9.1 Introduction

Male sexuality is set genetically during the time of fertilization by the presence of the Y chromosome within the spermatozoan since it fuses aided by the X-chromosome-containing ovum, therefore the sex-determining area associated with the Y chromosome (SRY) then drives the bipotential gonad associated with the embryo in order to become a testis through hormone-independent mechanisms 1,2. Nonetheless, after the testis that is early formed, growth of the total male phenotype, including further testicular development (masculinization), becomes totally influenced by a complex system of endocrine signals, especially hormones secreted through the testes 2. Individuals who lack any gonads are phenotypically female 1 and endocrine intervention is necessary to alter the standard feminine phenotype to be male 2. This will make both development and upkeep of masculinization at risk of endocrine-disrupting impacts at all developmental stages from very early embryo to adulthood; in particular, interruption of very very early embryonic developmental processes might have consequences for male health that is reproductive adult life 2. This chapter will deal with the results of endocrine interruption for growth of the tract that is urogenital for sperm production. It’s going to talk about the cap cap ability of endocrine-disrupting chemicals (EDCs) to bring about improper breast development (gynecomastia), alterations to puberty, and hyperplasia in prostatic muscle ( Figure 9.1 ). Continue reading →