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Biomedical subjects

E Roitman

Publications and source records attributed to E Roitman.

At least 19 recordsLinked to original sources
PubMed2002

Furosemide and 11beta-hydroxysteroid dehydrogenase activity, in man.

Mineralocorticoid receptors possess the same affinity for aldosterone and for cortisol and preferential binding of aldosterone is modulated by the 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) enzyme, which converts cortisol to its inactive metabolite cortisone. Several endogenous or exogenous compounds able to inhibit the enzyme have been described and, as a consequence, produce the syndrome of apparent mineralocorticoid excess (AME) characterized by hypertension, hypokalemia, volume repletion and suppression of the renin-angiotensin-aldosterone system. High doses of furosemide, a diuretic that works in the luminal surface of the thick ascending limb of Henle's loop, have been reported to inhibit 11 beta-OHSD activity to the same extent as licorice in vivo and in vitro, in rat. The aim of our study was to verify the effect of the drug on 11 beta-OHSD activity in man at the doses currently used in clinical practice. We tested the activity of 11 beta-OHSD following both acute and protracted administration of furosemide. In the acute study, the drug was administered at low (40 mg i.v. in bolo) and high doses (infusion of 10 mg/kg bw i.v for six hours); the protracted furosemide administration consisted in 50 mg/day for 20 days, by mouth. The ratios between the cortisol metabolites tetrahydrocortisol plus allo-tetrahydrocortisol to tetra-hydrocortisone and urinary free cortisol to urinary free cortisone were used to measure the activity of 11 beta-OHSD. Urinary cortisol, cortisone and their metabolites were tested by a gas-chromatographic/mass spectrometric method. Neither acute nor prolonged administration of furosemide did affect the activity of 11 beta-OHSD although the drug was able to modify plasma aldosterone and PRA secretion and to determine hypokalemia. Our results suggest that furosemide does not play a significant role in 11 beta-OHSD modulation in humans, at least at the dosage used in clinical practice.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2001

Dehydro-oestriol and dehydropregnanetriol are candidate analytes for prenatal diagnosis of Smith-Lemli-Opitz syndrome.

Gas chromatographic/mass spectrometric (GC/MS) analysis of maternal urine and serum steroids from 13 pregnancies at 25% risk for Smith-Lemli-Opitz syndrome (SLOS) was undertaken. All patients were between 12 and 31 weeks' gestational age. From dehydrocholesterol/cholesterol ratios determined in amniotic fluid and chorionic villus cells, five patients were shown to carry SLOS affected fetuses and eight patients were negative for the condition. Because it had previously been shown that dehydro-oestriol and dehydropregnanetriol were novel steroids produced in SLOS, these compounds were measured in the serum and urine samples of the 13 mothers. All five urine samples from SLOS affected pregnancies had high levels of both dehydrosteroid metabolites, which were below the detection limit in the non-affected pregnancies. The ratios of dehydro-oestriol/oestriol (DHE(3)/E(3)) were between 0.073 and 1.42 for the affected patients and less than 0.01 for unaffected patients. Corresponding values for dehydropregnanetriol/pregnanetriol (DHPT/PT) were 0.037-1.02 for affected and less than 0.01 for unaffected. In the positive serum sample available for analysis, the DHE(3)/E(3) ratio was 0.20 [unaffected (n=5), <0.014]. It is proposed that the measurement of DHE(3) and DHPT in maternal urine and serum may allow non-invasive antenatal diagnosis of SLOS.

Biomarkers↗
PubMed2000

Prostate formation in a marsupial is mediated by the testicular androgen 5 alpha-androstane-3 alpha,17 beta-diol.

Development of the male urogenital tract in mammals is mediated by testicular androgens. It has been tacitly assumed that testosterone acts through its intracellular metabolite dihydrotestosterone (DHT) to mediate this process, but levels of these androgens are not sexually dimorphic in plasma at the time of prostate development. Here we show that the 3 alpha-reduced derivative of DHT, 5 alpha-androstane-3 alpha,17 beta-diol (5 alpha-adiol), is formed in testes of tammar wallaby pouch young and is higher in male than in female plasma in this species during early sexual differentiation. Administration of 5 alpha-adiol caused formation of prostatic buds in female wallaby pouch young, and in tissue minces of urogenital sinus and urogenital tubercle radioactive 5 alpha-adiol was converted to DHT, suggesting that circulating 5 alpha-adiol acts through DHT in target tissues. We conclude that circulating 5 alpha-adiol is a key hormone in male development.

