Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to clarify the action of drugs for liver disease, the effect of protoporphyrin (PP) on CCl4-induced liver injury was studied. Attention was given to the levels of lysosomal enzymes, some components of the liver, and inhibition of enzymes and lysis of lysosomal membranes by lipid peroxides. Administration of PP to CCl4-poisoned rats was found to prevent the decrease in lysosomal lipolytic enzyme level in the liver, but not in other enzyme levels tested. The inhibition of lipolytic enzyme by CCl4 administered may be partially involved in lipid accumulation in the liver. A dose of PP administered to CCl4-poisoned rats for 8 days depressed the neutral lipid content in the liver nearly to the control value. Methyl linoleate hydroperoxide (hydroperoxide) at a lower concentration of 10(-6)% inhibited the lipolytic enzyme acitivity by 30% and in concentrations ranging from 10(-4) to 10(-3)% inhibited beta-glucuronidase activity. Addition of PP to the medium containing 10(-6) to 10(-5)% hydroperoxide and alpha-tocopherol reduced the enzyme inhibition further than in the absence of PP. The hydroperoxide in concentrations varying from 10(-6) to 10(-3)% caused a partial lysis of liver lysosomal membranes, but addition of PP slightly reduced the damage by the hydroperoxide in concentration lower than 10(-5)%.
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PMID:Effect of "drugs for liver disease" on hepatotoxic action of carbon tetrachloride. I. Changes of lysosomal enzyme levels and effect of protoporphyrin on the levels. 17 10

A simple, specific, and technically easy high-performance liquid chromatography (HPLC) method for the separation and quantification of unconjugated bilirubin, bilirubin monoglucoside-monoglucuronide, bilirubin diglucuronide, and bilirubin monoglucuronide has been developed. The method was used to determine the bilirubin compounds of bile obtained endoscopically from the common bile duct in 43 patients with gallstone disease and in 6 subjects without gallstones or liver disease. The bile samples were also assessed for the presence of beta-glucuronidase-producing bacteria. The amount of unconjugated bilirubin was significantly higher (p less than 0.01) in bile containing bacteria producing beta-glucuronidase than in bile without such bacterial strains. In six 'normal' bile samples the following quantities of bilirubin conjugates and unconjugated bilirubin were found (median and range): bilirubin monoglucoside-monoglucuronide (mixed conjugate), 61 (27-80) mumol/l; bilirubin diglucuronide, 632 (512-861) mumol/l; bilirubin monoglucuronide, 113 (70-175) mumol/l; and unconjugated bilirubin, 3 (1-7) mumol/l. These results are in good agreement with those obtained with other HPLC methods. The concentrations of unconjugated bilirubin were lower than those found when using conventional diazo methods and thin-layer chromatography. HPLC proved to be a useful tool in gallstone pathogenesis studies. Our results support bacterial glucuronidase as a possible pathogenic factor in pigment gallstone disease.
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PMID:High-performance liquid chromatography of bilirubin conjugates in bile: effect of beta-glucuronidase on the bile pigments. 281 36

Rat liver membrane vesicles were exposed to acetaldehyde, with or without reduction of the resultant adducts formed. Superoxide anion production and degranulation of rat neutrophils, upon stimulation with the liver membrane vesicles, were measured by cytochrome c reduction before and after the addition of superoxide dismutase, and beta-glucuronidase release respectively. Preincubation with acetaldehyde significantly enhanced superoxide anion production by both the reduced and non-reduced membrane samples (1.7-fold and 4.4-fold, respectively). Preincubation with acetaldehyde significantly enhanced degranulation (1.5-fold) of neutrophils in response to the non-reduced membranes only. The reductive process itself caused a marked increase (2.4-fold) in the ability of the membrane vesicles to stimulate degranulation. Cytochalasin B, an inhibitor of phagocytosis, did not reduce degranulation, implying that it occurred as a consequence of cell surface stimulation. Neutrophil superoxide anion production and lysosomal enzyme release in response to acetaldehyde-altered liver cell membranes could be an important mechanism of hepatocyte injury in alcoholic liver disease.
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PMID:Superoxide anion production and degranulation of rat neutrophils in response to acetaldehyde-altered liver cell membranes. 301 4

