Retinoic acid (RA) is an active metabolite of vitamin A (VA) and is involved in tissue organization, patterning, and growth. RA has been shown to regulate male reproduction, however information on its role in ovary development is limited. To investigate the functions of RA in the ovary, we examined its role in ovary development and ovulation using an in vivo dietary VA-deprivation animal model. Our preliminary results have shown that VA deficiency causes a variety of ovarian pathologies, including reduced numbers of total follicles and corpus lutea, formation of hemorrhagic and atretic follicles, and formation of bursa and follicular cysts. To further examine if the reduced numbers of corpus lutea represents a defect in ovulation, in this study, we investigated the effect of VA deficiency on ovulation. We fed CD-1 pregnant mice with either a VA deficient diet (VA-) or a control diet, and at weaning, female pups were maintained on their respective diet. These female pups were then induced super-ovulation at day 19 (D19) or week 7 (Wk7) via subcutaneous injection of pregnant mare’s serum gonadotropins (PMSG) followed by human chorionic gonadotropin (hCG) 48 hours later. Oviducts from these animals were collected 14-16 hours later and ovulated oocytes in the oviducts were counted and scored. Our preliminary data showed that although the total numbers of ovulated oocytes were similar in the control and VA- groups at day 19, VA- mice responded poorly to super-ovulation at week 7. Overall, our study suggests that vitamin A is critical for ovary development and ovulation.
"Vitamin A Deficiency Causes Ovulation Abnormalities in Mice,"
1, Article 4.
Available at: http://via.library.depaul.edu/depaul-disc/vol3/iss1/4