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The mammalian ovary is comprised of follicles at various stages of growth and is responsible for gamete and steroid hormone production. Conservation of ovarian function is vital for female reproductive and general health, and disruption can lead to infertility and/or ovarian senescence. Stressors affect the ovary by inflicting damage to the primordial oocyte and/or inducing follicular activation thereby depleting the follicular reserve and disrupting biological pathways or defense mechanisms necessary for maintaining proper ovarian function. Cyclophosphamide (CPA) is a chemotherapy drug that biotransforms into an ovotoxic metabolite phosphoramide mustard (PM) via hepatic biotransformation. Our previous findings demonstrated that PM (60 μM) exposure depleted primordial follicles as well as all follicle types in cultured postnatal day (PND) 4 rat ovaries. With the advancement of science and medicine, there has been a decline in mortality rates of females who receive chemotherapy. The viability and health of the ovary post-chemotherapy treatment is of major concern for female cancer survivors due to the harsh effects of anti-neoplastic agents. An ovarian defensive mechanism would challenge the adverse effects of PM-induced ovotoxicity. We hypothesized that the ovarian defense response to PM-induced damage involves both the ABCB1 and ABCC1 proteins to excrete PM from the ovary and that their regulation involved the PI3K pathway. ABCB1 and ABCC1 are involved phase III chemical biotransformation, having enzymatic activity that requires ATP derived energy for the transportation of endogenous and exogenous compounds. Briefly, PND4 rat ovaries were cultured in PM (60 μM), LY294002 (20 μM), or vehicle control (1% DMSO) followed by protein isolation and western blotting. Adult

Phase III biotransformation enzyme involvement in the ovarian response to ovotoxic environmental exposures