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We examined the response of rat female pituitary at different metabolic stages to treatments with estrogenic compounds and vitamin D analogs. Immature or ovariectomized (Ovx) female rats responded by increased creatine kinase specific activity (CK) to estradiol-17β (E2), genistein (G), daidzein (D), biochainin A (BA), quecertin (Qu), carboxy- G (cG), carboxy- BA (cBA), and raloxifene (Ral). The response was inhibited when Ral was injected together with the estrogens. CK was increased when hormones were injected daily into Ovx rats for 4 different time periods. Pretreatment with the less-calcemic vitamin D analogs JK 1624 F2-2 (JKF) or QW 1624 F2-2 (QW) followed by estrogenic injection resulted in increased response and sensitivity to E2 and loss of inhibition of E2 by Ral. CK was also increased by feeding with E2 or licorice or its components dose- and time- dependent in immature or Ovxrats. Diabetic female rats did not respond to increased doses of E2. In conclusion, rat female pituitary is estrogens-responsive organ, suggesting to consider its response for HRT in postmenopausal women for both beneficial and hazardous aspects. [ABSTRACT FROM AUTHOR]

Studies from our laboratory revealed that direct application of physical strain (PS) to cultured bone cells stimulated synthesis of prostaglandin E2 (PGE2) in a specific population of cells. We found that PGE2 induced the cellular production of cAMP in several bone cell types, whereas the induction of DNA synthesis was limited to osteoblastlike cells. Indirect evidence indicated that PS induced the osteoblastlike cells to synthesize PGE2. Other cell types, for example, chondrocytes, when activated by PS, can be induced to produce cAMP and induce DNA synthesis not mediated by PGE2. We have also found that electric stimulation of different populations of bone cells is specifically induced by a certain intensity of the electric field. It seems that electric stimulus circumvents the PGE2 effect and triggers the adenyl cyclase system in the cell directly. The electric field also induces DNA synthesis not via PGE2 production. [ABSTRACT FROM AUTHOR]

Cell cultures derived from young rat epiphyseal cartilage were grown for approximately 2 wk in BGJ medium supplemented with 10% fetal bovine serum to reach confluence. These cells were identified as chondrocytes as checked by morphology, the presence of alkaline phosphatase, and a positive type II collagen antibody reaction. The cells also responded to different hormonal treatment. Parathyroid hormone (PTH) increased cyclic AMP production by 50% within 15 min of treatment, whereas prostaglandin E (PGE) caused an increase of 160%. Calcitonin (CT) did not affect cAMP production in these cells. DNA synthesis 24 h after hormonal treatment was increased by PTH (2.5-fold) and PGE (2-fold), but not by CT. Among the vitamin D metabolites, 24,25(OH)D increased significantly the [H]thymidine incorporation into DNA, whereas 1,25(OH)D effect was minimal. These results provide evidence for the use of these cell cultures as a model for cartilage in vitro when studying biological and hormonal responsiveness. [ABSTRACT FROM AUTHOR]