Binding of oral contraceptive progestogens to serum proteins and cytoplasmic receptor

Article Abstract:

Drugs are usually administered in such a manner that the greatest effectiveness is achieved with the lowest dosage possible, to minimize the occurrence of side effects. This has led in recent years to the reduction of dosages of the estrogens and progesterones used in oral contraceptives. While this trend has been fairly widespread in estrogen dosage, adjustment of progestogens, progesterone derivatives, has not been uniform. Before doses are adjusted, it is best to understand the physiological factors underlying drug distribution and use by the body. Steroids like progesterone affect cell function by binding to receptors, proteins in the cells, which are then activated and ultimately cause numerous cell reactions. The amount of steroid available to enter the cell is determined by the total blood level of hormone or drug, which is made of free drug plus drug bound to sex hormone-binding globulin (SHBG, a protein which transports some steroid hormones). To provide a better basis for adjustment of progesterone dosages, the binding of some progestogens to cell receptors and to SHBG was characterized. Gestodene and levonorgestrel bound relatively well to SHBG, while 3-ketodesogestrel, a metabolite of desogestrel, bound about 10 times less well, and desogestrel and norgestimate bound poorly to the transport protein. In addition, complexes of SHBG with gestodene or levonorgestrel were relatively long-lived in the circulation, while those with 3-ketodesogestrel were not. Gestodene, levonorgestrel, and 3-ketonorgestrel bound well to receptors for the steroids progesterone, cortisol, and testosterone (male sex hormone), but not to the receptors for estrogen. Receptors for aldosterone, a steroid which regulates salt and water balance, were bound well by gestodene, levonorgestrel, and progesterone, but not 3-ketodesogestrel. These results were obtained with laboratory tests of binding, and are discussed in terms of biological effects of each drug, such as progesterone- and testosterone-like activities in animals and animal cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Progestational hormones, Synthetic, Progestational agents, Blood proteins

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Molecular tools to reestablish progestin control of endometrial cancer cell proliferation

Article Abstract:

Genetically engineering endometrial cancer cells with the receptor for progesterone can make the cells responsive to the anti-cancer effect of progesterone. Researchers used adenovirus to introduce the gene into endometrial cancer cells in culture.

Prevention, Cell proliferation

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Inhibition of human endometrial cancer cell growth in vitro and in vivo by somatostatin analog RC-160

Article Abstract:

The somatostatin analog RC-160 appears to inhibit the growth of endometrial cancer cells. It seems to interfere with the phosphorylation of the epidermal growth factor receptor, according to a study on mice.

Cancer cells, Somatostatin

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