In many mammalian species, including humans, folliculogenesis begins in fetal life and progresses throughout adulthood. The growing follicles progress from a reserve of primordial follicles that constitute the pool of female gametes for the entire life. Primordial follicles may begin to grow either immediately after forming or at clearly defined species-specific gap. Alternatively, some follicles may become quiescent before they either degenerate or resume growth several months or years afterwards. The rate of follicular assembly and the primordial to primary follicle transition is a critical step in female fertility. Therefore, disturbed coordination of the formation of primordial follicles and activation of their growth may entail some reproductive disorders. A poor initial reserve or the precocious primordial follicle depletion will result in infertility that, in women, is escorted by a shortened reproductive lifespan and early menopause. Therefore, it seems necessary to reach a profounder understanding of the molecular and cellular mechanisms controlling follicular development during preantral transition. In vitro growth of isolated immature ovarian follicles (IVGF) appears as an emerging technology, allowing to expand the fertility options in particular ovarian disorders or after cancer treatment
Part of the book: Insights from Animal Reproduction
Androgens, steroid hormones produced by follicular cells, play a crucial role in the regulation of ovarian function. They affect folliculogenesis directly through androgen receptors (ARs) or indirectly through aromatization to estrogens. Androgens are thought to be primarily involved in preantral follicle growth and prevention of follicular atresia. It also seems possible that they are involved in the activation of primordial follicles. According to the World Health Organization, endocrine-disrupting chemicals (EDCs) are substances that alter hormonal signaling. EDCs comprise a wide variety of synthetic or natural chemicals arising from anthropogenic, industrial, agricultural, and domestic sources. EDCs interfere with natural regulation of the endocrine system by either mimicking or blocking the function of endogenous hormones as well as acting directly on gene expression or through epigenetic modifications. Disruptions in ovarian processes caused by EDCs may originate adverse outcomes such as anovulation, infertility, or premature ovarian failure. In this chapter, we aim to point out a possible involvement of androgen excess or deficiency in the regulation of ovarian function. We will summarize the effects of EDCs expressing antiandrogenic or androgenic activity on female physiology. Continuous exposition to even small concentration of such compounds can initiate oncogenesis within the ovary.
Part of the book: Theriogenology