Male sexuality is set genetically during the time of fertilization because of the existence of the Y chromosome into the spermatozoan because it fuses because of the X-chromosome-containing ovum, therefore the region that brazilian bride is sex-determining of Y chromosome (SRY) then drives the bipotential gonad for the embryo in order to become a testis through hormone-independent mechanisms 1,2. But, when the testis that is early created, growth of the total male phenotype, including further testicular development (masculinization), becomes entirely influenced by a complex network of hormonal signals, specially hormones secreted through the testes 2. People who lack any gonads are phenotypically female 1 and endocrine intervention is necessary to modify the standard feminine phenotype to be male 2. This will make both development and upkeep of masculinization in danger of endocrine-disrupting impacts at all developmental phases from very very early embryo to adulthood; in specific, interruption of very very very early embryonic developmental procedures could have consequences for male reproductive health in adult life 2. This chapter will deal with the results of endocrine disruption for growth of the urogenital tract and for sperm production. It’s going to talk about the cap cap ability of endocrine-disrupting chemicals (EDCs) to carry about improper breast development (gynecomastia), alterations to puberty, and hyperplasia in prostatic muscle ( Figure 9.1 ).