Abstract
This chapter discusses testosterone metabolism and action in testicular feminization syndrome. The syndrome of testicular feminization (TF) is an intriguing abnormality of human sex differentiation. This inherited syndrome has been described in several species in addition to humans, including the cow, the dog, the rat, and the mouse. In most of the cases, the common feature is that, despite a normal rate of testosterone production, these genetically male subjects have external genitalia and breast characteristics of phenotypic females, an absence of internal genitalia other than the testis, and a striking resistance to endogenous and exogenous androgens. It is assumed that the lack of masculinization of these genetically male subjects is caused by a defect in testosterone action during fetal life and puberty. The cytoplasmic system binding dihydrotestosterone is possibly dependent on testosterone secretion because in vitro it decreases very rapidly after castration. The different steps involved in androgen activity at the cellular level are dependent on each other; in particular, the initial presence of active androgen within the cell seems to be necessary. The chapter also describes the 5α-reduction of testosterone in testicular feminization syndrome.
Published Version
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