o,p'-DDT as an estrogen: an evaluation of its ability to compete with 3H-estradiol for nuclear estrogen receptor sites in the quail oviduct.
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Biomedical subjects
Publications and source records attributed to R T Turner.
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The binding properties of estrogen to Japanese quail kidney cell nuclei were evaluated by 3H-17 beta-estradiol exchange. Kidney cell nuclei from estrogenized male, as well as laying female quail, had a single class of saturable (0.1-0.2 pmol/mg DNA), high affinity (Kd = 1-2 x 10-10M) nuclear binding sites for 17 beta-estradiol. High affinity estrogen binding sites were not found in kidney cell nuclei from untreated males. Various non-radioactive estrogens (17 beta-estradiol, estrone, estriol and diethylstilbestrol) competed effectively with 3H-17 beta-estradiol for the high affinity binding sites, whereas nonestrogens (testosterone and progesterone) did not complete. It is concluded that the 3H-estradiol binding characteristics of kidney cell nuclei provides strong evidence for a nuclear estrogen receptor in the avian kidney.
Medullary bone was induced in male Japanese quail by administration of estradiol valerate. An increase in the organic weight of the femur was observed by 36 h after estrogen and an increase in ash weight was observed by 96 h. A complex sequence of metabolic changes in the femur occurred after estrogen treatment. A large increase in uptake of 3H-proline associated with enhanced collagen formation began 36 h after estrogen and reached a peak 3.5 times the control rate at 60 h. The onset of mineralization of the newly formed bone matrix, as determined by 45Ca uptake, began about 24 h after onset of collagen synthesis indicating that synthesis of the bone matrix and its mineralization occur sequentially. Large increases in the rates of uptake of 3H-uridine and 3H-thymidine occurred prior to the onset of medullary bone formation and appear to reflect the differentiation of osteogenic precursors to bone-forming cells.
The effect of tamoxifen citrate on bone mass in immobilization osteoporosis was studied in 11 growing dogs. Immobilization osteoporosis was induced by fiberglass cast immobilization of the right hindlimb for 28 days, while the left hindlimb served as a nonimmobilized control. Six dogs received tamoxifen citrate (1.5 mg/kg per os) once daily for 28 days; five dogs received no treatment. All dogs were euthanatized on day 28 and bone samples were collected. Bone mineral content of the distal tibial metaphysis of casted and uncasted limbs was measured by single photon absorptiometry. Immobilization resulted in a significant reduction in bone mass in the casted limb of untreated and tamoxifen-treated dogs. However, tamoxifen-treated dogs had less severe immobilization osteoporosis than untreated dogs. The calculated bone mass sparing effect of tamoxifen was 24.4%. Because of the complexity of pathologic bone remodeling, use of a single therapeutic agent may not be the optimal means of preventing bone loss associated with immobilization.