety of animal species. TCDD is believed to exert its effects primarily through the ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR). Although the AhR is found at high levels in both thymocytes and thymic stroma, it is uncertai...

Reproductive and developmental disorders are the most sensitive toxic effects caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is thought to produce many, if not all, of these toxic effects by impairing steroidogenesis and/or steroid action during the prenatal or early postnatal stages. However, the mechanism of the antisex steroid effect of TCDD is not well understood. This study rev...

Rainbow trout were fed a diet containing 1.8, 18, or 90 pg/g 3H-2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for up to 320 d. Concentrations of TCDD were determined in muscle, liver, and ovaries at 100, 150, 200, and 250 d. Concentrations of TCDD reached an apparent steady-state concentration in liver after 100 d of exposure, whereas concentrations in other tissues continued to increase until 150...

Using zebrafish embryos, we reported that 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) evoked circulation failure through activation of the aryl hydrocarbon receptor type 2 (AHR2). However, the following molecular target after AHR2 activation is largely unclear. It has been reported that TCDD induces cyclooxygenase 2 (COX2), a rate-limiting enzyme for prostaglandin synthesis in some cells. In this...

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant that induces various types of immunotoxicity. One effect of exposure to this contaminant is alteration in cell adhesiveness. Leukocyte function-associated antigen-1 (LFA-1) plays an important role not only in T-cell recruitment into sites of inflammation and lymphoid tissues, but also in T-cell activation and i...

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced toxicity is particularly striking in adipose tissue, where it causes severe wasting. This phenomenon suggests that TCDD could have effects on adipocyte differentiation, now demonstrated using 3T3-L1 cells as a model system. When cells were treated with 10 nM TCDD before differentiation or during the first two days of induction in the presence o...

Adult zebra fish completely regenerate their caudal (tail) fin following partial amputation. Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibits this regenerative process. Proper regulation of transcription, innervation, vascularization, and extracellular matrix (ECM) composition is essential for complete fin regeneration. Previous microarray studies suggest that genes involved in E...

The aryl hydrocarbon receptor (AhR) mediates the carcinogenicity of a family of environmental contaminants, the most potent being 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Increased incidence of lymphoma and leukemia in humans is associated with TCDD exposure. Although AhR activation by TCDD has profound effects on the immune system, precise cellular and molecular mechanisms have yet to be de...

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread industrial environmental contaminant. Animal studies suggest that TCDD exposure alters the estrus cycle. Twenty years after a 1976 industrial explosion in Seveso, Italy, the authors interviewed female residents to determine whether there was an association between TCDD exposure and current menstrual cycle characteristics. The authors an...

We have used human ovarian carcinoma BG-1 cells to determine which steps in the pathway of estrogen signaling are disrupted by the aryl hydrocarbon receptor (AhR) ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We report that inhibition of estrogen signaling occurs between 7 and 18 h after TCDD treatment and that this effect is not caused by a decrease in estradiol concentration. TCDD decrea...