Human pubic skin was obtained from normal subjects and patients with abnormal sex differentiation. Skin samples (200 mg) supplemented with NADPH, were incubated for 1 h with labelled testosterone. The conversion of testosterone to dihydrotestosterone1), 3α- and 3β-androstanediol was calculated. This conversion averaged 14.9 ± 3.4 % (se) in 11 normal men and 3.6 ± 1.4 % (se) in 8 normal women. In 4 children as in 4 young hypogonadotrophic hypogonadal men, the conversion rate of testosterone to 5α-reduced metabolites was low (0.8 to 3.5%) and increased at puberty (13.5 to 19.2%). After administration of HCG for 3 months to 1 of the hypogonadal men, it reached 30.2 %. Inversely, the formation of dihydrotestosterone and androstanediols from testosterone was suppressed in 2 men treated with large doses of oestrogen. In 3 subjects with an incomplete form of testicular feminization syndrome, the conversion rate of testosterone to 5α-reduced metabolites was in the normal male range (6.4 to 18.3%), whereas it was low in one case of the complete form of the syndrome (1.5%). In 9 women with idiopathic hirsutism the rate of 5α-reduced metabolites recovered from testosterone was close to that of normal men (13.5 ± 5.5% (se).
From theseresults, it is postulated that in human subjects, there is a good correlation between hair growth in skin from a sexual area and the extent of testosterone 5α-reduction in this tissue. Such an enzymatic activity might be induced by active androgens; this latter hypothesis is in good agreement with the increase of 5α-reduction activity observed at puberty or after treatment of young hypogonadal males.
In addition, it is pointed out that a positive correlation is observed between the 5α-reductase activity present in each skin sample studied and the urinary 3α-androstanediol found for the same individual. This confirms our previous findings suggesting that the determination of urinary 3α-androstanediol might prove of clinical interest in the evaluation of the androgenic status in human subjects.