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PubMed1976

Distinct testicular 17-ketosteroid reductases, one in interstitial tissue and one in seminiferous tubules. Differential modulation by testosterone and metabolites of testosterone.

The final step in the biosynthesis of testosterone is the reduction of androstenedione, which is catalyzed by the microsomal enzyme 17-ketosteroid reductase. Evidence is presented which suggests that there are two distinct 17-ketosteroid reductases in rat testes, one in interstitial tissue and one in seminiferous tubules. The two enzymes have different pH optima, 5.6 for the one from interstitial tissue and 6.5 for the one from seminiferous tubules. At the optimum pH, a 70-fold difference in Km values was observed, 17 muM for the interstitial tissue enzyme and 0.25 muM for the enzyme from seminiferous tubules. Testosterone and metabolites of testosterone have very different effects of each of these enzyme activities. The interstitial tissue enzyme activity is inhibited by testosterone and several 5alpha-reduced metabolites of testosterone and by estrogens. The most potent inhibitor of the steroids investigated was 5alpha-androstane-3alpha, 17beta-diol, followed by 17beta-estradiol approximately equal to dihydrotestosterone greater than testosterone greater than estrone greater than estriol. 5alpha-Androstane-3alpha, 17beta-diol and 17beta-estradiol were shown to act by competitive inhibition with apparent Ki values of 2.2 and 3.7 muM, respectively. In contrast, it was demonstrated that among the above steroids, only dihydrotestosterone inhibits the 17-ketosteroid reductase activity of seminiferous tubules and this inhibition was only observed at very high concentrations of inhibitor. Testosterone stimulated the 17-ketosteroid reductase activity of seminiferous tubules. 5alpha-Androstane-3alpha, 17beta-diol at low concentrations stimulated the enzyme activity from seminiferous tubules, while it had no effect at high concentrations. The remainder of the steroids tested had no effect on the 17-ketosteroid reductase activity of seminiferous tubules. The difference in response of the two enzyme activities suggests a mechanism for local regulation of testosterone synthesis in each testicular compartment that does not involve directly pituitary gonadotropins.

17-Ketosteroids↗
PubMedDate not supplied

Urinary 17-ketosteroid fractions in young patients with breast cancer.

The main fractions of 17-ketosteroids were estimated in 30 young women (under 40 years) with breast cancer and 20 controls of the same age. The determination of the fractionated ketosteroids was made by thin layer chromatography on silicagel. The mean levels of etiocholanolone, androsterone, total ketosteroids and the sum of the fractions of 17-ketosteroids were significantly decreased in patients with breast cancer in comparison with the controls. No significant differences between the mean levels of dehydroepiandrosterone and 11-oxygenated-17-ketosteroids were noted in these groups.

17-Ketosteroids↗
PubMed1988

Rat Leydig cell and granulosa cell 17-ketosteroid reductase activity: subcellular localization and substrate specificity.

The potent gonadal steroids testosterone and estradiol are synthesized from the biologically weak precursors, androstenedione and estrone, by enzymatic reduction of the ketone group at carbon-17 of the steroid nucleus (17-ketosteroid reductase). To test the hypothesis that Leydig and granulosa cells may contain a distinct 17-ketosteroid reductase enzyme, the subcellular localization and the substrate specificity of the enzyme was examined in each cell type. In Leydig cells, the 17-ketosteroid reductase activity was concentrated in the microsomal fraction of the cell. In granulosa cells, the 17-ketosteroid reductase activity was concentrated in the cytosolic fraction of the cell. In Leydig cell microsomes, the apparent Michaelis-Menten constant for the conversion of androstenedione to testosterone was 0.41 mumol/L and for the conversion of estrone to estradiol it was 12 mumol/L. In granulosa cell cytosol, the apparent Michaelis-Menten constant for the conversion of estrone to estradiol was 1.1 mumol/L and for the conversion of androstenedione to testosterone it was 15 mumol/L. These results demonstrate that rat Leydig and granulosa cells each contain a 17-ketosteroid reductase enzyme with unique subcellular localization and substrate specificity.

17-Hydroxysteroid Dehydrogenases↗
PubMed1977

Correlation of the effects of dexamethasone administration on urinary 17-ketosteroid and serum androgen levels in patients with hirsutism.

