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PubMed1985

Lipid composition and acid hydrolase content of lamellar granules of fetal rat epidermis.

Lipids and acid hydrolases have been characterized in a subcellular fraction, enriched with lamellar granules (LG), derived from fetal rat epidermis. This fraction contains 23% glycosyl ceramides and ceramides, 15% free sterols, and 34% phospholipids. The lipid/protein ratio is 2.0. The sterols and sphingolipids were present in proportions similar to those previously reported in stratum corneum. These findings provide direct biochemical evidence for the widely accepted hypothesis that stratum corneum lipids are derived from exocytosis of lamellar granules into the intercellular space. The LG fraction was enriched in certain acid hydrolases including glucosidase, acid phosphatase, phospholipases A, and sphingomyelinase; other acid hydrolases, i.e., amino-glycosidases, glactosidase and aryl sulfatase (pH 5.5), and steroid sulfatase were not preferentially localized in this fraction. By modulation of phospholipids, glycolipids, and proteins in the membrane regions of stratum corneum, the acid hydrolases of LG may play a role relevant to the function and desquamation of stratum corneum.

Animals↗
PubMed2003

An Xp; Yq translocation causing a novel contiguous gene syndrome in brothers with generalized epilepsy, ichthyosis, and attention deficits.

PURPOSE: We describe two brothers with generalized epilepsy, attention deficits, congenital ichthyosis, and Leri-Weill dyschondrosteosis who harbor an unusual Xp; Yq translocation chromosome, resulting in a novel contiguous gene syndrome because of deletion of genes from the distal short arm of the X chromosome. METHODS: Physical examination, neuropsychologic testing, EEG, and neuroimaging studies were performed. Because of their unusual phenotype, karyotyping, fluorescence in situ hybridization, and further molecular analyses were carried out to refine the break points of the underlying unbalanced sex chromosome rearrangement. RESULTS: The subjects had generalized epilepsy, X-linked ichthyosis, Madelung deformities, mesomelia, normal intelligence, and attention deficits. The brothers' karyotype was unbalanced; they inherited a maternal derivative X chromosome. Deleted distal Xp genes included short-stature homeobox on the X chromosome (SHOX), aryl sulfatase E (ARSE), variably charged X-chromosome mRNA gene A (VCX-A), and steroid sulfatase (STS). The final karyotype was 46,Y,der(X)t(X; Y)(p22.3; q11.2).ish der(X) (DXZ1+, KAL+, STS-, SHOX-) mat. CONCLUSIONS: Loss of distal contiguous Xp genes resulted in a syndrome comprising bony deformities, ichthyosis, attention problems, and generalized epilepsy. Candidate epilepsy genes within the deleted segment, such as ASMT, a gene involved in the final synthesis of melatonin, are discussed. Cytogenetic analyses should be included in the clinical evaluation of patients with generalized epilepsy and complex phenotypes.

Adolescent↗
PubMed1998

Analysis of an interstitial deletion in a patient with Kallmann syndrome, X-linked ichthyosis and mental retardation.

Contiguous gene syndromes are an interesting clinical phenomenon, resulting from interstitial or terminal deletions of several adjacent genes. The phenotype results in a combination of two or more monogenic disorders and relates clinical findings to corresponding genotypes. We present the case of a male patient with Kallmann syndrome (KS), X-linked ichthyosis (XLI) and X-linked mental retardation (MRX). He was referred at the age of 15.4 years for delayed puberty and obesity. He had a previous history of pyloric stenosis, bilateral orchidopexy and surgical correction of a pes equinovarus adductus. On physical examination, generalised ichthyosis and hypoplastic external genitalia were found. KS was evident with hypogonadotropic hypogonadism, hyposmia and a hypoplastic anlage of the olfactory tract in magnetic resonance imaging. Lipoprotein electrophoresis, and lack of steroid sulfatase and arylsulfatase-C activity in leucocytes confirmed XLI. DNA investigation established an interstitial deletion in Xp22.3 involving the Kallmann (KAL) gene, the steroid sulfatase (STS) gene and a putative mental retardation locus (MRX). The novel MRX locus maps to a 1-Mb region between DXS1060 and GS1.

Adolescent↗
PubMed1996

A 13C-NMR study of the mechanism of bacterial metabolism of monomethyl sulfate.

