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The reduction of 4-[1,2-3H]androstene-3,17-dione (androstenedione) in vitro by scrotal skin was measured in samples from nine men (16–34 years old) with hypospadias and from ten male control subjects. The reduction of androstenedione was also studied in axillary and upper arm skin of seven control subjects. Androstenedione was reduced to material with chromatographic characteristics of 5α-androstane-3,17-dione and to 3α- and 3β-hydroxy-5α-androstan-17-one.
No difference in 5α-reductase activity (defined as the sum of these three metabolites formed) was found in scrotal skin from hypospadic and control men.
The mean concentration of 5α-dihydrotestosterone in serum from men with hypospadias was lower than that in serum from control subjects (P< 0·01). The mean ratio of the serum concentrations of testosterone and 5α-dihydrotestosterone was higher in hypospadic men than in control subjects (P< 0·05). No differences between the two groups were found in the mean serum concentrations of LH, FSH, prolactin, dehydroepiandrosterone, androstenedione, testosterone or testosterone-binding globulin.
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The metabolism of 4-[1,2-3H]androstene-3,17-dione in the prepuce, axillary skin and skin from the arm was investigated in 27 boys operated for phimosis (controls) and 13 unselected boys with hypospadias (a congenital defect of the male urethra). In all types of skin investigated, androstenedione was metabolized to 5α-androstane-3,17-dione, 3α-hydroxy-5α-androstan-17-one, 3β-hydroxy-5α-androstan-17-one and testosterone. Conversion to testosterone was found in the prepuce of two out of 11 boys with hypospadias.
Mild forms of hypospadias in the age group 1–4 years had a higher level of 5α-reductase activity in the prepuce than controls in the same age group (P < 0·05); no such differences were found in the few severe cases of hypospadias in this group. No other differences in 5α-reductase activity were found between hypospadic boys and controls. The ratio of 5α-reductase activity in the prepuce: 5α-reductase activity in skin from the arm was significantly higher (P<0·05) in hypospadic boys than in controls in the age group 1–4 years.
Serum levels of LH and FSH were the same in normal and hypospadic boys but the concentration of prolactin in the serum was lower in boys with hypospadias compared with control subjects in the age group 1–4 years (P<0·005). No differences were found in serum concentrations of androstenedione, testosterone, oestradiol and testosterone-binding globulin.
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SUMMARY
The concentrations of LH and FSH were measured by radioimmunoassay in sera from immature male and female rats of various ages. Fairly high levels of FSH were found in both sexes at birth but LH was not detected. FSH peaks appeared in the male at 13 and 19 days of age and in the female at 13 and 17–19 days of age. LH was undetectable in the male before 12 days of age, rose to a peak (440 ± 60 (s.d.) ng/ml) at 13 days of age and fell below the detection level again between 15 and 25 days of age. A further increase then occurred which almost reached adult levels. LH was first detectable in the female rat at 11 days of age with a peak value of 130 ± 35 ng/ml at 12 days. The hormone was undetectable on days 14 and 15, rose to a second peak on day 18 (148 ± 56 ng/ml), and was again absent between 19 and 25 days of age. The concentration rose, as in the male, between days 25 and 28 to a level similar to that of the adult. The results show sexual differences in prepubertal gonadotrophin surges.
The LH peak at 12–13 days in both sexes appears to be light-dependent. The FSH peak at this time was affected by light but was not strictly light-dependent.
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The metabolism of 4-[4-14C]androstene-3,17-dione in the microsomal fraction of livers from male and female rats was investigated after hypothalamic deafferentation at two levels. It was found that frontal deafferentation at the retrochiasmatic level caused a complete 'feminization' of hepatic steroid metabolism in the male rat but was without effect in the female animal. Transection rostral to the suprachiasmatic nuclei was without effect in both sexes. A complete transition from male to female hepatic steroid metabolism after retrochiasmatic deafferentation was reached on day 4 after the operation and persisted for at least 10 weeks. The present results, taken together with previous investigations, indicate that the release of a 'feminizing' factor from the pituitary gland of the male rat is inhibited by a factor produced in, or transported through, the periventricular anterior hypothalamic region including the suprachiasmatic area. No effect on the hepatic steroid metabolism was observed after blinding of the rats suggesting that a diurnal rhythm is not essential to this control mechanism.
