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Biomedical subjects

J Fevery

Publications and source records attributed to J Fevery.

At least 235 records · Page 13Linked to original sources
PubMed1971

Excretion in dog bile of glucose and xylose conjugates of bilirubin.

1. T.l.c. with neutral solvent systems of ethyl anthranilate azopigments derived from bile of man, dog and rat revealed pronounced species variation. The less polar components (alpha-group) could be separated conveniently by development with chloroform-methanol (17:3, v/v). 2. The azopigment material derived from gallbladder bile of dog contained about 10% of azobilirubin beta-d-monoxyloside (azopigment alpha(2)) and 30% of azobilirubin beta-d-monoglucoside (azopigment alpha(3)). The sugar moieties were identified by t.l.c. with acidic, neutral and basic solvent systems and by anion-exchange column chromatography of their boric acid complexes. Treatment of the purified azopigments with ammonia vapour led to the formation of the amide of azobilirubin, indicating that both pigments are ester glycosides. The beta-d configuration was demonstrated by enzymic studies with emulsin (an adequate source of beta-glucosidase activity) and with Mylase-P (an adequate source of beta-glucosidase and beta-xylosidase activities). 3. Hydrolysis studies with model substrates and with the alpha(2)- and alpha(3)-azopigments suggested that in Mylase-P the beta-glucosidase and beta-xylosidase activities reside in separate enzymes. 4. Compared with the accepted conjugation with glucuronic acid as a major route of detoxication in mammals, the detection of large amounts of xylose and glucose conjugates of bilirubin in dog bile suggests that the underlying biosynthetic pathways may be important alternative routes of detoxication.

Ammonia↗
PubMed1971

Mass-spectrometric structure elucidation of dog bile azopigments as the acyl glycosides of glucopyranose and xylopyranose.

1. The structures of the alpha(2)- and alpha(3)-azopigments, prepared by diazotization of dog bile with ethyl anthranilate, were shown by mass spectrometry and g.l.c. to correspond to azobilirubin beta-d-xylopyranoside and azobilirubin beta-d-glucopyranoside respectively. 2. Both azopigments consist of a mixture of two methyl vinyl isomers having structures (IIIa) and (IIIb) for the alpha(2)-azopigment and structures (IVa) and (IVb) for the alpha(3)-azopigment. Separation of methyl vinyl isomers was obtained by t.l.c. or column chromatography performed on the acetylated azopigments. Hydrolysis of the less polar acetates derived from components (IIIa) and (IVa) gave rise to the azopigment (Ia), whereas hydrolysis of the more polar acetates derived from components (IIIb) and (IVb) gave rise to the azopigment acid (Ib). The positions of methyl and vinyl substituents in compounds (Ia) and (Ib) were assigned on the basis of their n.m.r. spectra. 3. Molecular ions in the mass spectra of the trimethylsilyl and acetyl derivatives of the azopigments indicated the presence of a pentose and a hexose conjugating sugar. 4. The ester functions linking the sugars to the propionic acid side chain of azobilirubin were demonstrated by ammonolysis and identification of the amide of azobilirubin as the aglycone derivative. 5. The sugar moieties were shown to occur as xylopyranose (alpha(2)) and glucopyranose (alpha(3)), bound at C-1, by application of a sequence of reactions performed on a micro-scale. The sugar hydroxyl groups were acetylated and the 1-acyl aglycone removed selectively by treatment with hydrogen bromide in acetic acid. Hydrolysis of the 1-bromo sugar acetates followed by acetylation afforded the alpha- and beta-xylopyranose tetra-acetates and alpha- and beta-glucopyranose penta-acetates, identified by a combination of g.l.c. and mass spectrometry. 6. The validity of this degradation scheme was confirmed (a) by g.l.c.-mass spectrometry identification of the alpha- and beta-1-propionyl derivatives of glucopyranose tetra-acetate, obtained from the alpha(3)-azopigment after final reaction with propionic anhydride; (b) by subjecting the acetates of alphabeta-glucopyranose, alphabeta-xylofuranose and alphabeta-glucofuranose to the same sequence of reactions.

Acetates↗
PubMedDate not supplied

Analysis of bilirubins in biological fluids by extraction and thin-layer chromatography of the intact tetrapyrroles: application to bile of patients with Gilbert's syndrome, hemolysis, or cholelithiasis.

A method was developed to extract quantitatively the bilirubins from bile, urine, serum, stool, and preparations from liver with a chloroform-ethanol mixture at pH 1.8 in the presence of ascorbic acid and NaCl. Extracted pigment was submitted to thin-layer chromatography, and the separated bilirubins were either immediately eluted and determined spectrophotometrically or individually converted to ethyl anthranilate azo derivatives for thin-layer chromatographic analysis of each isolated pigment band. Bilirubins in duodenal bile of eight healthy adults comprised 1.5 +/- 1.3% unconjugated bilirubin-IX alpha, 69 +/- 6% bilirubin diglucuronide, and 16 +/- 4% bilirubin monoglucuronides. Mixed diconjugates containing one glucuronosyl moiety and either one xylosyl or one glucosyl group amounted to 10 +/- 3%. Most samples (6 of 8) contained trace amounts (0.6 +/- 0.6%) of unconjugated bilirubin-IX beta, in agreement with nearly exclusive cleavage of heme at the alpha-meso position. The composition of the bilirubins in bile was normal in 6 patients with cholesterol gallstones, 4 with chronic hepatitis, and 3 with hemolysis. In duodenal bile of individuals with Gilbert's syndrome (n = 10), the concentration of bilirubin conjugates was comparable to that in healthy adults, but the proportion of bilirubin diglucuronides (52 +/- 8%) was decreased. The concentration of unconjugated bilirubin-IX alpha showed a fair positive correlation with that of bilirubin monoglucuronide and was increased in half of the patients with Gilbert's syndrome.

