Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:1.16.3.1 (
ceruloplasmin
)
5,074
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The residual androgenic activity of two new combined oral contraceptives (OCs)--30 mcg of ethinyl estradiol in combination with either 150 mg of desogestrel or 75 mcg of gestodene--was investigated in 40 healthy volunteers. Measured in these volunteers were modifications in transport protein levels. These levels are known to be increased by estrogen, but this increase can be counterbalanced, to varying degrees, by gestagens. For both OCs, there was a marked percentage increase in sex hormone binding globulin (SHBG), corticosteroid binding globulin (CBG), thyroxine binding globulin (TBG), and
ceruloplasmin
(CP) and a similar reduction in total testosterone and the free androgen index. The modifications in SHBG, CBG, TBG, and CP are interpreted as an expression of the correlated value of the estrogenicity/gestagenicity ratio of the OCs studied and suggest that these particular formulations have greater estrogenicity. The relatively negligible biological androgenic activity of desogestrel and gestodene and their elevated affinity
progesterone receptor
/androgen receptor ratio reflect the high selectivity of these agents. Moreover, the lack of androgenic effects makes desogestrel and gestodene appropriate treatment agents for hyperandrogenism.
...
PMID:Sex hormone binding globulin, cortisol binding globulin, thyroxine binding globulin, ceruloplasmin: changes in treatment with two oral contraceptives low in oestrogen. 182 29
Captopril (D-3-mercapto-2-methylpropanoyl-L-proline) is an angiotensin converting enzyme (ACE) inhibitor, used widely in the treatment of hypertension and congestive heart failure. Captopril also inhibits proliferation of a variety of cell types, including several lacking ACE and renin acitvity. We have previously demonstrated that human mammary ductal carcinoma cells are among the cell types whose mitotic activity is inhibited by captopril. In those cells, captopril also reduces estrogen receptor (ER) and increases
progesterone receptor
(PR) concentrations. The present study evaluated the mechanism of captopril's antiproliferative action in an ER/PR-negative human mammary ductal carcinoma cell line, Hs578T. Cells grown in a 10% serum medium showed negligible changes in the presence of captopril alone. However, in the presence of subphysiologic concentrations of copper salts or copper-loaded
ceruloplasmin
, captopril caused a dose-dependent reduction in cell number, thymidine incorporation and mitochondrial dehydrogenase activity. In contrast, iron salts and iron-saturated transferrin had no effect on captopril activity. Catalase and horseradish peroxidase nullified the cytotoxic effects of captopril/Cu++, whereas H2O2 mimicked those effects. These data are consistent with the notion of a copper-catalyzed oxidation of captopril, leading to the generation of H2O2 as the cytotoxin to this clinically important cell type.
...
PMID:Mechanism of captopril toxicity to a human mammary ductal carcinoma cell line in the presence of copper. 1051 67