||Health Effects Research Lab., Research Triangle Park, NC. Perinatal Toxicology Branch. ;Purdue Univ., Lafayette, IN. Dept. of Foods and Nutrition. ;ManTech Environmental Technology, Inc., Research Triangle Park, NC.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant the produces adverse biological effects including carcinogenesis, reproductive toxicity, immune dysfunction, hyperderatosis, hepatotoxicity, thymic involution, and teratogenesis. The present study examines the expression of Ah receptor (AhR) and glucocorticoid receptor (GR) in the embryonic palate following exposure to TCDD, hydrocortison (HC), and HC + TCDD. C57BL/6N pregnant mice were treated with HC (25 or 100 mg/kg/day GD10-13, sc), TCDD (3 microgram/kg/day GD10-13, or 23 microgram/kg GD10, orally), or HC + TCDD (25 mg/kg/day SC and 3 microgram/kg/day orally, GD10-13). Craniofacial tissues were collected from the embryos on GD14 and examined for AhR and GR expression using in situ hybridization, Northern blots, and immunohistochemistry. The authors found that in the embryonic palate exposed to TCDD, the AhR was downregulated and the GR expression increased. Conversely, following HC exposure, the GR was downregulated and AhR levels were elevated. HC + TCDD produced increased expression of both receptors. Effects on AhR appeared to be regulated at the transcriptional level, as both protein and mRNA were altered in similar directions.