Digoxin-like immunoreactivity (DLI) has been found in serum from subjects with a variety of physiological and pathological conditions, including uremia, liver disease, pregnancy, and the neonatal period. The physicochemical nature of this material is still not known. Using gel filtration chromatography, extraction with methylene chloride, and treatment with beta-glucuronidase, we determined that serum DLI exists in three forms: protein-bound, glucuronidated, and free, with respective mol wt of 5000, 400, and 230. In serum, DLI exists in the protein-bound and free forms, while in urine, DLI is found in the glucuronidated and free states.
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PMID:Digoxin-like immunoreactivity: occurrence in three molecular forms and partial characterization. 357 29

Bilirubin monoglucuronide is rapidly deconjugated when incubated with UDP and rat liver microsomal preparations at pH 5.1. The following evidence was found that this reaction is catalyzed by UDP-glucuronyltransferase: (i) unconjugated bilirubin and UDP-glucuronic acid were identified as the reaction products; (ii) Gunn rat microsomal preparations lack bilirubin UDP-glucuronyltransferase deficiency and do not catalyze the deconjugation reaction, and (iii) neither saccharo-1,4-lactone, a beta-glucuronidase inhibitor, nor butylated hydroxytoluene, an inhibitor of spontaneous isomerisation, affect the rate of the deconjugation reaction. Deconjugation appears to be the reverse of UDP-glucuronyltransferase-catalyzed glucuronidation. The conditions for the reverse reaction differ in the following aspects from those of the forward reaction: (i) nucleotide triphosphates stimulate the reverse reaction probably allosterically; (ii) UDP-N-acetylglucosamine stimulates the forward reaction but has no effect on the reverse reaction; (iii) the optimal pH for the reverse reaction is pH 5.1 and for the forward reaction is pH 7.8, and (iv) Mg++ ion is not required for the reverse reaction but stimulates the forward reaction. Detergents stimulate both reactions. Stimulation of the reverse reaction by nucleotide triphosphates and detergents is mutually independent and additive which suggests different mechanisms of action. Deconjugation reactions may become important during parenchymatous liver disease when, as a result of anaerobic glycolysis, intracellular pH decreases. Elevated levels of unconjugated bilirubin in the serum of patients with parenchymatous liver disease may be a sign of sick liver cells rather than decreased UDP-glucuronyltransferase activity.
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PMID:UDP-glucuronyltransferase-catalyzed deconjugation of bilirubin monoglucuronide. 643 92

The activities of the lysosomal enzymes beta-hexosaminidase, beta-glucuronidase, and beta-galactosidase were confirmed to be elevated in serum from pregnant women. The increased activity of beta-hexosaminidase and beta-glucuronidase showed the same changes in the isoenzyme pattern as found in serum from patients with some liver affections. In the light of recent findings, the increased activity of beta-hexosaminidase (and some other lysosomal enzymes) in pregnancy and liver disease might depend upon the non-parenchymal liver cells not being able properly to clear these enzymes from the blood.
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PMID:A possible explanation for the occurrence of increased beta-hexosaminidase activity in pregnancy serum. 645 14

Sera from 9 persons with either biopsy-proven alcoholic liver disease or a history of chronic, excessive ethanol consumption were analyzed for their content of various hydrolases. Compared to controls, significant elevations in the following enzyme activities were seen in sera from the patient population: acid phosphatase (2.0-fold), beta-glucuronidase (2.1-fold), hexosaminidase (1.4-fold), and alpha-L-fucosidase (2.3-fold). In addition, alpha-mannosidase activity, previously reported to be unchanged in cases of hepatic cirrhosis [Reglero et al., Clinica chim. Acta 130: 155-158], (1980) was found to be significantly increased (p less than 0.001) when assays were performed at acid (pH 4.5) or intermediate (pH 5.5) hydrogen ion concentrations. Fractionation of sera on DEAE-Sephadex columns showed that the increase in alpha-mannosidase activity in the serum of patients with alcoholic liver disease was due to increases in the level of at least one 'acid alpha-mannosidase' and two intermediate pH optimum alpha-mannosidases. The general increase in the activity of a group of glycosidases is consistent with a hypothesis involving decreased clearance of glycoproteins from the blood of persons with hepatic cirrhosis.
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PMID:Serum alpha-mannosidase in patients with alcoholic liver disease. 671 94

