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)

Oligomers of hyaluronic acid were prepared by digestion of hyaluronic acid from rooster combs with testicular hyaluronidase (hyaluronate 4-glycanohydrolase, EC 3.2.1.35), leech head hyaluronidase (hyaluronate 3-glycanohydrolase, EC 3.2.1.36), and with fungal hyaluronidase (hyaluronate lyase from Streptomyces hyalurolyticus). The oligomers were fractionated by gel permeation, using Sephadex G-50. Oligomers isolated after incubation of the hyaluronic acid with the testicular hyaluronidase were further modified. To prepare oligomers with N-acetylglucosamine at both ends, terminal nonreducing glucuronic acid residues were removed with beta-glucuronidase. Reducing terminal N-acetylglucosamine residues were removed by reaction under mildly alkaline conditions. The reducing terminal N-acetylglucosamine residues were also reduced with sodium borohydride to form N-acetylglucosaminitol. The potentials of the various oligosaccharides to bind to the proteoglycan from bovine nasal septum cartilage were estimated by determining their effectiveness as inhibitors of the proteoglycan-hyaluronate interaction. The present study shows that, to bind maximally to the proteoglycan, the hyaluronate oligosaccharide must be at least 10 sugar residues in length and be terminated at the nonreducing and reducing ends with a glucuronate residue and an N-acetylglucosamine residue, respectively. Sugar residues extended beyond this basic decasaccharide, do not interact with the hyaluronate binding site on the proteoglycan.
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PMID:Interactions of cartilage proteoglycans with hyaluronate. Inhibition of the interaction by modified oligomers of hyaluronate. 43 8

The objectives of the study were to determine whether the follicular (F; days 6-11) and luteal (L; days 16-21) phases of the menstrual cycle were associated with changes in starch malabsorption, stool bulking, stool mucinase, and beta-glucuronidase activities in 10 women (24.1 +/- 0.7 years old) eating a standardized low-fibre diet. Starch malabsorption, measured by breath hydrogen excretion after a breakfast of pureed chickpea (days 10 and 20) versus 10 g lactulose (days 11 and 21), decreased from 9.7 +/- 1.8 g/50 g starch ingested (F) to 6.6 +/- 1.8 g/50 g starch ingested (L) (P less than 0.05). Stool wet weight decreased from 84.5 +/- 10.1 g/day (F) to 52.2 +/- 5.8 g/day (L) (P less than 0.002). Stool dry weight decreased from 20.2 +/- 1.9 g/day (F) to 14.2 +/- 1.1 g/day (L) (P less than 0.006). Stool nitrogen excretion decreased from 1.81 +/- 0.19 g/day (F) to 0.82 +/- 0.06 g/day (L) (P less than 0.006). Stool mucinase and beta-glucuronidase activities were unaffected by the menstrual cycle. These results indicate that women eating low-fibre Western diets may be more prone to constipation during the luteal phase of the menstrual cycle.
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PMID:Starch malabsorption and stool excretion are influenced by the menstrual cycle in women consuming low-fibre Western diets. 166 73

Mucinase and beta-glucuronidase enable colon bacteria to degrade protective mucins and recycle glucuronide conjugates of toxins and carcinogens. The response of these bacterial enzymes to dietary fiber was studied in the laboratory rat. Fiber-free basal diet was mixed with guar gum, pectin, carrageenan, or cellulose at levels of 5 and 15%. These diets were fed for 21 days to groups of six male Fischer-344 rats having an average weight of 150 g. Mucinase and beta-glucuronidase activities were assayed in fresh rat feces. Rats fed 15% guar gum or pectin gained significantly (P less than 0.05) less weight than the other rats. Mucinase specific activity was highest in the fiber-free diet group and lowest in the 15% guar gum group. Total daily output of mucinase was highest in rats fed fiber-free diet or cellulose and lower in rats fed more readily fermentable fiber. Specific activity and total output of beta-glucuronidase were highest in rats fed fiber-free diet and significantly lower in those fed 15% fiber diets. These data are consistent with the hypothesis that some kinds of dietary fiber may play a role in the etiology of intestinal disease.
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PMID:Effects of dietary fiber on fecal mucinase and beta-glucuronidase activity in rats. 629 39

The aim of the study was to compare the physiological consequences of two dietary fibre sources on the faecal microflora and colonic mucosal growth in rats. The studied sources, a moderately well-soluble fibre (rice bran, RB) and a less well-soluble fibre (wheat bran, WB), were included in diets of rats at a level of 10% for 3 weeks and compared with a totally fibre-deprived diet. RB significantly increased faecal water compared to the control diet (p < 0.05). Faecal nitrogen content and bacterial mass, as estimated from the 2,6-diaminopimelic acid (DAPA) output, were greatly and significantly increased by RB, and to a lesser extent by WB, compared to the control diet. Total bile acid excretion was significantly higher by rats fed RB than by those fed WB. Faecal bacterial enzyme activities tested (beta-glucuronidase, mucinase and nitroreductase) were significantly reduced by the two different fibre sources, but RB was more effective than WB, except for nitroreductase activity which was reduced at the same level for each fibre source. Although measurements of mucosal colonic weight and RNA content were significantly different between groups fed RB and WB (p < 0.05), DNA content and the ratio RNA/DNA did not significantly differ between these groups. Our results indicate that the differential changes observed in beta-glucuronidase and mucinase activities and DAPA and bile acid excretion may depend on the nature of the fibre consumed. They also suggest that RB, which had similar effects, sometimes more marked than WB, on the studied parameters, may be a new valuable fibre source.
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PMID:Comparative evaluation of the effects of two different forms of dietary fibre (rice bran vs. wheat bran) on rat colonic mucosa and faecal microflora. 753 89

