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The ovarian hormones stimulate the development of the reproductive system, induce the development of secondary sexual characteristics, and promote a receptive endometrium for the growth and development of the proconceptus. The development of the ovary is dependent on local and endocrine factors that can be the target of endocrine disruptors. The T-shaped uterus seen in women exposed to diethylstilbestrol (DES) could represent a narrow and more branched structure, similar to the structure of the fallopian tube. Müllerian development is dependent on coordinated gene expression and hormone exposure. The genes that control normal patterning of the reproductive tract are beginning to be identified. The most important hormones regulating mammary gland development are estrogen and progesterone. During pregnancy and lactation, prolactin contributes to lobular differentiation and milk production. Estrogen and progesterone play a fundamental role during puberty to develop a normal adult breast.
This chapter discusses the key events occurring at different stages of development in the normal human male and how this impacts the reproductive function in adulthood. Development of the normal male reproductive system can be divided into five periods: fetal, neonatal, infancy/childhood, puberty, adulthood. Normal hormonal functioning of the fetal testis is essential for masculinization and for development of a male reproductive system. In neonatal male and female babies there is activation of the hypothalamic-pituitary axis and consequent increase in circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). During the neonatal period, Sertoli cells continue to proliferate and this is arguably the most important period in life in terms of the magnitude of increase in Sertoli cell numbers. Sertoli cells start expressing androgen receptor (AR) at the onset of puberty and this is considered one sign of maturation of these cells, as they terminally differentiate and cease proliferating.
Many reproductive and developmental health problems are caused by exposure to chemicals that are widely dispersed in our environment. These problems include infertility, miscarriage, poor pregnancy outcomes, abnormal fetal development, early puberty, endometriosis, and diseases and cancers of reproductive organs. The compelling nature of the collective science has resulted in recognition of a new field of environmental reproductive health. Focusing on exposures to environmental contaminants, particularly during critical periods in development and their potential effects on all aspects of future reproductive life-course, this book provides the first comprehensive source of information bringing together the arguments that are spread out among various scientific disciplines in environmental health, clinical and public health fields. It provides a review of the science in key areas of the relationship between environmental contaminants and reproductive health outcomes, and recommendations on efforts toward prevention in clinical care and public policy.
Epidemiologic studies and animal studies increasingly suggest that exposures to environmental chemicals, nutrition, physical factors, and other factors early in development have a role in susceptibility to disease in later life. The mammalian female reproductive system arises from the uniform paramesonephric duct, the müllerian duct. The major subtypes of epithelial ovarian cancer (EOC) show morphologic features that resemble those of the müllerian duct-derived epithelia of the reproductive tract. Exposure of the developing female reproductive tract to diethylstilbestrol (DES), either in vivo or in organ culture, repressed the expression of HOXA10 in the uterus and resulted in uterine metaplasia. Epigenetic change in the molecular program of cell differentiation in the affected tissues may be a common mechanism. Most regions of the mammalian genome exhibit little variability among individuals in tissue-specific DNA methylation levels. Future analyses of epigenetic imprints of genes explain the developmental origins of disease.