Monocyte function has been studied in a total of 51 patients with biopsy-proven cirrhosis and 35 controls. There was significantly reduced monocyte spreading (p less than 0.05), chemotaxis (p less than 0.02), bacterial phagocytosis (p less than 0.05) and bacterial killing (p less than 0.02) in the cirrhotics compared to the controls. Monocytes from patients with cirrhosis produced significantly less of the lysosomal enzymes N-acetyl beta-glucosaminidase and beta-glucuronidase than those obtained from the controls (p less than 0.02). There was no significant difference in the number of monocytes obtained, the number of macrophage precursors, and the nitro-blue tetrazoline (NBT) reduction between the cirrhotic and the controls. The reduced function appeared to be mainly due to a circulating inhibitory factor and could be corrected by incubation of the cirrhotic cells in serum from control subjects. The response of monocytes from patients with cirrhosis did not differ from the controls in their response to added endotoxin or latex particles suggesting that they are capable of a normal response in the absence of the inhibitory factor. Paired specimens of portal and systemic serum were collected from patients with no evidence of liver disease undergoing vascular surgery. When added to normal human monocytes the portal serum caused a significant reduction in bacterial killing (p less than 0.02) and chemotaxis (p less than 0.05) compared to results obtained in the paired systemic serum. Mixing experiments suggests the presence of an active inhibitor in the portal serum. The results suggest that monocyte function is reduced in cirrhosis apparently due to a serum inhibitor which may have originated from the portal vein. The abnormalities may account in part for the increased susceptibility of these patients to infection.
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PMID:Monocyte function in cirrhosis. 711 29

"Direct reacting bilirubin" in serum of patients with cholestatic liver disease and in serum of bile duct-ligated rats consists of a complex mixture of bilirubin metabolites. These metabolites were studied by means of high-pressure liquid chromatography. Bilirubin glucuronides in normal bile are beta-glycosidic 1-O-acyl conjugates which are completely hydrolyzed on incubation with beta-glucuronidase. Cholestatic serum contains glucuronide and non-glucuronide bilirubin metabolites. The glucuronides were only partially hydrolyzable with beta-glucuronidase. Compernolle et al. [11] showed that the 1-O-acyl bond of bilirubin glucuronides is labile and prone to migrate from the C1 position at the glucuronosyl residue to positions C2, C3 and C4. The isomerisation products are non-beta-glycosidic, beta-glucuronidase-resistant conjugates. The main beta-glucuronidase-resistant conjugates in cholestatic serum were characterized as: non-beta-glycosidic bilirubin monoglucuronide, non-beta-glycosidic diglucuronide and a diglucuronide isomer with beta-glycosidic and non-beta-glycosidic glucuronosyl groups. Moreover, a substantial amount of bilirubin monoglucoside monoglucuronide was detected in cholestatic human serum.
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PMID:beta-Glucuronidase-resistant bilirubin glucuronide isomers in cholestatic liver disease--determination of bilirubin metabolites in serum by means of high-pressure liquid chromatography. 722 35

The authors have measured the activity of acid phosphatase, beta-glucuronaidase and cathepsin-D in tthe sera of patients with different liver diseases, and the actvity of beta-glucuronidase in granulocytes and the rate of its release. Using the method for the releaseof beta-glucuronidase from the granulocytes they drew conclusions to thedegree of the membrane-damage occurring in the liver diseases. They provided that in the sera of patients with different liver diseases the increase in the activity of the acid phosphatase and the beta-glucuronidase is different. According to their in vitro studies the decrease in the beta-glucuronidase activity measured in the granulocytes, and the release of enzyme is in connection with the type of liver disease and with the different degree of lysosomal membrane alteration.
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PMID:Lysosomal enzymes in sera and granulocytes of patients with chronic liver diseases. 728 55


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