Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0338671 (Steroids)
9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of human mammary tumors to convert 7alpha 3H-testerone to estrogens was examined in order to determine whether this bore any relationship to estrogen receptor and steroid sulfurylation levels; such levels being indicative of hormone dependency. In 8 out of 9 tumors, formation of estradiol-17beta from testosterone was demonstrated. Those tumors showing the lowest conversion of testosterone to estradiol-17beta possessed the highest levels of dehydroepiandrosterone sulfotransferase which lends support to data implicating sulfurylation in the regulation of steroid metabolism in human tumors. All tumors activated sulfate to adenosine-3'-phospho-5'-phosphosulfate and the concentrations were significantly correlated withe the recorded levels of dehydroepiandrosterone sulfate. Estrogen receptor levels did not show any obvious relationship to the other parameters.
Steroids 1976 Oct
PMID:Steroid metabolism by human mammary carcinoma. 13 57

Guinea pig adrenal estrogen sulfotransferase from either sex was eluted as a single peak, irrespective of buffer salt concentration, when subjected to fast protein liquid chromatography on gel filtration columns. The same enzyme was consistently eluted in two distinct peaks during chromatofocusing. Adrenal pregnenolone sulfotransferase was eluted during gel filtration in a heterogeneous pattern, dependent on salt concentration. These properties have made possible almost complete separation of the two sulfotransferases in one step, although adrenal estrogen sulfotransferase may possess a minute intrinsic ability to catalyze sulfation of pregnenolone. Pregnenolone sulfotransferase had no measurable activity toward estrone. Pregnenolone sulfotransferase from both sexes yielded variable elution patterns during chromatofocusing. Estrogen sulfotransferase from the adrenal, as well as that of guinea pig chorion, was strongly inhibited by N-ethylmaleimide and to a lesser degree by iodoacetamide and iodoacetate. Adrenal and chorion estrogen sulfotransferases were thermolabile and were activated, although not protected from the effect of heat, by binding to 3'-phosphoadenosine 5'-phosphosulfate. Adrenal pregnenolone sulfotransferase was inhibited only by high concentrations of N-ethylmaleimide and not at all by iodoacetamide or iodoacetate. It was more thermostable than the estrogen sulfotransferase and was not activated by binding to 3'-phosphoadenosine 5'-phosphosulfate.
Steroids 1992 Jun
PMID:Comparison of estrogen sulfotransferase and pregnenolone sulfotransferase of guinea pig. 144 Jul

A sulfotransferase which catalyzes transfer of the sulfate group from 3'-phosphoadenosine-5'phosphosulfate to cholesterol has been demonstrated in the rat gastric mucosa. The product of the reaction was characterized as cholesterol sulfate by two-dimensional thin-layer chromatographic behavior, and gas-liquid chromatography of cholesterol after acid solvolysis. The bulk of enzyme activity was found in the cytosol fraction. Sulfation of cholesterol did not require added Mg+2, Mn+2, or Ca+2, and was unaffected by ethylenediaminetetraacetate. Triton X-100 moderately enhanced the enzyme activity. A broad pH optimum from pH 6.0-9.0 was exhibited with a maximum at pH 7.0-7.5. The apparent Km for PAPS was 0.8 x 10(-6)M. The possible function of cholesterol sulfate in gastric mucosa is discussed.
Steroids 1980 Dec
PMID:Enzymatic sulfation of cholesterol by rat gastric mucosa. 693 87

Steroid sulfotransferase activity is present in the cytosol fraction of hamster epididymis. The activity of this enzyme is increased by magnesium ion. Cysteine is essential to assure optimal activity. Adenosine-3'-phosphate-5'-phosphosulfate is required as sulfate donor and an apparent Km of 62 microM was calculated. Inhibition studies suggest that this enzyme preferentially catalyzes the sulfurylation of the 3 beta-hydroxyl group of delta 5-steroids. An unusual feature of the enzyme is a pH optimum at pH 10.
Steroids 1981 Nov
PMID:Steroid sulfotransferase in hamster epididymis. 694 22