Total 24 hour urinary 17-ketosteroid and serum testosterone (T), androstenedione (delta), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DS), and cortisol levels were measured before and during four days of dexamethasone administration in 28 hirsute patients and 10 women with normal ovulatory cycles. Both the base-line urinary 17-ketosteroids and serum androgen levels were significantly higher (p less than 0.05) in hirsute than in normal subjects. Cortisol levels were similar in the two groups. Dexamethasone administration resulted in a significant suppression (p less than 0.05) of all the urinary and serum androgen and cortisol levels in both groups. At the end of suppression the serum DHEA, DS and cortisol levels were similar, while the urinary 17-ketosteroids and serum T and delta levels were still significantly higher (p less than 0.05) in the hirsute than in normal women. There was poor correlation between total urinary 17-ketosteroid and serum androgen results. These finding suggest there is a dual abnormality of androgen production in hirsute patients. The adrenal glands appear to secrete increased quatities of DHEA and DA, while the ovaries appear to produce elevated amounts of T and delta.

17-Ketosteroids↗
PubMed1990

Combined effects of two mutations of catalytic residues on the ketosteroid isomerase reaction.

delta 5-3-Ketosteroid isomerase (EC 5.3.3.1) catalyzes the isomerization of delta 5-3-ketosteroids to delta 4-3-ketosteroids by a conservative tautomeric transfer of the 4 beta-proton to the 6 beta-position with Tyr-14 as a general acid and Asp-38 as a general base [Kuliopulos, A., Mildvan, A. S., Shortle, D., & Talalay, P. (1989) Biochemistry 28, 149-159]. Primary, secondary, and combined deuterium kinetic isotope effects establish concerted substrate enolization to be the rate-limiting step with the wild-type enzyme [Xue, L., Talalay, P., & Mildvan, A. S. (1990) Biochemistry 29, 7491-7500]. The product of the fractional kcat values resulting from the Y14F mutation (10(-4.7)) and the D38N mutation (10(-5.6)) is comparable (10(-10.3)) to that of the double mutant Y14F + D38N (less than or equal to 10(-10.4)) which is completely inactive. Hence, the combined effects are either additive or synergistic. Quantitatively, similar effects of the two mutations on kcat/KM are found in the double mutant. Despite its inactivity, the Y14F + D38N double mutant forms crystals indistinguishable in form from those of the wild-type enzyme, tightly binds steroid substrates and substrate analogues, and immobilizes a spin-labeled steroid in an orientation indistinguishable from that found in the wild-type enzyme, indicating that the double mutant is otherwise largely intact. It is concluded that the total enzymatic activity of ketosteroid isomerase probably results from the independent and concerted functioning of Tyr-14 and Asp-38 in the rate-limiting enolization step, in accord with the perpendicular or antarafacial orientation of these two residues with respect to the enzyme-bound substrate. Synergistic effects of mutating two residues on kcat and on kcat/KM of enzyme-catalyzed multistep reactions are shown, theoretically, to occur when both residues act independently in the same step, and simple additivity occurs when this step is rate-limiting. Other conditions for additivity of the effects of mutations of kcat and kcat/KM are theoretically explored.

Binding Sites↗
PubMed1993

Effects of itraconazole on cytochrome P-450-dependent sterol 14 alpha-demethylation and reduction of 3-ketosteroids in Cryptococcus neoformans.

As in other pathogenic fungi, the major sterol synthesized by Cryptococcus neoformans var. neoformans is ergosterol. This yeast also shares with most pathogenic fungi a susceptibility of its cytochrome P-450-dependent ergosterol synthesis to nanomolar concentrations of itraconazole. Fifty percent inhibition of ergosterol synthesis was reached after 16 h of growth in the presence of 6.0 +/- 4.7 nM itraconazole, and complete inhibition was reached at approximately 100 nM itraconazole. This inhibition coincided with the accumulation of mainly eburicol and the 3-ketosteroid obtusifolione. The radioactivity incorporated from [14C]acetate in both compounds represents 64.2% +/- 12.9% of the radioactivity incorporated into the sterols plus squalene extracted from cells incubated in the presence of 10 nM itraconazole. The accumulation of obtusifolione as well as eburicol indicates that itraconazole inhibits not only the 14 alpha-demethylase but also (directly or indirectly) the NADPH-dependent 3-ketosteroid reductase, i.e., the enzyme catalyzing the last step in the demethylation at C-4. This latter inhibition obviates the synthesis of 4,4-demethylated 14 alpha-methylsterols that may function at least partly as surrogates of ergosterol. Eburicol and obtusifolione are unable to support cell growth, and the 3-ketosteroid has been shown to disturb membranes. The complete inhibition of ergosterol synthesis and the accumulation of the 4,4,14-trimethylsterol and of the 3-ketosteroid together with the absence of sterols, such as 14 alpha-methylfecosterol and lanosterol, which can partly fulfill some functions of ergosterol, are at the origin of the high activity of itraconazole against C. neoformans. Fifty percent inhibition of growth achieved after 16 h of incubation in the presence of 3.2 +/- 2.6 nM itraconazole.