Two different mechanisms have been proposed previously for initiating the biodegradation of monomethyl sulfate (MeSO4) in bacteria. For a Hyphomicrobium species, a sulfatase enzyme has been proposed to hydrolyse MeSO4 to methanol and inorganic sulfate. For an Agrobacterium sp., an alternative proposal involves monooxygenation of MeSO4 (hydroxylation) to produce methanediol monosulfate, which decomposes spontaneously to formaldehyde and inorganic sulfate. In the present study, 13C-NMR was used to monitor metabolic intermediates of [13C]MeSO4 in real time in each species in order to resolve the issue of mechanism of biodegradation. Agrobacterium sp. M3C grew on MeSO4 but not on methanol. MeSO4-grown cells catabolised [13C]MeSO4 but not [13C]methanol, and [13C]methanol did not accumulate from MeSO4 in the presence of a known inhibitor of methanol dehydrogenase (cyclopropanol). Hyphomicrobium MS223 grew on MeSO4 and, in contrast with the Agrobacterium sp., also on methanol. The normally rapid metabolism of [13C]methanol by methanol-grown cells was arrested by cyclopropanol, but metabolism of [13C]MeSO4 by MeSO4-grown cells was unaffected. Moreover there was no accumulation of [13C]methanol from [13C]MeSO4 under conditions in which methanol dehydrogenase was shown to be inactive. The results provided strong evidence against the intermediacy of methanol in the biodegradation of MeSO4 in either species, and thereby render untenable mechanisms involving sulfatase-mediated hydrolysis of MeSO4. The data are consistent with the hydroxylation of MeSO4 via a monooxygenation mechanism and subsequent spontaneous hydrolysis of the methanediol monosulfate intermediate.

Alcohol Oxidoreductases↗
PubMed2002

Glucuronidation and sulfation of the tea flavonoid (-)-epicatechin by the human and rat enzymes.

(-)-Epicatechin (EC) is one of the flavonoids present in green tea, suggested to have chemopreventive properties in cancer. However, its bioavailability is not clearly understood. In the present study, we determined the metabolism of EC, focusing on its glucuronic acid and sulfate conjugation using human liver and intestinal microsomes and cytosol as well as recombinant UDP-glucuronosyltransferase (UGT) and sulfotransferase (SULT) isoforms in comparison with that occurring in the rat. Surprisingly, EC was not glucuronidated by the human liver and small intestinal microsomes. There was also no evidence of glucuronidation by human colon microsomes or by recombinant UGT1A7, which is not present in the liver or intestine. Interestingly, in the rat liver microsomes EC was efficiently glucuronidated with the formation of two glucuronides. In contrast, the human liver cytosol efficiently sulfated EC mainly through the SULT1A1 isoform. For the intestine, both SULT1A1 and SULT1A3 contributed. Other SULT isoforms contributed little. High-performance liquid chromatography of the sulfate conjugates showed one major sulfatase-sensitive peak with all tissues. An additional minor sulfatase-resistant peak was formed by the liver and intestinal cytosol as well as with SULT1A1 but not by the Caco-2 cytosol and SULT1A3. In the rat, EC sulfation was considerably less efficient than in the human liver. These results indicate that sulfation is the major pathway in EC metabolism in the human liver and intestine with no glucuronidation occurring. There was also a large species difference both in glucuronidation and sulfation of EC between rats and humans.

Animals↗
PubMed1983

Initiation of Activation of a Preemergent Herbicide by a Novel Alkylsulfatase of Pseudomonas putida FLA.

The activation of the preemergent herbicide 2-(2,4-dichlorophenoxy)ethyl sulfate (Crag herbicide) is initiated by soil microorganisms that are presumed to act by removing the ester sulfate group via some type of sulfatase enzyme. An enrichment technique with the herbicide as the sole source of sulfur led to the isolation of several pure cultures that could produce 2-(2,4-dichlorophenoxy)ethanol from the herbicide. One of these, a strain of Pseudomonas putida, was particularly active. Polyacrylamide gel zymograms of extracts of cells grown on nutrient broth showed the presence of three secondary and three primary alkylsulfatases. One of the latter enzymes was active toward Crag herbicide as well as sodium dodecyl sulfate. Maximum activity was obtained in the late-stationary phase of growth, and enzyme yields were not affected by either the presence or the absence of the herbicide in the growth medium. The enzyme was purified 2,670-fold to homogeneity by a combination of streptomycin sulfate treatment, heat treatment, and column chromatography on DEAE-cellulose, Sephacryl 200-S, and butyl agarose. The pure enzyme was tetrameric (molecular weight, 295,000) and most active at pH 6.0. Saturation kinetics with inhibition by excess substrate were observed for Crag herbicide and octyl sulfate. 2-Butox-yethyl sulfate was a relatively poor substrate, and dodecyltriethoxy sulfate was not hydrolyzed at all. Enzymatic hydrolysis of each substrate in the presence of H(2)O led to incorporation of O exclusively into SO(4) ions in all three cases. The Crag herbicide sulfatase therefore acts by cleaving the O-S bond of the C-O-S ester linkage, in contrast with other alkylsulfatases acting on long-chain alkyl sulfates.

