| dc.description.abstract | Dioxins have historically been known to cause adverse health effects in humans1. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin), is a byproduct of forest fires, waste incineration, automobile exhaust, cigarette smoke, and other combustion processes2. While TCDD is a known teratogen, it has also been linked to lowered sperm counts in male rats3, cleft palate formation during embryogenesis4, and kidney blockage2. To better understand the teratogenic effects of dioxin, we studied its effect on cardiogenesis. By collecting embryonic hearts from various mouse strains, we investigated potential links between prenatal TCDD exposure and the expression of major genes involved in cardiogenesis. Embryonic hearts were dissected from mice that were prenatally exposed to 0, 1, or 100 ng/kg per day of dioxin. Preliminary data shows significant strain-dependent differences in expression of master regulator genes, such as GATA4. We also see delayed expression of other downstream genes involved in heart development that have been known to cause congenital heart defects. | en |