Cryptococcus neoformans↗
PubMed2002

Identification of human urine stains by HPLC analysis of 17-ketosteroid conjugates.

A new method for identifying human urine stains utilizing high-performance liquid chromatographic (HPLC) analysis of five major 17-ketosteroid conjugates: dehydroepiandrosterone sulfate, etiocholanolone sulfate, etiocholanolone glucuronide, androsterone sulfate, and androsterone glucuronide was examined. Samples of urine stains were extracted with borate buffer solution (pH 9.3) and the extracts were applied onto a Sep-Pak tC18 cartridge. The analytes were eluted from the cartridge with methanol. The eluates were prelabeled with 2,4-dinitrophenylhydrazine in trichloroacetic acid-benzene solution and were separated by HPLC on a reversed-phase ODS column using a mobile phase of 80% methanol in a buffer consisting of 25 mM sodium acetate in 2% acetic acid. The eluates were monitored by a spectrophotometer at 380 nm. While all five 17-ketosteroid conjugates were clearly detected in the human urine stain samples, traces of only some of these conjugates were detected in the animal samples. Therefore, the presence of all five 17-ketosteroid conjugates indicated human specificity. In addition to the above finding, the properties of those five 17-ketosteroid conjugates were confirmed by electrospray ionization liquid chromatography-mass spectrometry (ESI-LC-MS).

17-Ketosteroids↗
PubMedDate not supplied

17-Ketosteroids in leprosy.

Urinary 17-ketosteroids were estimated in 29 lepromatous leprosy cases. Correlation between 17-ketosteroid values, histopathologic findings, and serum G.G.P.T. values is discussed. Low values of 17-ketosteroids were associated with definite leproma to liver indicating the value of liver damage to 17-ketosteroids. This was more marked in males than in females.

17-Ketosteroids↗
PubMed1976

Simple determination of 3alpha-hydroxy fraction and 3beta-hydroxy fraction of urinary 17-ketosteroids.

We describe a method for determination of the 3alpha-hydroxysteroid fraction and 3beta-hydroxysteroid fraction of 17-ketosteroids in urine. The method includes enzymatic hydrolysis with beta-glucuronidase and extraction with ethyl acetate and color development of 3beta-hydroxysteroids by 3beta-hydroxysteroid oxidase and of total 17-ketosteroids by the Zimmermann reaction. The value for 3alpha-hydroxysteroids is calculated by subtracting the value for 3beta-hydroxysteroids from the value for total 17-ketosteroids. Recovery was assessed and results compared with those by an accepted method. Results were satisfactory for measuring these fractions of 17-ketosteroids.

17-Ketosteroids↗
PubMed2005

Ketosteroid profiling using Girard T derivatives and electrospray ionization tandem mass spectrometry: direct plasma analysis of androstenedione, 17-hydroxyprogesterone and cortisol.

A function of concentrations of three ketosteroids, [(androstenedione + 17alpha-hydroxyprogesterone)/cortisol], has been shown to provide better discrimination than the concentration of 17alpha-hydroxyprogesterone alone, for the diagnosis of the inherited disease congenital adrenal hyperplasia (CAH). A rapid, direct infusion electrospray ionization tandem mass spectrometry (ESI-MS/MS) method has been developed to measure this ratio in plasma (100 microL). Sensitivity and specificity result from the preparation of mono-Girard T derivatives. Androstenedione, 17alpha-hydroxyprogesterone and cortisol are individually quantitated by isotope dilution. Excellent statistical correlation with radioimmunoassay (RIA) results for the analysis of 17alpha-hydroxyprogesterone is demonstrated. The value of the ratio function of the three ketosteroids is 0.01-0.16 for normal controls (n=26) and 1.83-18.7 for patients with severe CAH (n=4). Profiles of ketosteroids derivatized with Girard T from the plasma of a child with severe CAH, generated by ESI-MS/MS analysis, are shown. Neutral loss scans for 29.5 and 59 Da assist in the identification of the ketosteroids.

