[Scintigrams of the normal placenta].
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Biomedical subjects
Publications and source records attributed to T Oka.
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Progesterone administered with estrogen to the intact female chick antagonizes the characteristic effects of estrogen to induce cell proliferation and cytodifferentiation of tubular gland cells in the oviduct, events that are accompanied by the appearance of lysozyme. Progesterone appears to exert its effect by preventing proliferation of cells destined to become tubular gland cells, but once such cells do proliferate, subsequent cytodifferentiation and appearance of lysozyme are not prevented.
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Daily administration of estrogen to immature female chicks results in marked oviduct growth and appearance of characteristic tubular gland cells which contain lysozyme. Although a rapid increase in total DNA and RNA content begins within 24 hr, cell specific protein, lysozyme, is first detectable after 3 days of estrogen. Progesterone administered concomitantly with estrogen antagonizes the estrogen-induced tissue growth as well as appearance of tubular gland cells and their specific products, lysozyme and ovalbumin. When the initiation of progesterone administration is delayed for progressively longer periods (days) during estrogen treatment, proportionally greater growth occurs with more lysozyme and tubular gland cells after 5 days of total treatment. Progesterone does not inhibit the estrogen-stimulated increase in uptake of alpha-aminoisobutyric acid and water by oviduct occurring within 24 hr or the estrogen-induced increase in total lipid, phospholipid, and phosphoprotein content of serum. The above results of progesterone antagonism can best be explained by the hypothesis that progesterone inhibits the initial proliferation of cells which become tubular gland cells but does not antagonize the subsequent cytodifferentiation leading to the synthesis of lysozyme and ovalbumin once such cell proliferation has occurred.
The effects of estrogen and progesterone on the function of chick oviduct tubular gland cells have been studied. Such function, as measured by the increase in specific cell products such as lysozyme and ovalbumin, requires the continuous presence of estrogen or progesterone. Withdrawal of hormone results in a rapid cessation of function and an involution of the oviduct accompanied by rapid decreases in total weight, lysozyme, and RNA. During such involution, tubular gland cells per se persist, as evidenced by a lack of comparable decrease in total DNA content and by histological demonstration of tubular gland cells. When estrogen administration is reinstituted, preexisting tubular gland cells rapidly synthesize ovalbumin and lysozyme without requiring new DNA synthesis. Administration of progesterone also stimulates the function of such cells. Furthermore, the effects of estrogen and progesterone are synergistic on the synthesis of lysozyme and ovalbumin, whereas progesterone antagonizes the estrogen-evoked formation of tubular gland cells. It is suggested that such complex interactions of estrogen and progesterone on oviduct development and function result from differences in responsiveness of the various cell types present in the tissue.
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In the microbial conversion of added hypoxanthine to 5'-inosinic acid, Mn(2+) concentration in the growth medium is known to have a profound effect both on the yield of 5'-inosinic acid and the morphology of cells of Brevibacterium ammoniagenes. To elucidate the mechanism in which Mn(2+) was concerned with cell morphology and 5'-inosinic acid production, effects of Mn(2+) on the macromolecular synthesis were measured. It was found that Mn(2+) strongly governed deoxyribonucleic acid (DNA) synthesis and that, in the medium lacking Mn(2+), DNA synthesis was stopped at the level corresponding to one-fourth to one-third that in the medium supplemented with Mn(2+) (100 mug/liter). On the other hand, cellular ribonucleic acid and protein synthesis was quite indifferent to Mn(2+) concentration. Consequently, cells showed so-called "unbalanced growth death" after 10 hr of culture, losing the ability to form colonies while cell mass was increasing. The elongated cells turned into irregular forms (bulbous, club-shaped, etc.) which finally lysed. Two main reaction components in the conversion of hypoxanthine to 5'-inosinic acid, phosphoribosylpyrophosphate and hypoxanthine phosphoribosyltransferase, were liberated into the medium during lysis. The role of Mn(2+) in the synthesis of DNA and the role of the unbalanced growth death in the conversion of hypoxanthine to 5'-inosinic acid are discussed.
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