Journal Article↗
PubMed1977

Release of beta-lysin from platelets caused by antigen-antibody complexes, purified enzymes, and platelet-aggregating substances.

The release of beta-lysin, which followed the intravenous injection of antigen-antibody complexes, did not take place when these complexes were added to citrated whole blood but did occur in heparinized blood. beta-Lysin release in heparinized blood was inhibited by citrate but were reversed by the addition of calcium ions that implicated complement reactions. Fourteen different enzymes were added to platelet-rich plasma (PRP). Streptokinase, neuraminidase, papain, phospholipase C, sulfatase, and trypsin caused platelets to release significant quantities of beta-lysin, whereas elastase, phosphatase, protease, ribonuclease A, hyaluronidase, lipase, and pepsin caused little or no increase in the plasma beta-lysin concentration. One enzyme, fibrinolysin, inactivated beta-lysin faster than it was released. The enzyme-induced release of beta-lysin from PRP was often accompanied by a reduction in the number of platelets. The intravenous injection of streptokinase, neuraminidase, and sulfatase caused in vivo releases of beta-lysin into the plasma. The platelet-aggregating substances collagen, arachidonic acid, and adenosine 5'-diphosphate caused beta-lysin to be released from PRP. The platelet-aggregating substances L-epinephrine, zymosan, fibrinogen, reserpine, and serotonin caused little or no release of beta-lysin from platelets. The results of this study indicate that the release of beta-lysin during antigen-antibody-complement reactions, blood coagulation, phagocytosis, and inflammation could be enzyme mediated.

Adenosine Diphosphate↗
PubMed1981

Hydrolytic enzymes of anaerobic bacteria isolated from human infections.

Thirty-three strains of anaerobic bacteria isolated from human clinical specimens were examined for the presence of heparinase, hyaluronidase, chondroitin sulfatase, gelatinase, collagenase, fibrinolysin, lecithinase, and lipase activities. Pronounced heparinase activity was limited to species of the genus Bacteroides. A number of species of the genera Bacteroides and Clostridium produced hyaluronidase and chondroitin sulfatase. Gelatinase, collagenase, and fibrinolysin activities were encountered in isolates of the genera Bacteroides, Clostridium, and Peptostreptococcus. All strains capable of degrading collagen also hydrolyzed other protein substrates. Lipolytic activity was minimal among these anaerobic bacteria. No specific hydrolytic activity was consistently associated with the isolates.

Anaerobiosis↗
PubMed2000

Accumulation of quercetin conjugates in blood plasma after the short-term ingestion of onion by women.

Quercetin is a typical flavonoid present mostly as glycosides in plant foods; it has attracted much attention for its potential beneficial effects in disease prevention. In this study, we examined human volunteers after the short-term ingestion of onion, a vegetable rich in quercetin glucosides. The subjects were served diets containing onion slices (quercetin equivalent: 67.6-93.6 mg/day) with meals for 1 wk. Quercetin was only found in glucuronidase-sulfatase-treated plasma, and its concentration after 10 h of fasting increased from 0.04 +/- 0.04 microM before the trial to 0.63 +/- 0.72 microM after the 1-wk trial. The quercetin content in low-density lipoprotein (LDL) after glucuronidase-sulfatase treatment corresponded to <1% of the alpha-tocopherol content. Human LDL isolated from the plasma after the trial showed little improvement of its resistance to copper ion-induced oxidation. It is therefore concluded that conjugated metabolites of quercetin accumulate exclusively in human blood plasma in the concentration range of 10(-7) approximately 10(-6) M after the short-term ingestion of vegetables rich in quercetin glucosides, although these metabolites are hardly incorporated into plasma LDL.

