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

Analysis of the secretion of the human apocrine gland has shown the presence of dehydroepiandrosterone and androsterone sulfates, two androgen steroids previously identified in axillary sweat. These steroid sulfates were characterized by the gas chromatographic/mass spectrometric analysis of the odorous steroids formed on direct injection of the apocrine secretion into the host gas chromatographic injector. No spectral evidence was found for the presence of the delta16-androgen steroids which have axillary-like odors and have also been reported in axillary sweat. Cholesterol was the major steroid component of the secretion.
Steroids 1979 Sep
PMID:Steroid analysis of human apocrine secretion. 15 59

Cholesterol side-chain cleavage (CSCC) and aromatase activities were measured in luteal mitochondria and tissue pieces, respectively, from rhesus monkeys on days 22, 49, 128 and 160 of gestation. CSCC activity did not vary significantly during gestation and thus probably does not respond to chorionic gonadotropin which is elevated on day 22 of pregnancy. It is not known, however, whether CSCC can be stimulated prior to day 22 when the corpus luteum is steroidogenically more active. Both 3H-pregnenolone and 3H-progesterone were synthesized from [1,2-3/]cholesterol. Aromatase activity declined from high levels on days 22 and 49 to a nadir on day 128 of pregnancy. Utilizing either [1beta-3H]androstenedione or [1beta-3H]testosterone as substrate yielded comparable results throughout gestation.
Steroids 1977 Feb
PMID:Cholesterol side chain cleavage and aromatase activities in the corpus luteum of the pregnant rhesus monkey. 40 20

The relationship of bile acid and cholesterol excretion to changes in plasma cholesterol during pregnancy were studied in guinea pigs. Plasma cholesterol level increased in the first trimester of pregnancy, reached to a peak during the second trimester and decreased in the third trimester reaching the lowest level at one week prior to parturition. Cholesterol level returned to the control level after parturition. Plasma triglyceride level followed a similar trend attaining peak values at second trimester and gradually returned to the control level at the third trimester of pregnancy. Bile acid and total sterol excretion were significantly higher in guinea pigs during the last phase of pregnanccy while they remained unchanged during early stage of pregnancy.
Steroids 1978 Jun
PMID:Bile acid and cholesterol excretion in the pregnant guinea pig: studies on the hypercholesterolemia of pregnancy. 69 68

Marked variations in the 3beta-hydroxysterol content of hamster spermatozoa were observed as they progress through the epididymis. Cholesterol is the major sterol of caputal spermatozoa while the concentration of precursors of cholesterol was higher than that of cholesterol in caudal spermatozoa. One of these precursors has been identified as desmosterol. A second sterol has now been identified as 5alpha-cholestra-7,24-dien-3beta-ol by GLC-MS and by NMR. Its concentration is approximately 3-fold higher than that of cholesterol. This 3beta-hydroxysterol is also found in epididymal tissue.
Steroids 1978 Dec
PMID:5alpha-Cholesta-7,24-dien-3beta-ol as a major sterol of the male hamster reproductive tract. 73 99

This review briefly summarizes key researches on the structure of the sterol molecule from its very beginnings to the definitive elucidation in 1932. Cholesterol biosynthesis treated in somewhat greater detail covers the period from the 1930s to the 1960s. As a historic contribution, it presents researches previously published in numerous books, reviews, and original papers. The selection of topics, dictated by limits of time and space, is necessarily arbitrary and a personal choice. Readers of this journal will be familiar with the relevant chemical structures. Structural formulas are therefore omitted.
Steroids 1992 Aug
PMID:Sterol molecule: structure, biosynthesis, and function. 151 68

