Abstract

The penis is a hydromechanical pump with unique and complex structural elements that are required for maintaining its physiological function. Penile erection is a complex neurophysiological process that depends on integration of signaling from hormones, neurotransmittersand vascular factors. The endocrine system produces a host of hormones critical for cellular differentiation during penile development in the young and maintaining cellular homeostasis and erectile physiology during adulthood. Endocrine-disrupting chemicals (EDCs) produce lasting and significant impact on penile development in the young and alter penile physiology in adulthood, with a negative impact on erectile function. EDCs are known to interrupt hormone biosynthesis and also interact with members of the steroid/thyroid hormone receptor superfamily. Disruption of hormone biosynthesis and interfering with hormone receptor interactions and signaling likely contribute to penile malformation during development and abnormal physiological function in the adult. Penile erection depends on release of neurotransmitters, such as neural and endothelial nitric oxide, and the function of the vascular endothelium, the trabecular smooth muscle, and adequate tissue elasticity to ensure compliance and maintain erection. EDCs produce a host of alterations in penile histoarchitecture and produce deformities in penile structural elements and negatively impact erectile physiology resulting in venoocclusive dysfunction and erectile dysfunction. In this chapter we reviewed the available data in the contemporary literature pertaining to endocrine disruption of tissue development, resulting in penile malformation in the young and the effects of endocrine disruption on erectile physiology in the adult male. A body of evidence exists indicating that EDCs exert a negative impact on erectile tissue development as well as erectile physiology.

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