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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of metabolites of testosterone and of anabolic androgens on bone marrow and thymus of ovariectomized mice were studied. Steroids contained in capsules made of silastic tubing were implanted on the day of castration or were injected at the day of castration (Noralone and T.P.), lymphatic organs were examined two weeks later. It was found that testosterone, 5 alpha-DHT, 3 alpha-diol, Dianabole, T.P., and Noralone caused increases in the relative number of large cells and in activity of 20 alpha SDH in bone marrow. Concomitantly, these steroids caused a marked reduction in thymus cell number and an increase in the responsiveness of the thymus cells to Con A and PHA. The steroid 3 beta-diol increased marrow cell 20 alpha SDH activity but did not affect the thymus cell number. Other steroids tested, Ad-dione 3 alpha or 3 beta-androsterone, 5 beta-DHT, epitestosterone, and progesterone had no effect on thymus or bone marrow.
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PMID:Effects of testosterone metabolites and of anabolic androgens on the bone marrow and thymus in castrated female mice. 657 19

The antiproliferative activity of previously synthesized (Z)-cholest-4-en-6-one oxime (1), (E)-cholest-4-en-6-one oxime (2), 7-aza-B-homocholest-4-en-6-one (3) and 6-aza-B-homocholest-4-en-7-one (4) and newly synthesized 6-thioxo-7-aza-B-homocholest-4-ene (5) and 6-aza-7-thioxo-B-homocholest-4-ene (6) was tested for their possible effects against two human tumor cell lines, cervical carcinoma (HeLa) and chronic myelogenous leukemia (K-562). Compounds 1-6, exerted a dose-dependent antiproliferative effect toward cell lines used in experimental design, showing high selectivity in their action for tumor cells in comparison to normal immunocompetent cells (non-stimulated PBMC and PHA-stimulated PBMC). Compounds 2, 3 and 4 exhibited a very high but selective antitumor activity, by inducing apoptosis in sensitive, for that purpose targeted tumor cell line (HeLa cells). Low toxic effect upon both non-stimulated, and PHA stimulated PBMCs from control, healthy volunteers, has been detected for compounds 1, 2, 3 and 4. The possible reasons for profound differences in the effects of this spectrum of steroidal compounds between tumor cell lines and normal stimulated and non-stimulated PBMCs are discussed. The molecular mechanisms for apoptotic events in HeLa cell line are suggested. The guidelines for further research are underlined.
Steroids 2007 May
PMID:Synthesis of some steroidal oximes, lactams, thiolactams and their antitumor activities. 1743 24

Glucocorticoids (GCs) and progesterone have been employed as immunosuppressive agents during pregnancy for many years. Intracellular acidification by GCs is due to a rapid non-genomic inhibition of membrane Na(+)/H(+)-exchange 1 (NHE1) activity and is followed by immunosuppression of PHA-stimulated proliferation. NHE1 is tethered to the cortical actin cytoskeleton through ezrin/radixin/moesin (ERM) proteins within lipid rafts; these regulate cell shape, migration and resistance to apoptosis. We explored whether mifepristone (RU486), an antagonist of GCs in T cells, is able to completely block rapid non-genomic responses, namely NHE1 activity and the phosphorylation C-terminal residues of ERM proteins at threonine (cp-ERM). GCs stimulate a rapid non-genomic cp-ERM response in cells within 5min. RU486 antagonized the GC-induced rapid decrease in NHE1 activity, and arrested PHA-stimulated T cells at G0/G1 phase but had no effect on the rapid increase in cp-ERM, which persisted for 24h. However, the cp-ERM response was blocked by staurosporine in both resting and GC stimulated cells. The results of RU486 antagonized the GC induced rapid decrease in NHE1 ion transport activity, but not the increase cp-ERM. This suggests that RU486 in T cells exerts its antagonistic effects at NHE1 containing plasma membrane sites and not where cp-ERM links lipid rafts to cortical cytoskeletons.
Steroids 2016 07
PMID:In human T cells mifepristone antagonizes glucocorticoid non-genomic rapid responses in terms of Na(+)/H(+)-exchange 1 activity, but not ezrin/radixin/moesin phosphorylation. 2677 50