Adult↗
PubMed2000

Male-pattern baldness in men with X-linked recessive ichthyosis.

BACKGROUND: X-linked recessive ichthyosis (XRI) is a genetic disorder of keratinization with extracutaneous manifestations due to deficiency of steroid sulfatase (STS). Because STS plays an important role in androgen metabolism, and elevated levels of dehydroepiandrosterone sulfate have been reported in young men with andogenetic alopecia (AGA), the hypothesis was advanced that men with XRI do not show AGA or develop only mild forms of common baldness. METHODS: Patients with a diagnosis of XRI confirmed by analysis of the microsomal sulfatases in our clinic between 1984 and 1998, and in whom study of the case histories depicted the typical clinical presentation of XRI, were sent a questionnaire with the Hamilton-Norwood scale of patterns of hair loss in men, inquiring them to designate the condition of their scalp hair. RESULTS AND CONCLUSIONS: Of 15 questionnaires returned, 7 indicated Hamilton-Norwood I, 3 Hamilton-Norwood II, 3 Hamilton-Norwood III-vertex, 1 Hamilton-Norwood IV and 1 Hamilton-Norwood VII. The results of this survey do not support the hypothesis that XRI and AGA are mutually exclusive, in as much as advanced AGA was found among these men.

Adolescent↗
PubMed1991

Ocular findings in X-linked ichthyosis: a survey on 38 cases.

The authors report on the occurrence of ocular abnormalities in X-linked ichthyosis (XLI) patients, in their carrier mothers and in healthy volunteers who served as controls. The diagnosis of XLI was based on: (1) demonstration of steroid sulfatase deficiency in cultured skin fibroblasts; (2) lack of hybridization of patient's deoxyribonucleic acid (DNA) with specific steroid sulfatase complementary DNA probe; (3) electrophoretic mobility of plasma lipoproteins. Cholesterol sulfate plasma levels were also determined. The incidence of corneal opacities was the same in XLI patients and in their carrier mothers (23.7 and 24.3%, respectively). Neither other corneal nor ophthalmological alterations were found. Moreover, in XLI patients the plasma levels of cholesterol sulfate were about twenty times higher than in controls. Our findings demonstrate that ocular changes do not seem to be an absolute criterion for a definite diagnosis of XLI and the fact that the pathogenesis of corneal opacities is not due to an accumulation of cholesterol sulfate, but rather that this compound probably induces physicochemical changes of the corneal tissue properties.

Adolescent↗
PubMed2004

Cerebral glycolipidoses: clinical characteristics of 41 pediatric patients.

A retrospective clinical and biochemical analysis of 41 pediatric patients with cerebral lipidoses seen between 1995 to 2003 was performed at a tertiary referral center for neurologic disorders in southern India. Enzyme assays in serum and leukocytes, including histopathology, neuroimaging, and neurophysiology studies, were performed. There were 20 cases of metachromatic leukodystrophy (infantile,14; juvenile, 6), 12 cases of Tay-Sachs disease (infantile, 9; late G(M2-M3) gangliosidoses, 3), 8 cases of Sandhoff's disease, and 1 male case with multiple sulfatase deficiency. Consanguinity was present in 51.2% of cases. The male-to-female ratio was 23:17. Similar illness in the families was noted in 24.4%. The prominent clinical features in sulfatide lipidoses were regression of motor and mental milestones, seizures, and speech impairment, and in G(M2) gangliosidoses, the features were delayed milestones, startle myoclonus, seizures, and the presence of cherry-red spots. The case with multiple sulfatase deficiency had low levels of arylsulfatase A and B. This study indicates that these autosomal recessive inherited disorders are indeed prevalent in India.

Adolescent↗
PubMed1984

Partial deficiency of glycoprotein neuraminidase in some patients with Morquio disease type A.

A deficiency of glycoprotein neuraminidase (sialidase, acylneuraminyl hydrolase, EC 3.2.1.18) activity was found in fibroblasts from a patient with the clinical symptoms of Morquio disease type A (mucopolysaccharidosis IV A). Residual neuraminidase activity was about 5% of the mean normal activity. N-Acetylgalactosamine-6-sulfate (GalNAc-6-S) sulfatase activity was reduced to less than 1% of normal with a pH-optimum of 3.0 as expected for the severe form of Morquio disease. In peripheral leucocytes of the patient, however, neuraminidase activity but not Ga1NAc-6-S sulfatase activity was in the normal range. Mixing experiments excluded the presence of excessive amounts of inhibitors of neuraminidase activity.