Androstane-3,17-diol↗
PubMed1999

Neonatal urinary steroids in Smith-Lemli-Opitz syndrome associated with 7-dehydrocholesterol reductase deficiency.

The biosynthetic abnormality in Smith-Lemli-Opitz syndrome (SLOS) is a deficiency of 7-dehydrocholesterol (7DHC) reductase, the enzyme responsible for catalyzing the final step in the Kandutsch-Russell pathway for cholesterol synthesis. Because the disposition of 7DHC and 8-dehydrocholesterol [8DHC; cholesta-5,8(9)-dien-3beta-ol] produced in this syndrome is little understood, we have analyzed urine from three young infants by gas chromatography/mass spectrometry to characterize its steroid metabolites. All steroid metabolites of adrenal origin found in normal infant urine were also found in urine from the patients with SLOS but in reduced amount. Quantitatively, the major steroids in these SLOS patients were identified by mass spectrometry as homologs of normal neonatal steroids possessing an additional double bond. Generally, two forms of each steroid were present in a similar amount. Because of the markedly increased levels of 7DHC and 8DHC in SLOS, these almost certainly represented the 5,7 and 5,8(9) unsaturated forms of each metabolite. The most abundant steroids were tentatively identified as 3beta,16alpha-dihydroxy-5,7-pregnadien-20-one and 3beta,16alpha-dihydroxy-5,8(9)-pregnadien-20-one, although similar 21-hydroxylated steroids and homologs of 16alpha-hydroxy-DHEA were also found. This study shows that all enzymatic steps used by cholesterol in the DHEA synthetic pathway are also functional for 7DHC and 8DHC.

Gas Chromatography-Mass Spectrometry↗
PubMed1999

Midgestational maternal urine steroid markers of fetal Smith-Lemli-Opitz (SLO) syndrome (7-dehydrocholesterol 7-reductase deficiency).

Smith-Lemli-Opitz syndrome (SLOS) is a malformation syndrome associated with 7-dehydrocholesterol (7DHC) 7-reductase deficiency. Although SLOS can be detected in an affected fetus before midpregnancy by measurement of 7DHC levels in amniotic fluid or chorionic villus cells, a noninvasive, more routine method is needed. Accordingly, this study was instigated to search for specific steroids in maternal urine in an affected pregnancy that reflect the 7-reductase deficiency of the fetus, ie, steroids retaining 7,8-unsaturation. Steroids were characterized by gas chromatography/mass spectrometry after urinary extraction, conjugate separation, and derivatization. Most steroids in maternal urine from a patient carrying a SLOS fetus were identified as progesterone metabolites, and these were entirely conventional, showing no evidence of additional unsaturation. Unsaturated homologues of the cortisol metabolites were also not detected. However, unsaturated homologues of pregnane-3,16,20-triols and pregnane-3,17,20-triol were found. Most likely, these are 7,8-unsaturated homologues, but 8,9-unsaturation is also possible because of the known activity of delta7-delta8-isomerase on 7DHC, which results in 8DHC being a prominent sterol in SLOS. Among these novel human steroids, the following were provisionally characterized: 5beta-pregn-7(or 8)-ene-3alpha,17alpha,20alpha-triol, 5beta-pregn-7(or 8)-ene-3alpha,16alpha,20alpha-triol, and 5alpha-pregn-7(or 8)-ene-3,16alpha,20alpha-triol. Confirmation of the position of unsaturation will require steroid synthesis. These novel steroids are not present in normal pregnancy urine and, therefore, are valuable for prenatal diagnosis of SLOS. In addition, separate studies have shown that 5beta-pregn-7(or 8)-ene-3alpha,17alpha,20alpha-triol is present in urine of children and adults with SLOS, and so is a useful analyte for confirmation of the disorder throughout life.

Adult↗
PubMed1999

Equine type estrogens produced by a pregnant woman carrying a Smith-Lemli-Opitz syndrome fetus.

