Aim: Oxidative stress (OS) is defined as an imbalance between oxidants and antioxidants in favor of the oxidants, and the disruption of redox signaling leads to molecular damages. This study was conducted to clarify the effect of OS in individual follicular fluid (FF) on oocyte fertilization and embryonic division. Methods: A total of 124 patients who underwent assisted reproductive technology treatment in our hospital underwent intracytoplasmic sperm injection and 211 FF were collected. The ova were fertilized, and embryos were individually cultured until cleavage stage or blastocyst stage and classified according to the Veeck classification system or Gardner classification system. Results: The follicular fluid corresponding to the ovum was analyzed by measuring the OS marker, the reactive oxygen metabolites (d-ROM test), and the antioxidant marker (biological antioxidant potential marker [BAP] test), and the relation between these markers and clinical parameters was analyzed. The value of d-ROM was correlated with the proper fertilization status and formation of good quality cleavage embryo, whereas the elevated value of BAP was observed in better embryonic development group. Oxidative stress index, defined as d-ROM/BAP × 100 clearly indicated that lower oxidative stress index was associated with better fertilization status and embryo development. Conclusion: Our results clearly indicate that the balance between OS and antioxidant capacity in FF at the time of oocyte retrieval is possibly important in the processes of fertilization and embryo division; thus, we propose that oxidative status and balance in FF might be used as novel biomarkers in assisted reproductive technology.

Ulipristal (UPA), a selective progesterone receptor modulator, has both agonistic and antagonistic effects on progesterone receptors. UPA suppresses ovulation by inhibiting the luteinizing hormone (LH) surge from the pituitary gland; however, the direct effect of UPA on ovarian tissue remains poorly studied. In the present study, we examined the effects of UPA on the ovaries of rats. Rats were treated for 28 d with 4, 20, and 100 mg/kg UPA. UPA treatment increased the number of primordial follicles at each treatment group, with the highest number found in the 4 mg/kg group, and the number of primordial follicles decreasing with increasing dose. The number of primary and antral follicles tended to increase with increasing UPA levels. Furthermore, the decrease in primary follicle number could be attributed to the exhaustion of follicles, but the examination of proliferation markers, oxidative stress markers, and cell death markers revealed no remarkable toxic effects on ovarian tissues. These results suggest that UPA treatment promotes follicle development at each stage but inhibits ovulation by suppressing the LH surge, resulting in an increase in atretic follicles or unruptured luteinized cysts. UPA may not have toxic effects on the ovary because the expression of antioxidant genes and cell death markers was not dramatic in follicles treated with UPA. Taken together, these results suggest that UPA may not have a direct local effect on ovarian follicles. Hence, we hypothesized that prolonged UPA treatment in patients with uterine fibroids may not be harmful and may not decrease future fecundity.