Child↗
PubMed2003

Congenital hypopituitarism as a cause of undetectable estriol levels in the maternal triple-marker screen.

We are reporting a child with congenital panhypopituitarism, in whom deficient fetal steroidogenesis was suspected prenatally because of undetectable estriol levels measured in the maternal triple-marker screen. No fetal abnormalities were detected by ultrasonography. Amniocentesis demonstrated a normal 46,XX karyotype. Measurement of maternal urinary steroids failed to show elevation in the excretion of the major precursor for estriol, 16 alpha-hydroxydehydroepiandrosterone, indicating that the fetus did not have steroid sulfatase deficiency (placental sulfatase deficiency), the most common genetic cause of extremely low estriol. The steroid analysis excluded other rare single gene defects, including aromatase deficiency and 17 alpha-hydroxylase deficiency. We therefore suspected that the cause of low estriol in this fetus was adrenal insufficiency. Postnatal evaluation was consistent with panhypopituitarism, characterized by deficiency of all anterior pituitary hormones. Because this screen is now offered to more than half the pregnant women in the United States, reports of low estriol levels have become increasingly common. Therefore, it is essential that physicians be familiar with the various etiologies, perform the appropriate antenatal evaluation to determine the specific cause, and closely monitor both mother and child ante- and postnatally.

Adrenal Gland Diseases↗
PubMed1990

Effects of DHA-S on placental 3 beta-hydroxysteroid dehydrogenase activity, progesterone and 20 alpha-dihydroprogesterone concentrations in placenta and serum.

To study the effects of dehydroepiandrosterone sulfate (DHA-S) on placental steroid metabolism and maternal steroidal profiles at term, the following in vivo and in vitro experiments were performed. Two hundred mg of DHA-S was given to five pregnant women 30 minutes prior to delivery. After delivery, the placenta was collected and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and sulfatase activity was determined by measuring the rate of conversion of pregnenolone to progesterone and DHA-S to DHA. The amount of C21-delta 4-steroid in the placental tissue was measured by gas chromatography mass spectrometry (GC-MS) and compared with the control groups. The maternal serum concentration of several steroids was also measured by GC-MS before and after the administration of DHA-S. 3 beta-HSD activity in the placentae from the mothers who received DHA-S before delivery was significantly lower than in the controls. On the other hand, no significant change was observed in the activity of sulfatase. The serum concentration of progesterone (P) and 20 alpha-dihydro-P (20-P) before DHA-S loading decreased following the administration whereas estradiol (E), DHA, and androstenedione (A) levels increased. To study the direct effect of DHA-S and its related steroids on placental 3 beta-HSD activity, placental tissue samples were incubated with pregnenolone in vitro. Several other steroids were added simultaneously into the medium. It was observed that placental 3 beta-HSD activity was directly inhibited by DHA-S. These results indicate that DHA-S inhibits 3 beta-HSD activity in the placenta and subsequently causes a reduction in P and 20-P.

20-alpha-Dihydroprogesterone↗
PubMed2006

Low estriol levels in the maternal triple-marker screen as a predictor of isolated adrenocorticotropic hormone deficiency caused by a new mutation in the TPIT gene.