The equine-type estriols 1,3,5(10),7-estratetraene-3,16alpha,17beta-triol (16alpha-hydroxy-17beta-dihydroequilin) and 1,3,5(10),6,8-estrapentaene-3,16alpha,17beta-triol (16alpha-hydroxy-17beta-dihydroequilenin) constituted over half of the estrogens excreted by a woman carrying a Smith-Lemli-Opitz syndrome (SLOS) affected fetus. The steroids were characterized by gas chromatography-mass spectrometry (GC/MS), and mass spectra of the dehydro estriols as trimethylsilyl ethers are illustrated. SLOS is associated with 7-dehydrocholesterol (7DHC), delta 7-reductase deficiency; the enzyme catalyzing the final step in cholesterol biosynthesis. Identification of these equine estrogens show that an estrogen biosynthetic pathway parallel to normal is functional in the feto-placental unit and uses 7DHC as precursor, therefore P450scc, P450c17, and 3betaHSD and P450arom are all active on 7-dehydrometabolites. Patients with affected fetuses have low plasma estriol values (probably due to deficient production of the cholesterol precursor) and this is often a warning sign which instigates further evaluation for SLOS. The estriol deficiency is not quantitatively made up by the dehydrometabolites, and the combined excretion was found to be about one-third of the mean of gestational age matched controls. The importance of these findings lies in the potential value of dehydroestriol measurement for non-invasive diagnosis of SLOS at mid-gestation. Currently diagnosis relies on imaging, since SLOS is a malformation syndrome, and measurement of 7DHC levels in amniotic fluid and chorionic villus tissue.

Adult↗
PubMed1998

Plasmapheresis in the treatment of posttransplant cardiomyopathy.

After heart transplantation a number of factors such as pre- and postoperative hypoxia of the myocardium, myocardial failure of the early postoperative period, acute rejection episodes, cytomegalovirus infection, and finally the progressive atherosclerosis of the coronary arteries lead to the development of transplanted heart failure. Severe alterations of the myocardial function at this end stage of the process correspond to incurable cardiomyopathy. The target of plasmapheresis in this case is to decrease the extent of the disturbances in the lipoprotein contents and blood rheology for the improvement of the coronary perfusion of the transplanted heart. Nine patients with 3-7 year survival periods after heart transplantations underwent plasmapheresis twice a year using the Haemonetics PCS-plus machine. 2,100-2,700 ml of plasma was removed. Biochemical data, rheology and coagulation, and the concentration of Sandimmune (Sandoz Pharma Ltd., Basel, Switzerland) were controlled, and radionuclide scintigraphy of the myocardium, coronarographia, and transesophageal ultrasound investigations were completed for these patients. The result was the significant improvement of the coronary perfusion of the myocardium. The level of immunosuppression after the plasmapheresis procedures did not change and therefore did not demand any correction. Thus, we think that plasmapheresis can be an effective method of treatment of posttransplantation cardiomyopathy; the improvement of coronary perfusion decreases the extent of chronic ischemia. Further studies are necessary to answer the question as to whether it is possible to prolong the time before retransplantation with the help of plasmapheresis.

Adult↗
PubMed1998

Steroid sulphatase deficiency is the major cause of extremely low oestriol production at mid-pregnancy: a urinary steroid assay for the discrimination of steroid sulphatase deficiency from other causes.

A method for determining whether a pregnant woman with an extremely low serum oestriol (ELSE) measurement of mid-trimester is carrying a fetus with steroid sulphatase deficiency or another more serious disorder is described. We undertook GC/MS analysis of steroids in random maternal urine samples and quantified oestriol, oestriol precursors (dehydroepiandrosterone (DHEA), 5-androstene-3 beta, 17 beta-diol, 16 alpha-hydroxy-dehydroepiandrosterone and 5-androstene-3 beta, 16 alpha, 17 beta-triol), pregnanediol, and five other steroids largely unaffected by pregnancy (androsterone, etiocholanolone, tetrahydrocortisol, 5 alpha-tetrahydrocortisol and tetrahydrocortisone). Thirty-two samples collected from seven normal pregnant women between the 7th and 27th week of pregnancy and 22 from individuals with ELSE were analysed. Diagnostic ratios of excreted products were developed. These included ratios of oestriol and oestriol precursors to the cumulative value for the five non-pregnancy-related steroids and ratios of oestriol and oestriol precursors to pregnanediol and to each other. Our data demonstrated high 3 beta-hydroxy-5-ene steroid excretion in all ELSE patients together with low urinary oestriol excretion, a situation only consistent with deficiency of steroid sulphatase. The normal individuals had high oestriol and low excretion of oestriol precursors. No patient in our series showed the low oestriol levels and low oestriol precursor values that would indicate a fetal adrenal abnormality as the underlying defect.