Recent studies have described an association between high-risk lipoprotein profiles and anabolic steroid abuse by athletes. However, none have included a comprehensive evaluation of diet as a confounding variable. The risk of cardiovascular disease (CVD) and its associations with drug abuse, dietary patterns, and training regimens were evaluated in 18 steroid-using (SU) and 17 non-steroid-using (NSU; no history of drug use or greater than or equal to 1 year drug-free) male bodybuilders. CVD risk was also evaluated in 10 control males. Fasting serum total cholesterol (TC), high-density lipoprotein cholesterol (HDL) and HDL subfractions 2 and 3, low-density (LDL) and very-low-density (VLDL) lipoprotein cholesterol, apoproteins (APO) A-1 and B, and triglycerides (TG) were analyzed at baseline (greater than or equal to 6 months drug-free) and the peak of steroid self-administration in SU. NSU were tested at similar times. Baseline CVD risk factor ratios (TC/HDL) were elevated (greater than 4.97) in 44% of SU and 24% of NSU. When baseline LDL and HDL values were compared to National Cholesterol Education Program CVD risk guidelines, these percentages stayed the same. At the peak of steroid administration significant changes were observed in LDL (22% increase), HDL (63% decrease), HDL-2 (86% decrease), HDL-3 (54% decrease), and TC/HDL (85% increase). No similar measures were observed among NSU or controls. Diets of all bodybuilders were similar, and included a daily intake of 5739 (+/- 2500) kcal, 324 (+/- 163) g protein, 637 (+/- 259) g carbohydrate, 214 (+/- 109) g fat, 5 (+/- 8) g alcohol, 1413 (+/- 1151) mg cholesterol, and a P/S ratio of 0.6 (+/- 0.3). Significant relationships between dietary fats and serum lipids were observed in the NSU. Polyunsaturated fatty acids were correlated with TG and VLDL (r = 0.69; p = 0.01), and TC/HDL (r = 0.06; p = 0.04). Total fats were correlated with TG (r = 0.57; p = 0.05), HDL-3 (r = -0.62; p = 0.04), and VLDL (r = 0.57; p = 0.05), and saturated fats with HDL-3 (r = -0.59; p = 0.055). Diet was moderately associated with lipoproteins in SU, but steroids had a much greater influence on CVD risk. Despite disease promoting diets NSU had relatively average CVD risk that may be attributed to protective effects of rigorous training.
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PMID:Dietary influences on cardiovascular disease risk in anabolic steroid-using and nonusing bodybuilders. 270 28

Cholesterol, pregnenolone, progesterone, 11-deoxycorticosterone (11-DOC) and corticosterone were quantitated in subcellular fractions isolated from in vivo adrenocorticotropin (ACTH)-stimulated rat adrenal zona fasciculata/reticularis. Six adrenal subcellular fractions separated by discontinuous sucrose gradient centrifugation (lipid, 0.125 M sucrose, cytosolic, microsomal, mitochondrial and nuclear) were extracted with alkaline ether/ethanol and assayed by high pressure liquid chromatography (HPLC). Lipid fractions contained the major cholesterol stores, while most pregnenolone and progesterone was found in lipid, microsomal and mitochondrial fractions. The 0.125 M sucrose and cytosol fractions together contained approximately 75% of the total 11-DOC and corticosterone. The five steroids were only present in small amounts in organelle fractions containing steroidogenic enzymes. Homogenate and lipid fraction cholesterol decreased between 10 and 15 min and again 30 min after ACTH injection. In the homogenate, lipid, microsomal and mitochondrial fractions, pregnenolone and progesterone were increased after ACTH injection; peak pregnenolone and progesterone concentrations were often measured in adrenal gland sucrose, cytosolic, microsomal and mitochondrial fractions 15 to 20 min after rats were injected with ACTH. Although ACTH increased 11-DOC and corticosterone in all but the mitochondrial and nuclear fractions, the sucrose, cytosolic and microsomal 11-DOC, and cytosolic corticosterone increased most dramatically. In many fractions, peak 11-DOC and corticosterone concentrations were most often observed between the 10 and 15 min periods and again at 30 min.
Steroids
PMID:Extraction of corticosterone from cell homogenates and subcellular fractions of the rat adrenal cortex. III. ACTH-induced temporal subcellular redistributions of steroid precursors to corticosterone. 301 51

