The long-term objective of our laboratory research is to elucidate the molecular mechanism of ovulation, the process of egg release from the ovary. The program of ovulation is activated by a surge of pituitary luteinizing hormone that initiates dramatic changes in molecular, biochemical, and physical events in the ovary, eventually expelling eggs from the ovary. Ovulatory failure has been associated with the development of numerous ovarian disorders such as polycystic ovarian syndrome (PCOS), hemorrhagic cyst formation, hormonal imbalance and infertility, all of which are major risk factors for women’s health. My laboratory’s current research is focusing on the following areas: endothelin system in ovulation and luteal function, steroids and prostaglandins in leukocyte trafficking, steroid receptors in PCOS pathogenesis and reproductive aging. We generate transgenic animal models and used them for those projects. Once noble findings are made from the animal studies, molecular mechanisms behind are sought using in vitro experiments. Routinely applied skills/approaches include but not limited to tissue specific gene targeting, microsurgery, organ transplantation, fertility test, histology, immunohistochemistry, hormone assays, DNA microarray, real-time PCR, tissue culture, and bioinformatics. The ultimate research goal of our lab is to help women who suffer from reproductive disorders and to develop safe and effective contraceptive strategies for humans and animals.


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Prenatal exposure to DEHP induces premature reproductive senescence in male mice  
(Barakat et al., 2017 Toxicological Science)

Di-(2-ethylhexyl) phthalate (DEHP) is the most commonly used phthalate, and it is an endocrine-disrupting chemical. This study tested a hypothesis that prenatal exposure to DEHP lays the foundation for premature gonadal dysfunction and subsequent reproductive senescence in male mice. Pregnant female CD-1 mice were orally dosed with vehicle control (tocopherol-stripped corn oil) or with 20 μg/kg/day, 200 μg/kg/day, 500 mg/kg/day or 750 mg/kg/day of DEHP from gestational day 11 to birth. Overall, the prenatal DEHP exposure did not cause any overt physical health problems in male offspring, as no significant differences in their body nor gonadal weight were seen up to the age of 23 months. However, an age- and dose-dependent gonadal dysfunction was observed. As early as 7 months of age, the 750 mg/kg/day group of mice exhibited significantly reduced fertility. At 19 months of age, 86% of the 750 mg/kg/day mice became infertile, whereas only 25% of the control mice were infertile. At this age, all of the DEHP-exposed mice had lower serum testosterone levels, higher serum estradiol levels, and higher LH levels compared to control mice. Histological evaluations showed that mice prenatally exposed to DEHP displayed a wide array of gonadal and epididymal abnormalities such as increased germ cell apoptosis, degenerative seminiferous tubules, oligozoospermia, asthenozoospermia, and teratozoospermia in comparison to age-matching control mice. In summary, this study shows that prenatal exposure to DEHP induces premature reproductive senescence in male mice.