Changes in colonic faecal microflora, enzymes of colonic energy metabolism, of cell proliferation and lipid profile in the serum and colon were studied in 48 mice exposed to cycas and fed a Nigeria-type diet. The animals were divided into three diet classes of 16 mice per class, and each class of animals was fed ad libitum either a normal diet, a high-carbohydrate high-fibre (HCF) diet or a high-protein high-fat (HPF) diet. Each diet class was subdivided into two equal groups of 8 animals each. One group was fed a diet type (acted as the diet control) without cycas, and the other group was fed the corresponding diet with cycas. The study period lasted for 3 weeks. The colonic faecal materials were acidified in the HCF-fed mice compared with the other diet-fed mice. Faecal beta-glucuronidase activity was significantly (p < 0.05) increased in the cycas-fed mice compared with the diet controls. Feeding mice with the HPF diet significantly (p < 0.05) increased beta-glucuronidase and mucinase activities. Colonic phosphofructokinase, glucose 6-phosphate dehydrogenase, lactate dehydrogenase and hyaluronidase activities were also significantly (p < 0.05) elevated in the cycas-treated mice. Feeding mice with the HPF diet also significantly (p < 0.05) increased these enzyme activities. Mice fed with the HCF diet significantly (p < 0.05) lowered serum total cholesterol, triglyceride and colonic total lipid. Colonic phosphatidylethanolamine and phosphatidylcholine were significantly (p < 0.05) increased in the HPF-fed mice. This study shows that the HCF diet alters the colonic faecal environment, colonic energy metabolism and hyaluronidase activity in ways which suggest its protective ability against the development of colon cancer in mice.
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PMID:Early biochemical events in mice exposed to cycas and fed a Nigerian-like diet. 787 55

In the presence of a known colon carcinogen, 1,2-dimethyl hydrazine (DMH), the activity of beta-glucuronidase was found to be significantly increased in the distal colon, distal intestine, liver and colon contents and the activity of mucinase was increased in both the colon and fecal contents when compared to control rats. Chilli (Capsicum annum L., Solanaceae) administration also showed an increase when compared to control rats, whereas supplementation with cumin (Cuminum cyminum L., Apiaceae) and black pepper (Piper nigrum L., Piperaceae) in the presence of DMH, showed more or less similar values as that of the control rats. The increase in beta-glucuronidase activity may increase the hydrolysis of glucuronide conjugates, liberating the toxins, while the increase in mucinase activity may enhance the hydrolysis of the protective mucins in the colon. Thus cumin and black pepper may protect the colon by decreasing the activity of beta-glucuronidase and mucinase. Histopathological studies also showed lesser infiltration into the submucosa, fewer papillae and lesser changes in the cytoplasm of the cells in the colon in cumin and black pepper groups when compared to the DMH and chilli treated animals.
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PMID:Influence of spices on the bacterial (enzyme) activity in experimental colon cancer. 972 Jun 7

The effect of fenugreek seeds on the activities of beta-glucuronidase and mucinase during 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats was studied. Rats were given a weekly subcutaneous injection of DMH at a dose of 20 mg/kg body weight, for 15 weeks. Fenugreek seed powder was weighed depending upon the weight of individual rats and incorporated in the powdered pellet diet at a dose of 2 g/kg body weight. After an experimental period of 30 weeks the activity of beta-glucuronidase significantly increased in the colon, intestine, liver and colon contents in DMH administered rats when compared to an untreated control group. Increase in beta-glucuronidase may increase the hydrolysis of carcinogen-glucuronide conjugate, liberating carcinogen and/or co-carcinogen within the colonic lumen. Inclusion of fenugreek seed powder in the diet significantly decreased the activity of beta-glucuronidase in all the tissues studied. This may prevent the free carcinogens from acting on colonocytes. Mucinase helps in hydrolysing the protective mucin. Mucinase activity was increased in the colon content and fecal content of animals given DMH when compared to control, while the activity was significantly reduced in animals given DMH + fenugreek when compared to animals given DMH only. Our study shows that supplementation of fenugreek seeds in the diet inhibits colon carcinogenesis, by modulating the activities of beta-glucuronidase and mucinase. The beneficial effect may be attributed to the presence of fibre, flavonoids and/or saponins.
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PMID:Fenugreek affects the activity of beta-glucuronidase and mucinase in the colon. 1459 93

