Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the androgenic activity of steroidal and nonsteroidal anti-androgens, the effect of several compounds on some parameters as an androgenic activity was measured in the ventral prostate (VP) and seminal vesicle gland (SV) of castrated male rats. Ornithine decarboxylase (ODC) activity, arginase activity, androgen receptor (AR) in cytosol and nucleus, histological examination and weight of accessory sex organs were used as parameters for androgenic activity. The ventral prostate weight was increased by the administration of not only steroidal anti-androgen, medroxyprogesterone (MPA), chlormadinone acetate (CMA) and cyproterone acetate (CPA), but also estradiol-17 beta(E2) and nonsteroidal anti-androgen, AA 560. However flutamide (Flu) failed to increase VP weight. In SV, the tendency to increase weight by the administration of these compounds was also observed. However, it was not obvious as in VP. It was proven by the measurement of the parameters that all tested compounds except Flu had an androgenic activity. It seems that the androgenic activity was caused by a different mechanism because the parameter response to the administrated compounds was not identical.
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PMID:[A study of the androgenic activity of anti-androgen]. 169 15

This paper reports an investigation of the mechanism involved in the response of endometrial adenocarcinoma to MPA. The following protocol was used for a period of 8 years: 1 g/day MPA per os for 30 days and 60 days after surgery, following by 500 mg/day for 1 year. Adenocarcinoma glycolytic activity, G-6-P cycle, polyamine concentration, and the activity of ornithine decarboxylase (ODC), i.e. the first enzyme in polyamine synthesis, were compared before and after the 30/day treatment. The modifications induced by MPA are discussed and related to the pathological picture in an attempt to determine the characteristics of responding tumors.
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PMID:Biochemical aspects of the hormonal therapy of endometrial adenocarcinoma. 224 10

There is an extensive background on the androgen responsiveness of the mouse kidney which can be demonstrated histologically by hypertrophy of the Bowman's capsule and the proximal convoluted tubule. Although androgens increase many renal proteins, beta-glucuronidase and ODC are distinguished by exquisite genetic regulation of the magnitude of the response induced by testosterone. Both the qualitative and quantitative expression of the genes for these enzymes are strain specific, and are dependent upon regulatory alleles. Ornithine decarboxylase is of particular interest since the response of this enzyme is rapid compared to that of beta-glucuronidase. Recent studies using a newly developed androgen receptor assay have demonstrated that the duration of retention of the androgen receptor complex in the nucleus correlates with the magnitude of the androgenic response. Progestins can mimic, inhibit, or potentiate the action of androgens. These responses have been termed the androgenic, antiandrogenic and synandrogenic actions of progestins, respectively. The androgenic and antiandrogenic action of this class of steroids are manifest on many tissues and on many endpoints within a given organ. These effects are believed to involve an early step(s) of androgen action which is common to all sensitive tissues. Results to date suggests that this early step involves the androgen receptor. By contrast, the synandrogenic action of progestins is limited in that it is not observed on all tissues, and not even on all endpoints within a single organ. In the mouse kidney, the synandrogenic actions of progestins have been most extensively studied on beta-glucuronidase. With this enzyme this unusual response to progestins can be demonstrated only in mice which carry the Gus-ra allele. This observation suggests that the potentiating action of progestins on beta-glucuronidase is manifest directly on the Gus gene complex. It is not certain at this time whether a similar mechanism is involved in the potentiation of androgen action on other organs such as the prostate. The androgenic action of progestins is believed to be similar to that of other androgens. Androgenic progestins such as MPA bind to the androgen receptors and translocate them to nuclei. This is followed by a dose dependent increase of proteins similar to what is observed after testosterone administration. In addition, the regulatory genes which modulate androgen action have the same effect on the androgenic effect of progestins. The fact that the potency of progestins such as MPA is less than that of testosterone is believed to relate in part to their lower affinity for the androgen receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Progestins can mimic, inhibit and potentiate the actions of androgens. 637 45