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Biology of Reproduction, Vol 12, 599-608, Copyright © 1975 by Society for the Study of Reproduction
1 Department of Obstetrics and Gynaecology and Department of Physiology, University of Western Ontario, London,
Ontario, Canada Homogenates of non-luteal tissue (interstitial cells plus follicles) from immature rat ovaries have
been incubated in phosphate buffer, pH 6.9 containing 10-3 M NADPH and 10-4 M progesterone-4-14C. Thirteen radioactive metabolites have been isolated, nine of which have been identified by
recrystallization to constant specific radioactivity following addition of carrier steroids. The others have
been identified provisionally, on the basis of chromatographic mobility in several thin layer
chromatography systems, both as free compounds and as acetate derivatives. The effect, upon
progesterone metabolism, of pre-treatment with 4 IU pregnant mare serum gonadotropin (PMS) to
induce a single crop of corpora lutea, and of prolactin treatment (100 µg NIH-P-B2 twice daily)
beginning 5 days before autopsy was investigated in a 2 x 2 factorial design experiment. Pre-treatment
with PMS significantly decreased the rates of formation, by non-luteal tissue, of metabolites identified
as androstenedione, 3
-hydroxy-5
-pregnan-20-one, 3
-hydroxy-5
-androstan-17-one, and provisionally as androsterone, 3
, 17
-dihydroxy-5
-pregnan-20-one. 3
, 17
-dihydroxy-5
-pregnan-20-one, and
testosterone. The same treatment was associated with significantly increased production of compounds
identified as 5
-pregnan-3,20-dione, 20
-hydroxypregn-4-en-3-one, and provisionally as 5
-pregnan-3
,20
-diol. Prolactin caused significant decreases in production of 20
-hydroxypregn-4-en-3-one,
5
-pregnan-3
,20
-diol and of 5
-androstan-3
, 17
-diol and/or 5
-androstan-3
,l7
-diol. In addition, prolactin resulted in statistically significant reduction in overall conversion of progesterone to all
metabolic products examined. No statistically significant interactions of treatments were detected, for
any metabolites. There was no evidence of formation of either estrone or estradiol-17
in any of the
treatment groups.
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