Abstract
In the rhesus monkey ( Macaca mulatta) the fetal testis appears to be more active than the fetal ovary in synthesizing steroids. This occurs despite the relative abundance of potential hormone precursors in the circulation. The possibility was investigated that this discrepancy in activity may be related to the activities of two rate-limiting enzymes, estrogen synthetase (ES) and C 17–20lyase (LA). ES and LA activities were characterized in monkey fetal gonads during late gestation from the rate of formation of 3H 2O from [1,2- 3H]-androstenedione (ES) and metabolism of [4- 14C]-17-hydroxyprogesterone to [ 14C]-androstenedione (LA). Ovaries and testes exhibited LA activity with apparent K m values of 3.4 × 10 −6M and 7.1 × 10 −7 M, respectively. Reaction rate was 1.8 ± 0.3 × 10 −3 nmol/min × mg protein ( n = 3) in the ovary which was significantly less than LA rate in the testis (8.3 ± 1.6 × 10 −3 nmol/min × mg −1 protein, n = 5). ES activity was detected only in the fetal ovary; it averaged 1.5 ± 0.4 × 10 −4 nmol/min × mg −1 protein ( n = 5). The apparent K m was 5.3 × 10 −8 M. Isolation of the [ 3H]-estrogens formed revealed the synthesis of estrone and estradiol-17β. During the 30 min incubation the amount of 3H 2O synthesized diverged from the combined quantity of tritiated estrone and estradiol-17β that was produced suggesting that other estrogens were synthesized. The reason fetal ovarian synthetic capacity is lower than that of the testis may be due to a low level of LA and ES activity in the ovary and additional metabolism of estrone and estradiol-17β.
Published Version
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