In utero exposure to cigarette smoke dysregulates human fetal ovarian developmental signalling.

Study Question: How does maternal cigarette smoking disturb development of the human fetal ovary?

Summary Answer: Maternal smoking increases fetal estrogen titres and dysregulates several developmental processes in the fetal ovary.

What Is Known Already: Exposure to maternal cigarette smoking during gestation reduces human fetal ovarian cell numbers, germ cell proliferation and subsequent adult fecundity.

Study Design, Size, Duration: The effects of maternal cigarette smoking on the second trimester human fetal ovary, fetal endocrine signalling and fetal chemical burden were studied.

Maternal cigarette smoking and effects on androgen action in male offspring: unexpected effects on second-trimester anogenital distance.

Introduction: Fertility, sperm counts, and testis weights are reduced in men whose mothers smoked in pregnancy. Animal studies suggest this could be due to impaired androgen action. Anogenital distance (AGD) provides a readout of fetal androgen exposure and is reduced by in utero exposure to harmful chemicals in rodents.

Development of steroid signaling pathways during primordial follicle formation in the human fetal ovary.

Context: Ovarian primordial follicle formation is critical for subsequent human female fertility. It is likely that steroid, and especially estrogen, signaling is required for this process, but details of the pathways involved are currently lacking.

Objective: The aim was to identify and characterize key members of the steroid-signaling pathway expressed in the second trimester human fetal ovary.

Gene expression analysis of human fetal ovarian primordial follicle formation.

Context: Primordial follicle formation dictates the maximal potential female reproductive capacity and establishes the ovarian reserve. Currently, little is known about this process in the human.

Objective: The aim of the study was to identify genes associated with the onset of human fetal primordial follicle formation in morphologically normal human fetuses.