Isolated adrenocorticotropic hormone (ACTH) deficiency (IAD) is a rare cause of adrenocortical insufficiency, especially in children, and may be an underestimated cause of neonatal death. Early postnatal diagnosis may prevent hypoglycemic seizures, Addisonian crises, and death. There are also occasional reports of prenatal diagnosis of IAD by findings on the maternal triple-marker screen (TMST), a combined serum analyte test that measures levels of alpha-fetoprotein, human chorionic gonadotropin, and unconjugated estriol for the detection of Down syndrome and open neural-tube defects. An isolated low estriol level is usually correlated with compromised uteroplacental perfusion and frequently associated with fetal death. A low estriol level in the context of normal fetal sonography and growth, after exclusion of placental sulfatase deficiency and Smith-Lemli-Opitz syndrome, should raise the suspicion of deficient fetal steroidogenesis, which leads to decreased production of adrenal dehydroepiandrosterone sulfate. We describe 2 brothers with adrenal insufficiency resulting from IAD. The parents are first cousins whose first son is healthy. During the pregnancy of the second son, who died at the age of 7 weeks as a result of presumed cardiomyopathy, a low estriol level on the TMST was ignored because of a normal fetal ultrasound. In the third pregnancy, a low level was found again, and the mother was referred to our tertiary center. Ultrasonography revealed no abnormalities, and karyotype was normal. Normal levels of steroid sulfatase activity and 7-dehydrocholesterol ruled out X-linked ichthyosis and Smith-Lemli-Opitz syndrome, respectively. Postnatally, basal and stimulated cortisol and ACTH levels were low. Other pituitary functions were normal, suggesting the diagnosis of IAD. The patient was treated with a stress dose of hydrocortisone on day 2 of life, which was tapered to a maintenance dose. At the time of this writing, he was 7 months old, with normal growth and development. Recently, loss-of-function mutations in the human TPIT gene were detected in autosomal recessive IAD. TPIT is a cell-restricted T-box transcription factor that is important for the terminal differentiation of pituitary corticotrophs. Therefore, we performed molecular analysis of the TPIT gene, which revealed a new mutation (IVS4+1G>A) that affects the first nucleotide of the splice site at the 5' end of the fourth intron. This stop codon probably leads to loss of TPIT function by nonsense-mediated mRNA decay, as it does for other TPIT nonsense mutations. We recommend that pregnant women with an isolated low estriol level of unexplained etiology be referred for additional evaluation by a multidisciplinary team that includes a geneticist and pediatric endocrinologist. Prompt ACTH testing in the first postnatal days will allow for early diagnosis. The immediate institution of glucocorticoid therapy, with proper instructions for stress management, can prevent unnecessary neonatal death secondary to an easily treatable disease.

Adrenal Insufficiency↗
PubMedDate not supplied

Seminal profiles of lysosomal enzymes in normal and infertile men.

Human seminal plasma is known to possess considerable proteolytic activity, much of which is associated with lysosomes. The activities of lysosomal hydrolases like alkaline proteinase, cathepsin-D, aryl-sulfatase and N-acetyl-beta-D-glucosaminidase in seminal plasma from randomly chosen infertile and vasectomised men have been compared. These enzymes have been implicated in the coagulation and liquefaction processes. The role of fructose and proteins in these processes has also been studied. The results indicate that cathepsin-D and aryl-sulfatase activity in infertile men were significantly lower than normo-spermic subjects. N-acetyl-beta-D-glucosaminidase was lowest in azoospermia suggesting that it could be used as a biochemical marker for azoospermia. Conversely, alkaline proteinase showed increased levels in all the infertile cases.

Fructose↗
PubMed2002

Identification of guanfu base A hydrochloride phase I and phase II metabolites in rat bile by liquid chromatography mass spectrometry.

AIM: To study metabolites of guanfu base A hydrochloride (GFA) in rat bile. METHODS: An analytical method was developed to identify guanfu base A and its metabolites by liquid chromatography mass spectrometry (LC-MS) and electrospray ionization tandem mass spectrum (MS-MS). Rat bile was collected after iv injection of GFA. Phase I metabolite was identified by comparison with authentic standard for their retention time, molecular ion peaks, fragment ions, and UV spectrums. In order to identified Phase II conjugates, the aglycones were identified after rat bile was treated with either glucuronidase or sulfatase firstly. Phase II conjugates were also separated and determined for their molecular ions by LC-MS, at last they were verified by identifying characteristic product ions or precursor ions by MS-MS. RESULTS: Phase I metabolite, guanfu base I (GFI), was identified in rat bile. After phase II conjugates were treated with glucuronidase or sulfatase, GFA and GFI occurred in chromatograms. Quasi molecular ions m/z 606 and 510 were separated and detected in rat bile. They were indicated to be GFA glucuronide and GFA sulfate, respectively. Furthermore, GFA glucuronide was confirmed to exist in rat bile by identifying two characteristic ions, m/z 177, [M+H]+ of glucuronic acid, and m/z 430, [M+H]+ of GFA, as product ions of m/z 606. CONCLUSION: Phase I metabolite GFI and phase II conjugates, GFA glucuronide and sulfate, GFI glucuronide and sulfate, were identified in rat bile.

Alkaloids↗