Sex hormone effects; Sex hormone synthesis, regulation, and function
20/11/2008 · Androgens Ppt - Download as ..
Testosterone is converted to two other important hormones. It is reduced to dihydrotestosterone in specific tissues like the skin and the prostate and it is oxidized to estradiol. In men this oxidation mainly takes place in adipose tissue and in the testes. In women the biosynthesis of estradiol takes place in the ovaria.
Ppt Androgen | Powerpoint Presentations and Slides » …
Much research has been devoted to unravel the biosynthesis of steroid hormones, because promising medical applications were expected. Many reviews have appeared in the literature about the biosynthetis of the male and female sex hormones . The main features of the biosynthetic pathways of testosterone, dihydrotestosterone, estrone and estradiol are know today as they are depicted in Schemes 1 and 2.
Breastfeeding and Autism and Childhood Cancer
In this paper we describe the effect of androgen on glycogen metabolism in different prostate cancers. We used PC3-AR-V and PC3-AR-E7 cells, which ectopically expresses AR and in case of PC3-AR-E7 the HPV-E7 protein. Additionally, LNCaP, which maintains a functional AR, was tested for glycogen content and its correlation to the number of cells. The PC3-AR-V and PC3-AR-E7 cell lines demonstrated a response to androgen leading to G1 arrest with a corresponding increase in the glycogen content (2 to 5 fold). PC3 cells lacking AR did not increase glycogen content in response to androgen. PC3 (AR-) cells demonstrate that intracellular glycogen content corresponds with the growth and/or survival of cells harbouring a functional AR. Intracellular stores of glycogen correlated inversely with the cell number: when cell numbers are low the glycogen content is high. This inverse relationship suggests that glycogenesis participates in growth arrest. However, glycogenesis is most likely not sufficient to induce ATP-dependent apoptosis, as the inhibition of glycogenolysis with the GP inhibitor CP-91149 does not induce cell death in these prostate cell lines. Glycogen content normalized to the number of cells is about 50% higher in PC3-AR cells treated with R1881 than treated with CP-91149. The additional increase in glycogen content of R1881-treated PC3-AR-V/E7 cells upon CP-91149 treatment further results in a reduction of cell number by growth inhibition and reduction in cell viability, which suggests that a certain intracellular glycogen content has to be reached to affect cell viability. Alternatively, certain effects of hormone treatment on cell survival may be enhanced by inhibition of glycogenolysis using CP-91149. Similarly, LNCaP cells responded with glycogen accumulation and growth arrest upon androgen removal, which was further enhanced by the GP inhibitor CP-91149.