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)

The effects of short-term treatment with orally-administered zinc sulphate and/or a mixture of cholesterol/choleate on serum lipoprotein and hepatic enzyme levels were studied. Administration of graded doses of zinc sulphate (20 or 40 mg/kg, as zinc ion) for 5 days, dose-dependently increased serum and hepatic zinc levels but depressed the serum high-density lipoprotein-cholesterol (HDL-C) concentration and liver cytochrome P-450 activity. However, it did not affect hepatic concentrations of malondialdehyde and free beta-glucuronidase. Cholesterol/choleate treatment for 5 days markedly damaged the liver, as reflected by elevations of hepatic concentrations of malondialdehyde (both in the mitochondrial and microsomal fractions) and of free beta-glucuronidase; total cholesterol and low-density lipoprotein-cholesterol in the blood were increased, whereas HDL-C was decreased significantly. Concomitant administration of zinc sulphate with cholesterol/choleate further lowered HDL-C levels, but reversed the high hepatic concentrations of both malondialdehyde and free beta-glucuronidase. The present study indicates that both zinc ions and cholesterol can decrease circulatory HDL-C levels and that zinc protects against cholesterol-induced hepatic damage by reducing lysosomal enzyme release and preventing lipid peroxidation in the liver.
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PMID:Effects of zinc and cholesterol/choleate on serum lipoproteins and the liver in rats. 273 9

Twelve serum analytes [triglycerides, cholesterol, total and conjugated bilirubin, high-density-lipoprotein cholesterol (HDL-C), alkaline phosphatase (AP), gammaglutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), beta-glucuronidase (beta-glu), alanine aminopeptidase (AAP), and 5'-nucleotidase (5'nuc)] were measured to investigate their correlation with exposure to polychlorinated biphenyls (PCBs) and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT). The relationship between serum lipids, lipophilic toxicants, and the analytes was also evaluated. The beta-glu, 5'nuc, triglycerides, cholesterol, and total bilirubin correlated positively and significantly with log concentrations of serum total PCBs and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), a metabolite of DDT. The more highly chlorinated PCBs (Aroclor 1260) had significant, positive correlations with several serum analytes, but the less chlorinated PCBs (Aroclor 1242) correlated significantly and negatively only with HDL-cholesterol. Triglyceride- and cholesterol-rich lipoproteins were added to serum to determine the effects of lipids on these assays. Several were spuriously elevated. AP and beta-glu were not affected by lipoprotein addition with the methods used in this study. AAP was increased significantly only at triglyceride concentrations exceeding 400 mg/dl. Lipoproteins may be elevated because of deranged lipid metabolism in response to PCBs, or PCBs may be elevated because elevated lipoproteins are present, as in familial triglyceridemia, a relatively common dyslipoproteinemia. Because this relationship is not well understood with respect to cause and effect, we propose the further use in epidemiological investigations of assay methods that are little affected by blood lipids yet are correlated with PCB concentrations. Congener-specific quantification of PCBs would help elucidate the effects of PCBs on assays used to monitor health effects.
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PMID:Effects of polychlorinated biphenyls and lipemia on serum analytes. 302 64

Activation of human peripheral blood monocytes could enhance their attachment and or migration into the arterial intima and their various secretory and other functions, thus influencing the pathogenesis of atherosclerosis. In these experiments the authors have explored the role of lipoproteins in the activation of human blood monocytes. Monocytes were purified from citrated blood by Histopaque density gradient centrifugation and countercurrent centrifugal elutriation and cultured in DMEM in the presence of 20% acid-treated autologous serum or 100 micrograms/ml each of VLDL, LDL, Ac-LDL, and HDL. Secretion of beta-glucuronidase activity into the media was measured as a marker of activation. All of the lipoprotein density classes as well as serum stimulated secretion of beta-glucuronidase activity, with LDL and Ac-LDL having a greater influence than serum, VLDL, or HDL. Serum and LDL also stimulated secretion of prostaglandin E into the culture medium. Incubation of monocytes with serum or LDL in the presence of inhibitors of arachidonate metabolism (NDGA and indomethacin) resulted in a significant decrease in secreted and intracellular beta-glucuronidase activity, indicating a role for products of arachidonate metabolism in the activation of monocytes by lipoproteins.
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PMID:Activation of human peripheral blood monocytes by lipoproteins. 312 26