[1,2-3H]Cholesterol, 5 beta-[21-14C]cholestan-3 beta-ol (coprostanol), and 3 beta-hydroxy-5 beta-[21-14C]pregnan-20-one were injected into intact Bufo arenarum toads. Arenobufagin, the main bufadienolide present in the venom of the mentioned toad, was isolated and purified by means of chromatographic procedures. The first two compounds, having an intact cholesterol side chain, were incorporated, at comparable levels, into the bufadienolide while the labeled pregnane derivative yielded non-radioactive arenobufagin. The above results support the hypothesis that cholesterol and those steroids having an intact cholesterol-type side chain are able to penetrate to the site of bufadienolide biosynthesis and are converted into bufadienolides by a still-unknown mechanism. On the other hand, those steroid derivatives bearing a degraded side chain, e.g., 20-keto-pregnanes, are not converted into bufadienolides because they are not incorporated into the bufadienolide-producing cells.
Steroids
PMID:Biosynthesis of bufadienolides in toads. VI. Experiments with [1,2-3H]cholesterol, [21-14C]coprostanol, and 5 beta-[21-14 C]pregnanolone in the toad Bufo arenarum. 312 47

5 alpha-[2,4-3H]Cholest-8(14)-en-3 beta-ol-15-one was administered to a series of male Sprague-Dawley rats by intragastric intubation in the form of an emulsion in a mixture of triolein, sodium taurocholate, bovine serum albumin, and glucose. [4-14C]Cholesterol was similarly administered to a second series of rats. The distribution of 3H and 14C was studied at 12 and 48 h after the administration of the sterols. The results demonstrated that the 15-ketosterol is absorbed and metabolized to material with the chromatographic properties of fatty acid esters of the 15-ketosterol, to cholesterol, and to fatty acid esters of cholesterol. The [3H]cholesterol formed from the 15-ketosterol was characterized by its behavior on silicic acid-Super Cel column chromatography, by the chromatographic behavior of its acetate derivative on alumina-AgNO3 column chromatography, and by purification by way of its dibromide derivative without significant change in specific activity. The general distribution of 3H was similar to that of 14C. No unusual concentration of 3H in any of the organs studied was observed.
Steroids
PMID:Inhibitors of sterol synthesis. Studies of the distribution and metabolism of 5 alpha-[2,4-3H]cholest-8(14)-en-3 beta-ol-15-one after intragastric administration to rats. 324 71

1. The substrate specificity of microsomal carboxyesterase(s) responsible for the formation of cholesteryl [2R]-2-(4-chlorophenyl) isovalerate from fenvalerate was investigated by incubating mouse kidney microsomes with 14C-cholesterol and the following substrates: fenvalerate isomers, fenvalerate analogues, other pyrethroids, methoprene and cycloprate analogues. Among the four isomers of fenvalerate, only the [2R, alpha S]-isomer yielded a cholesterol ester, being identical with the result obtained in the in vivo study. Some fenvalerate analogues produced cholesterol ester conjugates, but no other pyrethroids nor methoprene produced such conjugates. Some cycloprate analogues gave the corresponding cholesterol ester, the yields of which were dependent on their carbon-chain lengths. 2. Cholesterol ester formation in vitro from these fenvalerate analogues was well correlated with granuloma formation observed when the analogues were given to mice at 3000 ppm for a month. 3. Steroids other than cholesterol were also investigated as acceptors of the acid moiety of the [2R, alpha S]-isomer by incubating solubilized carboxyesterase(s) with the [2R, alpha S]-isomer in the presence of egg lecithin and several steroids. Dehydroisoandrosterone and pregnenolone were found to give the corresponding ester conjugates.
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PMID:Substrate specificity for formation of cholesterol ester conjugates from fenvalerate analogues and for granuloma formation. 335 27


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