Androstenediol↗
PubMed1997

Androstanediol and 5-androstenediol profiling for detecting exogenously administered dihydrotestosterone, epitestosterone, and dehydroepiandrosterone: potential use in gas chromatography isotope ratio mass spectrometry.

The basis of a potential method for confirming intake of four natural androgens (testosterone, epitestosterone, dihydrotestosterone, and dehydroepiandrosterone is presented. The method relies on isolating from urine a steroid fraction containing androstenediol and androstanediol metabolites of these natural steroids and analyzing their 13C content by gas chromatography, combustion, isotope ratio mass spectrometry. The steroids were recovered from urine by conjugate hydrolysis with a Helix pomatia preparation (sulfatase and beta-glucuronidase), Girard T reagent separation to obtain a nonketonic fraction, and Sephadex LH-20 chromatography for purification. Metabolites appropriate for all of the natural steroids could be separated (as diacetates) by gas chromatography on a DB-17 capillary column viz.: 5 alpha (and beta)-androstane-3 alpha,17 alpha-diol (epitestosterone as precursor); 5 alpha (and beta)-androstane-3 alpha,17 beta-diol (testosterone as precursor); 5-androstene-3 beta,17 beta-diol (dehydroepiandrosterone precursor); and 5 alpha-androstane-3 alpha,17 beta- (and 17 alpha-) diol (dihydrotestosterone precursor). Measurement of the 13C content of the specific analytes after ingestion of the androgen precursors demonstrated a lowering of delta 13C/1000 value compared to normal values. Typically, in the male individual studied, delta 13C/1000 values for all components were -26 to -27 before drug administration and -29 to -30 at 6 h after, the latter values reflecting those obtaining for commercial synthetic steroid compared to in vivo synthesized steroid. While generally the metabolism of the steroids was as expected, this was not the case for 5 alpha-dihydrotestosterone. A major metabolite was 5 alpha-androstane-3 alpha,17 alpha-diol, which had presumably been formed by 17 beta/17 alpha isomerization, a process previously known for unnatural anabolics but not for natural hormones. The isolation, purification, and isotope ratio mass spectrometry techniques described may form the basis of a general method for confirming natural steroid misuse by sports participants.

Androstane-3,17-diol↗
PubMed1997

Maternal tobacco smoke exposure and persistent pulmonary hypertension of the newborn.

We propose that in utero exposure to tobacco smoke products places a newborn at risk for persistent pulmonary hypertension of the newborn (PPHN). To test this hypothesis, infants with PPHN were identified. Healthy newborns of similar ethnicity were identified as a comparison group. Cord blood cotinine concentrations and maternal questionnaires were obtained. The number of women exposed to tobacco smoke in each group ascertained by questionnaire was borderline significantly different (38.7% vs. 20.5%; p = 0.080). However, more PPHN infants had detectable cotinine in their cord blood (64.5% vs. 28.2%; p = 0.002), and the median cotinine concentrations were significantly higher (5.2 ng/ml vs. 2 ng/ml; p = 0.051) than the comparison infants. Among infants delivered to nonsmoking women, more PPHN infants had detectable cotinine (50% vs. 19%; p = 0.015), and the cotinine concentrations were higher (3.5 ng/ml vs. 1.65 ng/ml; p = 0.022) than the comparison group. We conclude that active and passive smoking during pregnancy is a risk factor for PPHN. Therefore, we recommend that pregnant women cease smoking and avoid environmental tobacco smoke. Key words. cotinine, newborns, passive, persistent pulmonary hypertension, smoking, tobacco smoke pollution.

Adult↗
PubMed1996

Quantitation of cortisol and related 3-oxo-4-ene steroids in urine using gas chromatography/mass spectrometry with stable isotope-labeled internal standards.