17-alpha-Hydroxyprogesterone↗
PubMed1990

Spectral properties of 3-ketosteroid-delta 1-dehydrogenase from Nocardia corallina.

3-Ketosteroid-delta 1-dehydrogenase from Nocardia corallina is a flavoenzyme that catalyzes 1,2-desaturation of 3-ketosteroid. The dehydrogenase generated complexes with 3-ketosteroids and phenolic steroids such as estradiol with remarkable perturbations of the visible spectrum. The enzyme did not make the adduct with sulfite ion, but could use molecular oxygen as the electron acceptor. The CD spectra of oxidized and steroid-bound enzymes exhibited positive dichroisms in the visible region which resembled those of flavoenzyme oxidases. The dehydrogenase led isosbestically to the stable red semiquinone species with large yields upon photochemical or dithionite reduction (at pH 7.4) in the presence of the steroid product, 1,4-androstadiene-3,17-dione, but in the absence of the steroid the yield of semiquinone was low and the fully reduced enzyme was obtained. Substrate titration also yielded the red flavo-semiquinone stoichiometrically and it was hard to generate the fully reduced form. The reduced enzyme was oxidized with molecular oxygen, but did not oxidize with ferricyanide. An EPR study of these half-reduced forms confirmed the presence of the radical species with the g = 2.004 signal. The dehydrogenase was rapidly reduced with an excess amount of 3-ketosteroid at about 80% yield at pH 7.4 under anaerobic conditions and the reduced species was altered to the stable red semiquinone species. The rate of this reaction was t1/2 = 28 min at pH 7.4, 130 min at pH 9.0 and 34 min at pH 6.4, respectively. These results indicate that the semiquinone species does not act directly in turnover of the dehydrogenase reaction. The results were compared with the spectral properties of general acyl-CoA dehydrogenases and acyl-CoA oxidase toward the mechanism of C1,2-dehydrogenation.

Androstenedione↗
PubMed1962

17-ketosteroid and 17-hydroxycorticosteroid excretion in patients with duodenal ulceration.

The 24-hour excretion of 17-ketosteroids and 17-hydroxycorticosteroids has been estimated in a series of male duodenal ulcer subjects and compared with that of 56 normal male controls. It has been found that both 17-ketosteroid and 17-hydroxycorticosteroid excretion is less in ulcer subjects than in the control group; these differences are not large but in the case of 17-hydroxycorticosteroids they are statistically significant. For active ulcers (107 men) 17-hydroxycorticosteroid excretion is approximately 78% of normal and 17-ketosteroid excretion 93% of normal; in the quiescent phase (50 men) the differences are rather larger, being respectively 71% and 86% of normal. This reduced excretion persists after operation in both the short term, six months after operation (53 men), and the long term, 10 years and more after gastric resection (39 men).

17-Hydroxycorticosteroids↗
PubMed1995

Daily excretion levels of an unidentified ketosteroid in the urine of patients with Cushing's syndrome and healthy subjects measured by a new method.

