Date of Award

Fall 1971

Degree Type

Thesis - Restricted

Degree Name

Master of Science (MS)




Ovulation and luteinization were artificially induced in prepubertal rats by administration of 50 IU PMS followed 60±5 hours later by 25 IU HCG. Hypophysectomy, pituitary transplantation, and treatment with anti-LH serum were used to investigate the nature of hypophyseal involvement in the precursor and steroid metabolism of the luteinized ovary. Plasma and ovarian levels of progesterone and 20α-OH-pregn-4-ene-3-one and ovarian levels of cholesterol and esterified cholesterol were determined. The uptake of 14C-acetate into these compounds both in vivo and in vitro was also determined. Hypophysectomy was shown to cause a rapid reduction in plasma and ovarian steroid levels. However, hypophysectomized animals that were provided with pituitary transplants maintained steroids at intact levels even after repeated injection with anti-LH serum. This indicates that LH is not directly involved with steroid synthesis. Ovarian cholesterol and esterified cholesterol levels were greatly depressed by hypophysectomy. The presence of transplanted pituitaries in hypophysectomized animals resulted in a partial recovery of precursor levels. This recovery did not take place in transplanted animals that were treated with anti-LH serum. These results strongly suggest that transplants do produce some LH, that LH is directly involved in maintaining precursor pools, but that high precursor pools are not critical in maintaining steroid production in the superovulated rat. The uptake of 14C-Acetate into steroids and steroid precursors was greatly increased following hypophysectomy but hypophysectomized animals that had received pituitary transplants did not show this increase unless they were treated with anti-LH serum. It is apparent from this investigation that the uptake of acetate is not proportional to the magnitude of precursor or steroid formation. A compatible explanation would be that LH stimulated the production of acetate, perhaps by enhancing glycolysis. This would dilute the specific activity of the labeled acetate, resulting in a reduced uptake of the label into steroid precursors and steroids.



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