A method for the profiling of several important 3-oxo-4-ene urinary steroids is reported. The methodology is combined gas chromatography/mass spectrometry (GC/MS) utilizing stable isotope-labeled internal standards. The following standards were obtained or easily synthesized: [9, 11, 12, 12-2H4]cortisol, [1,2-2H2] and [9, 12, 12-2H2]cortisone, [1,2-2H2]6 beta-hydroxycortisol, and [1,2-2H2]18-hydroxycortisol. We found the following excretions of free steroids for normal adult males and females: cortisol (males mean +/- SD, 35 +/- 13; females mean +/- SD, 23 +/- 13), cortisone (males mean +/- SD, 58 +/- 23; females mean +/- SD, 50 +/- 22), 6 beta-hydroxycortisol (males mean +/- SD, 164 +/- 59; females mean +/- SD, 108 +/- 55), and 18-hydroxycortisol (males mean +/- SD, 148 +/- 55; females mean +/- SD, 71 +/- 30). For 18-hydroxycortisol in particular, the excretions were much higher for males than for females. We found that the larger part of urinary cortisol and cortisone is not free but is released from conjugation by enzymes present in snail digestive juice. Using a pooled urine sample from an equal number of male and female subjects, we found that for cortisol 29% was excreted free, 28% as glucuronide and 43% as other conjugates (probably sulfates). For cortisone 41% was free, 45% beta-glucuronide and 14% as other conjugates. Relatively little (3-8%) of the hydroxylated cortisols were excreted conjugated.

Adolescent↗
PubMed1992

Chlorohydrin formation from unsaturated fatty acids reacted with hypochlorous acid.

Stimulated neutrophils produce hypochlorous acid (HOCl) via the myeloperoxidase-catalyzed reaction of hydrogen peroxide with chloride. The reactions of HOCl with oleic, linoleic, and arachidonic acids both as free fatty acids or bound in phosphatidylcholine have been studied. The products were identified by gas chromatography-mass spectrometry of the methylated and trimethylsilylated derivatives. Oleic acid was converted to the two 9,10-chlorohydrin isomers in near stoichiometric yield. Linoleic acid, at low HOCl:fatty acid ratios, yielded predominantly a mixture of the four possible monochlorohydrin isomers. Bischlorohydrins were also formed, in increasing amounts at higher HOCl concentrations. Arachidonic acid gave a complex mixture of mono- and bischlorohydrins, the relative proportions depending on the amount of HOCl added. Linoleic acid appears to be slightly more reactive than oleic acid with HOCl. Reactions of oleic and linoleic acids with myeloperoxidase, hydrogen peroxide, and chloride gave chlorohydrin products identical to those with HOCl. Lipid chlorohydrins have received little attention as products of reactions of neutrophil oxidants. They are more polar than the parent fatty acids, and if formed in cell membranes could cause disruption to membrane structure. Since cellular targets for HOCl appear to be membrane constituents, chlorohydrin formation from unsaturated lipids could be significant in neutrophil-mediated cytotoxicity.

Arachidonic Acid↗
PubMed1992

Measurement of estradiol-17-fatty acid esters in human tissues.

We have developed a gas chromatographic/mass spectral method for the sensitive and reproducible measurement of estradiol-17-fatty acid esters in human tissues and blood. To provide an internal standard for quantification, a trideuterated analog of a representative estradiol ester is added to the tissues. Estradiol (E2) released from the nonpolar ester fraction by alkaline hydrolysis is derivatized to form the ditrimethylsilyl ether and then analyzed by gas chromatographic/mass spectral, monitoring the molecular ions mass per U charge of the ditrimethylsilyl derivative of E2 and [2H3]E2. There are low but detectable levels of E2 ester in the blood of cycling females; there are none in urine. While the E2 ester is present in breast cyst fluid, its concentration, 77-140 pmol/L, is considerably less than E2, 110-2,863 pmol/L. But there is a large amount of E2 ester in fat. In premenopausal women the average E2 ester in fat (sc and omental) is 957 +/- 283 38 fmol/g (SEM); in women who are menopausal less than 12 yr, the E2 ester in fat is 669 +/- 158 fmol/g; in women who are menopausal at least 15 yr, the fat level is 399 +/- 146 fmol/g. Muscle from the same women have lower concentrations of the ester; in 8 out of 12 muscle specimens it was not detectable. The E2 esters are extremely potent estrogens. Although they are hormonally active they require enzymatic hydrolysis to exert their hormonal action. These studies show that these long chain esters of E2 are sequestered in fatty tissues, wherein they represent a protected store of preformed hormone. Under the proper stimulation, adipose tissue can activate the estrogenic signal through the action of hormonally sensitive esterases. Thus, through signaling between estrogen sensitive tissues and neighboring fat cells, a local paracrine loop may exist.

