OVARIAN ENZYMATIC DIVERGENCE IN PATIENTS WITH POLYCYSTIC OVARY SYNDROME EXCRETING URINARY PREGNANETRIOLONE

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Abstract
When ovarian mitochondria from patients with polycystic ovary syndrome (POS) were incubated with [7-3H]17.alpha.-hydroxypregnenolone and [4-14C]-17.alpha.-hydroxyprogesterone, 11.beta.-hydroxylated metabolites were obtained. The mitochondria, prepared from pooled, frozen, polycystic ovarian tissue of 5 patients, converted [7-3H]17.alpha.-hydroxypregnenolone to 3.beta.,11.beta.,17.alpha.-trihydroxy-5-pregnen-20-one (yield 0.065%) and to 3.beta.,17.alpha.-dihydroxy-5-pregnene-11,20-dione (0.22%), while [4-14C]17.alpha.-hydroxyprogesterone was converted to 21-deoxycortisol (0.1%). Incubation of mitochondria, prepared from 4 pooled samples of frozen, normal ovarian tissue, yielded no evidence of 11.beta.-hydroxylation of either of the substrates. Mitochondria obtained from fresh, polycystic ovarian tissue of a single patient with POS converted [7-3H]17.alpha.-hydroxypregnenolone to 3.beta.,17.alpha.-dihydroxy-5-pregnene-11,20-dione (2.1%) and [4-14C]17.alpha.-hydroxyprogesterone to 21-deoxycortisol (0.1%). When the same mitochondrial preparation was incubated simultaneously with [7-3H]17.alpha.-hydroxypregnenolone and [4-14C]11-deoxycortisol, it converted 17.alpha.-hydroxypregnenolone to 3.beta.,17.alpha.-dihydroxy-5-pregnene-11,20-dione (1.9%), but no 11.beta.-hydroxylated derivatives of 11-deoxycortisol were found. These results demonstrate that ovaries of patients with POS contain an 11.beta.-hydroxylase active towards C-21-deoxysteroids but inert to C-21-hydroxysteroids such as 11-deoxycortisol.

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