We developed a new method for measuring an unidentified ketosteroid glucuronide (US-G) detected by the method of Iwata et al. for measuring 17-ketosteroid glucuronides by reversed phase HPLC on a Capcell-Pak C8 column with three kinds of mobile phase solutions (Iwata method; Clin Chem 35: 795-799, 1989). The Iwata method inadequately separated US-G and two hydroxy 17-ketosteroides, 11 beta-hydroxyetiocholanolone and 11 beta-hydroxyandrosterone, and it exhibits insufficient sensitivity for measuring traces of US-G in the urine of healthy subjects. We solved these problems by developing a new method which measures US-G in urine, as a free type by hydrolyzing the glucuronide type enzymatically, by normal phase HPLC on a Capcell-Pak Silica column with one kind of mobile phase solution. By this method, the levels of US excreted as a glucuronide in the urine of healthy subjects and of patients with Cushing's syndrome were determined as proportions of the levels of 11 beta-hydroxyandrosterone. The average daily urinary excretion of US was 971 micrograms (125-4,995 micrograms) in patients with Cushing's syndrome (n = 22: two males and 20 females aged 26 to 65 years), and 34 micrograms (0-141 micrograms) in healthy subjects (n = 63: 49 males, and 14 females aged 21 to 54 years), and the differences were clearly significant. However, there were no differences between the urinary US levels of patients with pituitary adenoma and patients with adrenal adenoma. Furthermore, no US was detected in the urine of patients with aldosteronism (two males and eight females aged 34 to 61 years).(ABSTRACT TRUNCATED AT 250 WORDS)

17-Ketosteroids↗
PubMed1976

Mass spectra of delta 4- and 5 alpha-3-ketosteroids formed during the oxidation of some 3 beta-hydroxysteroids by cholesterol oxidase.

Thirty-six delta5- and 5'alpha-3beta-hydroxysteroids have been oxidized with cholesterol oxidase to give the corresponding delta4- and 5alpha-3-ketosteroids, respectively. The mass spectral characteristics of the products (or their trimethylsilyl ether derivatives, in the case of 3-keto-hydroxysteroids) varied considerably, depending especially on the nature of the C-17 sidechain. The ion of m/e 124 (or its equivalent) from cleavage of ring B was frequently a major fragment from delta4-3-ketosteroids, but in some instances was of insignificant abundance. Trimethylsilylation of the product of the oxidation of neoergosterol gave neoergosterone enol-trimethylsilyl ether. Fragmentations of the sidechain predominated in the mass spectra of the 5alpha-3-ketosteroids.

Cholesterol↗
PubMed1985

Derivatization of ketosteroids for fast atom bombardment mass spectrometry.

Girard's reagents were used to derivatize ketosteroids and conjugates for analysis by positive ion fast atom bombardment mass spectrometry. Spectra contain an abundant ion corresponding to the cation (C+) of the newly formed ionic derivative (C+A-) and relatively little fragmentation. With derivatization, detection of ketosteroids at a concentration of 1 microgram microliter-1 in glycerol was straightforward. Such derivatization schemes may prove useful in the analysis of ketosteroids in complex biological mixtures.

Indicators and Reagents↗
PubMed1998

Determination of C-21 ketosteroids in serum using trifluoromethanesulfonic acid catalyzed precolumn dansylation and 1,1'-oxalyldiimidazole postcolumn peroxyoxalate chemiluminescence detection.

A new procedure for the quantitation of C-21 ketosteroids using trifluoromethanesulfonic acid-catalyzed precolumn dansylation and coupled column liquid chromatographic separation, followed by postcolumn 1,1'-oxalyldiimidazole peroxyoxalate chemiluminescence detection is presented. In the simultaneous optimization of chromatographic resolution and chemiluminescence intensity, a coupled column chromatographic system and a stopped-flow system were used. An eluent containing 20 mM phosphate buffer at pH 6.7 accomplished an efficient separation of 3 alpha-hydroxy-5 beta-pregnan-20-one from a mixture containing 10 C-21 ketosteroids. Phosphate buffer also proved to be the most advantageous, among the six buffers tested, for sensitive detection. Experimental design and multivariate data analysis were used to characterize and optimize the postcolumn reaction chemistry in the chromatographic system. A valid full factorial design with excellent predictability showed that the flow rates for both 1,1'-oxalyldiimidazole and hydrogen peroxide were the factors most strongly affecting the sensitivity of the system. The theoretical plate numbers were above 11,000 for all 10 dansylated ketosteroids. The 3 sigma detection limit estimated from 3 alpha-hydroxy-5 beta-pregnan-20-one calibration curve data was 1.6 pmol (n = 4, 125 microL injected) and spiked serum containing 0-74 pmol of this compound showed overall recoveries of 73 +/- 9% (n = 12). Quantitation of 3 alpha-hydroxy-5 beta-pregnan-20-one was finally carried out on 45 serum samples and the results compared to those from a radioimmunoassay (RIA) method. The data acquired with the procedure described in this work compare well with the results from RIA, which confirms the reliability of the new analytical procedure.

