[Attribution processes of the fourth age: strategies of distinction and self-enhancement in dealing with the social devaluation].

Steroid 5α-reductases (5αRs) are a family of enzymes that catalyze the irreversible reduction of the Δ double bond in steroids such as testosterone, progesterone, and glucocorticoids. By converting these hormones into 5α-reduced metabolites with distinct biological activities, this reaction redirects steroid signaling toward physiological programs essential for sexual differentiation, neuroendocrine regulation, and stress adaptation. The first 5α-reduced steroid was identified in 1931, when Adolf Butenandt isolated androsterone from male urine (). The biochemical basis for the formation of 5α-reduced steroids, however, remained unresolved until 1951, when Schneider and Horstmann detected 5αR activity in rat liver preparations during studies of deoxycorticosterone (DOC) metabolism (). Subsequent work showed that this activity was NADPH-dependent and could reduce multiple steroid substrates, establishing 5α-reduction as a general enzymatic pathway rather than an isolated substrate-specific reaction (). Yet the physiological significance of this pathway did not become clear until the late 1960s, when steroid 5α-reduction was linked to the conversion of testosterone into dihydrotestosterone (DHT). This conceptual transition was driven by evidence that DHT generates a more potent androgen-receptor signal than testosterone in key target tissues and accumulates preferentially within prostatic nuclei (; , ). Studies in androgen-responsive tissues, particularly the prostate () and perineal skin (), then established 5α-reduction as a tissue-selective mechanism for the local amplification of androgen signaling. The developmental relevance of this mechanism was defined soon thereafter. In rabbit and rat embryos, 5αR activity was enriched in the primordia of the prostate and external genitalia before the onset of virilization, whereas it remained undetectable in Wolffian duct derivatives until later stages of differentiation (). These findings showed that 5α-reduction is not only tissue-selective but also developmentally regulated. They also led to a decisive prediction: hereditary disruption of this pathway should dissociate Wolffian-derived, testosterone-dependent differentiation from DHT-dependent development of the external genitalia. This prediction was confirmed shortly thereafter by independent clinical reports of 46,XY individuals born with ambiguous external genitalia who underwent marked virilization at puberty (; ). The disorder, originally termed pseudovaginal perineoscrotal hypospadias and later reclassified as 5αR type 2 deficiency, features normal circulating testosterone but markedly reduced DHT, indicating a selective impairment in testosterone 5α-reduction rather than a generalized defect in androgen production. These cases established a central principle of androgen biology: DHT is required for masculinization of the external genitalia and prostate, whereas testosterone is sufficient for Wolffian duct differentiation and several aspects of pubertal virilization (). The syndrome also revealed a clinically important pattern: affected males typically develop markedly hypoplastic prostates and appear largely protected from benign prostatic hyperplasia (BPH).