Estrogen receptor (ER) levels, formation of 3'-phosphoadenosine-5'phosphosulfate (PAPS), and sulfate transfer to estradiol-178, have been determined in 62 human primary carcinoma cytosol preparations. Whilst no differences between ER positive and ER negative tumors were found in the synthesis of [35S]PAPS, formation of estradiol-3-[35S]sulfate catalysed by estrogen sulfotransferase was significantly higher in ER positive tumors [84 +/- 10 (mean +/- S.E.M.) versus 32 +/- 9 pmole estradiol-3-sulfate per mg protein per 2 hr for ER positive and ER negative tumors, respectively, p less than 0.02]. By choosing a discriminating value for estrogen sulfurylation of 40 pmole per mg protein per 2 hr, then 16/19 (84%) of the ER negative tumors were below this point. Since previous data had shown that 20/23 (87%) progesterone receptor negative tumors were also below this value (Pewnim, Adams and Ho, CANCER RES. 40, 1360 (1980), an alternative simple method, having a high potential for the evaluation of hormone responsiveness in mammary cancer, is suggested.
Steroids 1982 Jan
PMID:Estrogen sulfurylation as an alternative indicator of hormone dependence in human breast cancer. 695 16

The metabolism of 3H-androsterone was studied in homogenates (fortified with uridine 5'-diphosphoglucuronic acid and adenosine 3'-phosphate 5'-phosphosulfate) of eighteen breast tumors, one muscle underlying the primary breast carcinoma and metastatic axillary lymph nodes from a patient with suspected primary breast cancer. The major metabolites identified were less polar than androsterone. On saponification these lipoidal derivatives afforded androsterone as the only product (3 to 48%). Unmetabolized androsterone and lesser quantities of epiandrosterone, 5 alpha-androstane- alpha, 17 beta-diol and 5 alpha-androstane-3,17-dione comprised the free steroid fraction. Androsterone glucosiduronate was isolated (0.17-4.1%) from weight breast tumor homogenates and from the node tissue incubation (17%). There was no apparent correlation between glucuronyltransferase activity and histopathology or estrogen receptor content.
Steroids 1981 Apr
PMID:Glucosiduronidation and esterification of androsterone by human breast tumors in vitro. 724 87

Anti-phospholipid Antibody Syndrome or Hugh's syndrome is a heterogeneous disorder, first fully described in 1980s. The syndrome is caused by the presence of specific antibodies against phospholipid binding plasma proteins in the serum of the patient, with or without underlying autoimmune diseases, that causes prolongation of tests of coagulation. High index of clinical suspicion is required for diagnosis of Anti-phospholipid Antibody Syndrome. Stroke or myocardial infarction in young, unprovoked recurrent deep vein thrombosis and recurrent pregnancy loss are typical scenarios where Anti-Phospholipid Antibody Syndrome should be suspected. Presence of non-criteria manifestations like livedo reticularis, skin ulcers, nephropathy, valvular heart disease and thrombocytopenia adds to diagnostic clue for presence of Anti-Phospholipid Antibody Syndrome. Treatment of Anti-Phospholipid Antibody Syndrome has preventive and therapeutic aspects that usually focus on thrombotic and obstetric manifestations of the disease. Therapeutic anti-coagulation with heparin followed by warfarin is required for patients presenting with acute thrombosis. Those with venous thrombosis are given moderate intensity warfarin International Normalized Ratio, 2-3), whereas those with arterial thrombosis or recurrent venous thrombosis even on warfarin are treated with high intensity warfarin (International Normalized Ratio, 3-4). Similarly, anticoagulation with heparin is advised in patients with obstetric Anti-Phospholipid Antibody Syndrome throughout pregnancy and up to six weeks postpartum. Treatment recommendations are still not clear for asymptomatic Anti-Phospholipid Antibody Syndrome positive patients and in those with non-criteria manifestations of the disease. Steroids, intravenous immunoglobulin and immunosuppressant are reported to be effective in severe cases of catastrophic antiphospholid syndrome characterized by rapid small vessel thrombotic involvement of multiple organ systems. Studies are evaluating the efficacy of direct thrombin inhibitors in the management of refractory cases. Keywords: anticoagulants; anti-phospholipid syndrome; obstetric APS; thrombotic APS.
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PMID:A Simplified Understanding of the Black Swan: Anti-phospholipid Antibody Syndrome. 3147 50