Catalysis↗
PubMed1995

Ultraviolet spectroscopic evidence for decreased motion of the active site tyrosine residue of delta 5-3-ketosteroid isomerase by steroid binding.

delta 5-3-Ketosteroid isomerase (EC 5.3.3.1) from Pseudomonas testosteroni catalyzes the highly efficient conversion of delta 5-3-ketosteroids to delta 4-3-ketosteroids by a stereoselective and intramolecular transfer of the 4 beta-proton to the 6 beta-position. Tyr-14 is the critical general acid and Asp-38 is the general base involved in catalysis. The UV absorption bandwidths of Tyr-14 were much narrower than those of the other two tyrosines (Tyr-55 and Tyr-88) of isomerase or of the N-acetyltyrosine ethyl ester in aqueous solution, suggesting that Tyr-14 is restricted in its mobility. Further immobilization of this residue occurs upon steroid binding. Thus, 5 alpha-estrane-3,17-dione, an A-ring saturated steroid, induces significant narrowing of the tyrosine absorption bands (pi-->pi*) of the main peak (279.5 nm) and the shoulder (285.5 nm) of Tyr-14, with no significant changes in lambda max. No effects of steroid binding were found on the absorption bandwidths of Tyr-55, Tyr-88, or the phenylalanine residues. The ratio of the absorbance (Amax) at the absorption maximum (lambda max) to that at lambda max plus 4 nm (Amax +4) was used as a measure of peak sharpness. Specifically, the ratios of A279.5/A283.5 (main peak) and A285.5/A289.5 (shoulder) of Tyr-14 of the free enzyme at 25 degrees C were 1.25 and 1.89, respectively, and they increased to 1.41 and 2.70, respectively, in the complex. A more precise measurement of the band narrowing from 4.2 to 3.1 nm between the inflection points was obtained from the derivative spectra. The absorption bands of free and steroid-bound isomerase were narrowed significantly by lowering the temperature and were broadened by denaturation, suggesting that the unusual peak-sharpening effects induced by steroid binding arise from the restricted motion of Tyr-14, as well as from more directional hydrogen bonding resulting from the displacement of water molecules from the active site and decreased flexibility of the protein. Larger enthalpy of the sharpening effects was observed for the steroid-bound enzyme (-0.527 +/- 0.016 kcal/mol) than for the free enzyme (-0.250 +/- 0.018 kcal/mol) by lowering the temperature, indicating that interactions of Tyr-14 with its environment, which restrain its motion, are stronger in the steroid-bound enzyme than in the free enzyme. Hydrogen-bonding modes of Tyr-14, mobility of the active site, and protein flexibility are the environmental factors determining the absorption bandwidths of the critical Tyr-14 residue.

Binding Sites↗
PubMed1989

Fractionation of urinary 17-ketosteroids by gas chromatography: a neglected procedure in the assessment of hyperandrogenicity in the hirsute female.

17-Ketosteroids were determined by gas chromatography in twenty four-hour urine samples from 62 hirsute females. The method permitted the determination of androsterone (A), aetiocholanolone (E) and dehydroepiandrosterone (D). Elevated concentrations of one or more of these metabolites were detected in 81% of the samples. Two main patterns of hyperandrogenicity were observed: 1) Hyper A + E (27%) and 2) Hyper A (26%). Elevated AD, AED, D, ED or E were less common, but in total these patterns comprised another 28%. The plasma testosterone and total urinary 17-ketosteroid concentrations were elevated in only 21% and 23% of the samples, respectively. Thirty two out of 33 patients with elevated urine metabolites showed significant suppression following dexamethasone administration (2 mg/day during 6 days). Thus, dexamethasone suppressable hyperandrogenicity was predominant in this group of hirsute females. Elevations of urinary androsterone and aetiocholanolone are probably contingent on the relative activities of 5 alpha- and 5 beta-reductases) in the presence of increased androstenedione secretion. Elevations of urinary dehydroepiandrosterone suggest decreased adrenal cortical 3 beta-hydroxysteroid dehydrogenase) activity. Thus, fractionation of urinary 17-ketosteroids seems to be an effective test in the evaluation of hirsutism.

17-Ketosteroids↗