Bile↗
PubMedDate not supplied

Are nuclear particles specific for non-A, non-B hepatitis?

This study reports the findings of an electron microscopic search for so-called non-A, non-B nuclear particles in liver biopsies from patients with mainly chronic or prolonged liver disease and from chimpanzees. In patients without hepatitis B virus or acute hepatitis A virus serological markers, non-A, non-B-like nuclear particles were seen in hepatocytes in 28 of 31 cases of presumed non-A, non-B hepatitis, but also in 11 of 12 cases of liver disease not usually attributed to hepatitis viruses. They were also seen in 22 of 24 patients with HBsAg, in 3 of 3 patients with anti-HBc and no HBsAg, in 1 of 2 patients with hepatitis A, in a case of cytomegalovirus hepatitis, and in 16 of 19 patients whose serology was not available or inconclusive. The particles were present in 1 of 8 untreated HBsAg-negative chimpanzees and in 2 of 2 HBsAg-positive chimpanzees. They appeared in 4 of 4 chimpanzees developing non-A, non-B hepatitis following exposure to various inocula. Three patterns of particle aggregates were distinguished, all of which had been shown by others in non-A, non-B hepatitis. Dense aggregates were predominant, while others have shown intermediate aggregates more often; reasons for this difference could be technical. No pattern was specific for any condition. Either non-A, non-B-like nuclear particles, although associated with non-A, non-B hepatitis, are not specific for this condition, or non-A, non-B hepatitis viruses are extremely more common than is currently appreciated.

Animals↗
PubMedDate not supplied

Franco-Belgian cooperative study of ursodeoxycholic acid in the medical dissolution of gallstones: a double-blind, randomized, dose-response study, and comparison with chenodeoxycholic acid.

A double-blind randomized, multicenter study was carried out to determine the efficacy and safety of ursodeoxycholic acid (UDCA) at 4 doses of 2.1 to 16.2 mg X kg-1 X day-1, and chenodeoxycholic acid (CDCA) at the dose of 16.9 mg X kg-1 X day-1, in 197 patients treated for up to 1 year for radiolucent gallstones in functioning (opacified) gallbladders. There was confirmed complete dissolution in 5.9% of patients receiving UDCA at the dose of 2.1 mg X kg-1 X day-1, 18.9% in those receiving 4.2, 28.9% in those receiving 8.4, 14.6% in those receiving 16.2, and 20.0% in patients receiving CDCA. Partial (over 50%) or complete dissolution occurred in 29.4% of patients receiving 2.1 mg X kg-1 X day-1 of UDCA, 37.8% of those receiving 4.2, 55.2% in those receiving 8.4, 48.7% in those receiving 16.2, and 50.0% in patients receiving CDCA. Complete dissolution occurred significantly more frequently in small (less than 5 mm in diameter) than in large (5 to 15 and more than 15 mm) stones. There was no significant influence of treatment on serum cholesterol and triglycerides in any of the groups. Serum aminotransferases remained normal (or lower than twice the upper normal limit) in all patients treated with UDCA. Diarrhea leading to cessation of treatment occurred in 5% of patients receiving UDCA, but was significantly less frequent than in those receiving CDCA. These results confirm that, within a 1-year period, UDCA is equally effective and induces diarrhea less frequently than CDCA, with an optimal dose (8 mg X kg-1 X day-1) approximately twice lower than that of CDCA.

Adult↗
PubMedDate not supplied

Conjugation and maximal biliary excretion of bilirubin in the rat during pregnancy and lactation and during estroprogestogen treatment.

Hepatic bilirubin conjugation and excretion were investigated during pregnancy and lactation in the rat. Bilirubin uridine diphosphate-glucuronyltransferase activity was decreased by 30% in pregnant rats, both when expressed per milligram of protein or as specific activity and per unit of liver weight. Liver size increased during pregnancy, and, as a consequence, total hepatic glucuronyltransferase activity was unchanged. The biliary bilirubin output was normal in pregnant rats, and when loaded with bilirubin, the maximal output in bile for the whole liver was also normal. In lactating rats, specific glucuronyltransferase activity returned to control values, but the activity per unit of liver weight was still lower, due to the decreased hepatic protein concentration. The liver remained enlarged during lactation, and total hepatic glucuronyltransferase activity was increased, together with the maximal output of bilirubin in bile. Two weeks after delivery, hepatic bilirubin conjugation and excretion in nonlactating mothers were comparable to those of virgin females. Parallel modifications of bilirubin glucuronyltransferase assayed in vitro and of maximal biliary output of the pigment in vivo were observed in all animals studied. The output of bilirubin diconjugates in bile was decreased during pregnancy but no changes of the proportion of the mono-to diconjugates in bile were observed 2 weeks after delivery both in lactating and in nonlactating rats. The modifications observed during pregnancy could not be reproduced by treatment with beta-estradiol and progesterone. This suggests that different hormones or modifications of steroid metabolism are probably involved in the alterations of hepatic bilirubin metabolism in pregnant and lactating rats.

Animals↗