Lipid peroxidation has been induced by means of an atherogenic diet causing hypercholesterolaemia, hypertriglyceridaemia, increased LDL and decreased HDL serum fractions in addition to the fatty degeneration, vacuolization of the liver cells and accumulation of malondialdehyde in the liver. Increased release of acid phosphatase and N-beta-glucuronidase was also observed pointing to cholesterol-induced lysosomal membrane damage. In response to pretreatment with, and simultaneous administration of, 6,6'-methylene bis (2,2-dimethyl-4-methane sulphonic acid sodium salt-1,2-dihydroquinoline) the signs and symptoms of fatty liver degeneration, the tissue, plasma and platelet malondialdehyde concentrations and the LDL serum fraction significantly decreased and HDL serum fraction increased. Lisosomal membrane stability was restored, resulting in physiological acid phosphatase and N-beta-glucuronidase activities. The pathological and clinical aspects of lipid peroxidation in several diseases of the digestive organs and the suggested therapeutic uses of non-toxic radical scavengers have been outlined.
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PMID:Liver lipid peroxidation induced by cholesterol and its treatment with a dihydroquinoline type free radical scavenger in rabbits. 653 29

It is known that urinary excretion of glucaric acid (GA) is an indirect index of hepatic P-450 microenzyme induction. We measured and analyzed urinary excretion of GA and plasma lipids in non-pregnant women, pregnant women and postpartum women. GA was measured by a new method for the inhibition of beta-glucuronidase activity and plasma lipids were measured by routine laboratory methods and we obtained the following results. 1. The concentration of urinary GA was correlated with that of urinary creatinine in pregnant women. 2. The urinary GA and plasma HDL-cholesterol did not change during the first of gestation, but steeply increased in the middle of gestation, and postpartum values were lower than at term. 3. Plasma total lipids, triglycerides, and total cholesterol continuously increased throughout gestation. 4. Plasma free fatty acids and lipid peroxide steeply increased in late in gestation. These results and several reports suggested that the change in GA in pregnant women reflected their own metabolism not fetal or placental metabolism. It seems that grasping and understanding their metabolism can make their disease clear.
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PMID:[Measurement and fluctuation of urinary glucaric acid in pregnant women]. 808 94

The purpose of this study was to perform a comprehensive analysis of hepatic gene expression in a standard model of an alcohol-induced fatty liver using the cDNA microarray analysis. Male Sprague-Dawley rats were randomly divided into two groups and were given either an ethanol diet (ED), or a control diet (CD) for eight weeks. The ED rats showed significantly elevated levels of plasma total and HDL cholesterol as well as hepatic cholesterol and triglyceride compared to the pair-fed control rats. Among the 5185 genes on the rat cDNA microarray used in the current study, 74 genes were up-regulated and 108 genes were down-regulated greater than 2.0-fold in the liver of ED rats compared with those in the CD rats. The microarray results were verified by conducting real-time RT-PCR on the fourteen selected genes with varied expression ratios. After clustering the regulated genes based on their biological function, it was found that chronic ethanol consumption regulated mainly the genes implicated in the processes of signal transduction, transcription, immune response, and protein/amino acid metabolism. The microarray results obtained in this study revealed, for the first time, that several genes, including beta-glucuronidase, UDP-glycosyltransferase 1, UDP-glucose dehydrogenase, apoC-III, and gonadotropin-releasing hormone receptor, were regulated by chronic ethanol exposure in the rat liver.
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PMID:Changes in the hepatic gene expression profile in a rat model of chronic ethanol treatment. 1792 Jul 46

The experiment was aimed at studying the effects of easily fermentable oligosaccharides and phenolic compounds from chicory root meal (CRM) on the fermentative processes in the caecum, the antioxidative status and the lipoprotein profile of rats. Five different diets were fed ad libitum to 40 Wistar rats (eight animals per group, individually housed): a control group (C); group PCM (10% processed CRM, deprived of polyphenolic fraction); group PCMO (8% processed CRM and 1.6% oligofructose); group UCM (10% unprocessed CRM); and group FP (8.3% fructan-polyphenol concentrate from CRM). Diets PCM, PCMO, UCM and FP induced favourable metabolic changes in the caecum, blood lipid profile and the antioxidative status of the body. In the caecum, the experimental diets increased the production of volatile fatty acids (VFA) and acidification of digesta as well as a decrease in the ammonia concentration and bacterial beta-glucuronidase activity. In blood serum, the total cholesterol concentration was reduced and, simultaneously, the proportion of HDL in the total cholesterol concentration was increased. The presence of the polyphenolic fraction in the unprocessed meal (diets UCM and FP) evoked a significant increase in the total antioxidative status in blood serum. Dietary fibre and the polyphenolic fraction present in diet UCM and the FOS-polyphenol concentrate in diet FP did not exhibit an antagonistic activity regarding the physiological parameters analysed, except for in the intensity of caecal fermentation. The results of the experiment point to the benefits of dietary supplementation with chicory preparations containing both prebiotic saccharides and polyphenolic compounds, which enable us to take advantage of the physiological traits of both components.
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PMID:Physiological effects of chicory root preparations with various levels of fructan and polyphenolic fractions in diets for rats. 2145 15