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Transplacental carcinogenesis with dibenzo[def,p]chrysene (DBC): timing of maternal exposures determines target tissue response in offspring.
|Title||Transplacental carcinogenesis with dibenzo[def,p]chrysene (DBC): timing of maternal exposures determines target tissue response in offspring.|
|Publication Type||Journal Article|
|Year of Publication||2012|
|Authors||Shorey LE, Castro DJ, Baird WM, Siddens LK, Löhr CV, Matzke MM, Waters KM, Corley RA, Williams DE|
|Date Published||2012 Apr 1|
|Keywords||Animals, Aryl Hydrocarbon Hydroxylases, Benzopyrenes, Carcinogens, Female, Fetus, Gene Expression Regulation, Developmental, Gene Expression Regulation, Enzymologic, Gestational Age, Male, Maternal Exposure, Maternal-Fetal Exchange, Mice, Mice, 129 Strain, Neoplasms, Experimental, Placental Circulation, Pregnancy, Prenatal Exposure Delayed Effects, Time Factors, Tissue Distribution|
Dibenzo[def,p]chrysene (DBC) is a transplacental carcinogen in mice (15mg/kg; gestation day (GD) 17). To mimic residual exposure throughout pregnancy, dams received four smaller doses of DBC (3.75mg/kg) on GD 5, 9, 13 and 17. This regimen alleviated the previously established carcinogenic responses in the thymus, lung, and liver. However, there was a marked increase in ovarian tumors (females) and hyperplastic testes (males). [(14)C]-DBC (GD 17) dosing revealed transplacental distribution to fetal tissues at 10-fold lower concentrations than in paired maternal tissue and residual [(14)C] 3weeks post-dose. This study highlights the importance of developmental stage in susceptibility to environmental carcinogens.
|Alternate Journal||Cancer Lett.|