Adipose Tissue↗
PubMed1983

Characterization of the major steroids present in amniotic fluid obtained between the 15th and 17th weeks of gestation.

In pooled amniotic fluid obtained between the 15th and 17th weeks of gestation the concentration of free steroids and steroid glucuronides was found to be 40 micrograms/dl. The concentration of steroid monosulfates and disulfates was 19 micrograms/dl. About half of the characterized steroids are progesterone metabolites. The "fetal type" 3 beta-hydroxy-5-ene steroids were found exclusively in the sulfoconjugated form. Their concentration represents 20% of the total steroid content. The identification of two 15 beta-hydroxylated C21 steroids, 3 beta,15 beta,17 alpha-tridoxy-5-pregnen-20-one and 5-pregnene-3 beta,15 beta,17 alpha,20 alpha-tetrol isolated from mid-pregnancy amniotic fluid is reported here. Metabolites of cortisol and 17-deoxycorticosteroid metabolites had similar quantitative importance, 8.6 and 9.4%, respectively.

17-alpha-Hydroxypregnenolone↗
PubMed1983

Human stratum corneum lipids: characterization and regional variations.

The lipids of mammalian stratum corneum are known to be important regulators of skin permeability. Since the human stratum corneum displays remarkable regional variations in skin permeability, we assessed the total lipid concentration, the distribution of all major lipid species, and the fatty acid composition in Bligh-Dyer extracts from four skin sites (abdomen, leg, face, and sole) that are known to display widely disparate permeability. Statistically significant differences in lipid weight were found at the four sites that were inversely proportional to their known permeability. In all four sites, among the polar lipids, the stratum corneum contained negligible phospholipids, but substantially more cholesterol sulfate (1-7%) than previously appreciated. As in the stratum corneum from other mammals, the bulk of the lipids consisted of neutral (60-80%) and sphingolipids (15-35%). Of the neutral lipids, free sterols (4- to 5-times greater than esterified sterols), free fatty acids, triglycerides, and highly nonpolar species (n-alkanes and squalene) predominated. n-Alkanes, which were present in greater quantities than previously appreciated, comprised a homologous series of odd- and even-chained compounds ranging from C19 to C34. The sphingolipids comprised over 80% ceramides vs. lesser quantities of glycosphingolipids. In all four sites, the sphingolipids were the major repository of long-chain, saturated fatty acids. The neutral lipid:sphingolipid ratio generally was proportional to the known permeability of each site: higher neutral lipids and lower sphingolipids generally were associated with superior barrier properties. These studies provide: 1) the first detailed, quantitative analysis of human stratum corneum lipids and 2) information about the variability in lipid composition at four skin sites with known differences in permeability. The latter results suggest that variations in neutral lipids, rather than sphingolipids, may underlie local variations in skin permeability.

Alkanes↗
PubMed1981

Steroid excretion in urine during suppression and stimulation of adrenals in the 17 alpha-hydroxylase deficiency syndrome.

Twenty-three steroids were determined by capillary column gas chromatography in urine specimens from a patient with the 17 alpha-hydroxylase deficiency syndrome during dexamethasone suppression and ACTH stimulation tests. These steroids included pregnanediols and pregnenediols, 21-deoxy metabolites of corticosterone (e.g. 3 alpha, 20 alpha-dihydroxy-5 alpha-pregnan-11-one), and 21-hydroxy metabolites [e.g. allo-tetrahydrocorticosterone (3 alpha, 11 beta, 21-trihydroxy-5 alpha-pregnan-20-one)]. During dexamethasone suppression or ACTH stimulation, the excretion of all steroids decreased and increased, respectively, indicating the pituitary-dependent adrenal origin of each compound. The changes in excretion of 21-deoxy steroids responded slowly (compared with the 21-hydroxylated metabolites) to these maneuvers, thereby providing further evidence for extensive enterohepatic circulation of corticosterone metabolites. 21-Dehydroxylated corticosterone metabolites accounted for approximately 40% the total steroids excreted during the control period, and this percentage probably approximates the proportion of corticosterone excreted in bile.

Adrenal Glands↗