The aim of the present study was to unravel the chemopreventive effect of luteolin on bacterial enzymes such as beta-glucuronidase and mucinase in a colon carcinogenesis model induced by 1, 2-dimethyl hydrazine (DMH). Twenty mg/kg body weight of DMH were administered subcutaneously once a week for the first 15 weeks and then discontinued. Luteolin (0.1, 0.2, or 0.3 mg/kg body weight/everyday (p.o.) was administered in a dose dependent manner at the initiation and also at the post-initiation stages of carcinogenesis to DMH treated rats. The animals were sacrificed at the end of 30 weeks. Colon cancer incidence and the activities of bacterial enzymes beta-glucuronidase (in the proximal colon, distal colon, intestines, liver and colon contents) and mucinase (colon and fecal contents) were significantly increased in DMH -treated rats compared to the control rats. On luteolin administration, colon cancer incidence, number of tumors per rat and the activities of beta-glucuronidase and mucinase, were significantly decreased both in the initiation and post-initiation stages of colon carcinogenesis dependent on the three different doses given. The increase in beta-glucuronidase activity may augment the hydrolysis of glucuronide conjugates, liberating toxins, while the increase in the mucinase activity may enhance the hydrolysis of the protective mucins in the colon. Thus our results demonstrate for the first time that luteolin, a dietary flavonoid, exerts chemopreventive and anticarcinogenic effects against DMH induced colon cancer.
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PMID:Protective role of luteolin in 1,2-dimethylhydrazine induced experimental colon carcinogenesis. 1685 May 23

Diet-induced changes in the activities of bacterial enzymes are known to play a role in colon cancer development. Resveratrol has been implicated as a protective agent in carcinogenesis. In the present study, the effect of resveratrol on the activities of faecal and colonic biotransforming enzymes such as beta-glucuronidase, beta-glucosidase, beta-galactosidase, mucinase, nitroreductase and faecal sulfatase activity was assessed. The total number of aberrant crypt foci and their distribution in the proximal, medial and distal colon were observed in 1,2-dimethylhydrazine (DMH)-induced rats (group 3) and other treatment groups (groups 4-6). DMH (0.02 g/kg body weight) was given subcutaneously once a week for 15 consecutive weeks, and the experiment was terminated at 30 weeks. DMH-treated rats showed elevated levels of cancer-associated bacterial enzyme activities, whereas on resveratrol supplementation in three different regimens, rats showed lowered activities. Resveratrol supplementation throughout the experimental period (group 6) exerted a more pronounced effect (P < 0.01) by modulating the development of aberrant crypt foci and the activities of bacterial enzymes than did the other treatment regimens (groups 4 and 5). Thus, the present results demonstrate the inhibitory effect of resveratrol on DMH-induced colon carcinogenesis in rats.
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PMID:Dietary supplementation of resveratrol suppresses colonic tumour incidence in 1,2-dimethylhydrazine-treated rats by modulating biotransforming enzymes and aberrant crypt foci development. 1687 3

Colon cancer is becoming increasingly common in Asian countries and still remains the second leading cause of cancer death in the United States. Ginger, a natural spice having both antioxidant and antimutagenic property, is known to inhibit chemical carcinogenesis. This study was designed to investigate the chemopreventive efficacy of ginger on the activity of bacterial enzymes in rats induced colon cancer by 1,2-dimethylhydrazine. Twenty milligrams per kilogram body weight of 1,2-dimethylhydrazine was administered subcutaneously once a week for the first 15 weeks and then discontinued. Ginger (50 mg/kg body weight/per day, oral) was given at the initiation and also at the postinitiation stages of carcinogenesis to 1,2-dimethylhydrazine-treated rats. The animals were killed at the end of 30 weeks. The macroscopic findings in the colon and the incidence of tumors were recorded in each group, and the activity of beta-glucuronidase and mucinase was estimated in the tissues and fecal contents of rats. After a total experimental period of 32 weeks (including 2 weeks of acclimatization), tumor incidence was 100% in 1,2-dimethylhydrazine-treated rats. The incidence of cancer as well as the number of tumors in the colon was significantly reduced both in the initiation and postinitiation stages of carcinogenesis on ginger administration. The activities of bacterial enzymes beta-glucuronidase (proximal colon, distal colon, intestines, liver and colon contents) and mucinase (colon and fecal contents) were significantly elevated in 1,2-dimethylhydrazine-treated rats as compared with the control rats. The increase in beta-glucuronidase activity may augment the hydrolysis of glucuronide conjugates, liberating the toxins, while the increase in the mucinase activity may enhance the hydrolysis of the protective mucins in the colon. Ginger administration to 1,2-dimethylhydrazine-treated rats significantly decreased the incidence and number of tumors as well as the activity of beta-glucuronidase and mucinase. Thus, ginger has a chemopreventive and anticarcinogenic effect against 1,2-dimethylhydrazine-induced colon cancer by virtue of its ability to lower the activities of the microbial enzymes beta-glucuronidase and mucinase.
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PMID:Effect of ginger on bacterial enzymes in 1,2-dimethylhydrazine induced experimental colon carcinogenesis. 1691 65


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