Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Fenugreek affects the activity of beta-glucuronidase and mucinase in the colon. 1459 93

High amylose maize starch (HAS) is not digested in the small intestine and most of it reaches the large intestine. In the large intestine, HAS is fermented by intestinal bacteria, resulting in production of short-chain fatty acids (SCFA), particularly butyrate. Clostridium butyricum can utilize HAS and produce butyrate and acetate. It has been proposed that butyrate inhibits carcinogenesis in the colon. In this study, we examined the inhibitory effects of HAS and C. butyricum strain MIYAIRI588 (CBM588) on azoxymethane-induced aberrant crypt foci (ACF) formation in rats. In the group of rats administered only CBM588 spores, the concentration of butyrate in the cecum increased, but there was no decrease in the number of ACF. In the group of rats fed an HAS diet, a decrease in the number of ACF was observed, and in the group of rats administered HAS and CBM588, the number of ACF decreased significantly. In these two groups, the concentrations of acetate and propionate in intestinal contents significantly increased, but the concentration of butyrate did not change. It was found that the beta-glucuronidase activity level of colonic contents decreased significantly in the two groups of rats fed HAS. This study showed that HAS and CBM588 changed the metabolism of colonic microbiota and decreased the level of beta-glucuronidase activity, phenomena that may play a role in the inhibition of ACF formation in the rat colon.
 ...
PMID:Effects of high amylose maize starch and Clostridium butyricum on metabolism in colonic microbiota and formation of azoxymethane-induced aberrant crypt foci in the rat colon. 1469 45

Different vitamins and other micronutrients in vegetables, fruits, and other natural plant products may prevent cancer development (carcinogenesis) by interfering with detrimental actions of mutagens, carcinogens, and tumor promoters. The goal of current studies in cancer prevention is to determine the mechanisms of synergistic action of the natural source compounds known to inhibit one or more stages of carcinogenesis, that is, initiation and promotion/progression. Many natural cancer preventive agents are effective inhibitors of tumor initiation, promotion, and/or progression. The mechanism of action is related to their abilities to prevent critical carcinogen metabolism and to increase detoxification of carcinogens and tumor promoters. The authors review here the potential role of the detoxification system and, in particular, the roles of D-glucaric acid and the enzyme beta-glucuronidase in early detection and prevention of cancer. There is now growing evidence for the possible control of different stages of the cancer induction by inhibiting beta-glucuronidase with D-glucaric acid derivatives, especially with its salts (D-glucarates). D-Glucaric acid has been found in many vegetables and fruits. Therefore, the consumption of fruits and vegetables naturally rich in D-glucaric acid or self-medication with D-glucaric acid derivatives such as calcium D-glucarate offers a promising cancer prevention approach.
 ...
PMID:Detoxifying cancer causing agents to prevent cancer. 1503

Yoghurt feeding inhibits induced colon cancer in mice. Several studies showed the immunomodulatory effect of yoghurt which can explain this inhibition. It is possible that yoghurt bacteria can also affect gut flora enzymes related to colon carcinogenesis as reported for other probiotics in different animal tumours. The aim of this work was to evaluate the role of yoghurt starter bacteria and their cell-free fermentation products on the reduction of procarcinogen enzyme activities (beta-glucuronidase and nitroreductase). Mice injected with 1,2-dimethylhydrazine (DMH) and fed with yoghurt were used for this study. Mice given milk or yoghurt supernatant (cell free extract) were used to evaluate if the yoghurt antitumour effect is due to the starter bacteria or other components released during fermentation, that could inhibit these enzymes. We determined that yoghurt by itself maintained enzymes activities similar or lower than non-treatment control group, and the enzyme activity was also lower than milk or yoghurt supernatant groups. DMH increased the activity of the enzymes. Mice injected with DMH and fed cyclically with yoghurt presented lower enzymes activities than the tumour control group. Feeding yoghurt decreased procarcinogenic enzyme levels in the large intestine contents of mice bearing colon tumour. The results of this study provide another mechanism by which yoghurt starter bacteria interact with the large intestine of the mice and prevent colon cancer.
 ...
PMID:Reduction of beta-glucuronidase and nitroreductase activity by yoghurt in a murine colon cancer model. 1595 63

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.
 ...
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.
 ...
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.
 ...
PMID:Effect of ginger on bacterial enzymes in 1,2-dimethylhydrazine induced experimental colon carcinogenesis. 1691 65

2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is a genotoxic/carcinogenic compound formed in meat and fish during cooking. Following absorption in the upper part of the gastrointestinal tract, IQ is mainly metabolized in the liver by xenobiotic-metabolizing enzymes. Among them, UDP-glucuronosyl transferases lead to harmless glucuronidated derivatives that are partly excreted via the bile into the digestive lumen, where they come into contact with the resident microbiota. The purpose of this study is to investigate if microbial beta-glucuronidase could contribute to IQ genotoxicity by releasing reactive intermediates from IQ glucuronides. We constructed a beta-glucuronidase-deficient isogenic mutant from a wild-type Escherichia coli strain carrying the gene uidA encoding this enzyme and compared the genotoxicity of IQ in gnotobiotic rats monoassociated with the wild-type or the mutant strain. The Comet assay performed on colonocytes and hepatocytes showed that the presence of beta-glucuronidase in the digestive lumen dramatically increased (3-fold) the genotoxicity of IQ in the colon. This deleterious effect was paralleled by slight modifications of the pharmacokinetics of IQ. The urinary and faecal excretion of the parent compound and its conjugated derivatives reached a maximum 24-48 h after gavage in rats harbouring the beta-glucuronidase-deficient strain. In rats associated with the wild-type strain, the kinetics of urinary excretion showed a biphasic curve with a second, smaller peak after 144 h. This is the first in vivo demonstration that bacterial beta-glucuronidase plays a pivotal role in the genotoxicity of a common food-borne carcinogen.
Carcinogenesis 2007 Nov
PMID:Beta-glucuronidase in human intestinal microbiota is necessary for the colonic genotoxicity of the food-borne carcinogen 2-amino-3-methylimidazo[4,5-f]quinoline in rats. 1766 May 8

Quercetin exhibits a potent anticarcinogenic activity. However, ingested quercetin circulates as the glucuronide/sulfate conjugates, which are less active compared to the aglycone in healthy individuals. This study aimed to develop further understandings of the cancer-preventing mechanism with dietary quercetin. According to a two-stage hepatocarcinogenesis model with N-diethylnitrosamine (DEN) and phenobarbital (PB), preneoplasms were induced specifically in the liver of Fisher 344 rats. In the liver, glutathione S-transferase placental form (GST-P) positive foci were produced 14 weeks later. beta-Glucuronidase activity increased significantly in the liver by 1.2-fold in the DEN/PB group compared to the activity in a saline group. In the kidney, thymus, lung, heart, and plasma, the activities were similar between both groups. When quercetin was dosed intragastrically 15 min before sacrifice, the aglycone level of quercetin in liver was significantly 1.9-fold higher in the DEN/PB group than in the saline group. On the other hand, quercetin was dosed to rats 3 times a week for 14 weeks. The treatment kept the aglycone level of quercetin at a significantly higher level and tended to suppress the formation of GST-P positive foci. The increase in beta-glucuronidase activity with carcinogenesis induction became insignificant following the frequent doses of quercetin. It was considered that quercetin aglycone played a preventative role and, thus, the conjugates were converted to the active aglycone by beta-glucuronidase that was induced by the generation of preneoplasms.
 ...
PMID:Metabolic conversion of dietary quercetin from its conjugate to active aglycone following the induction of hepatocarcinogenesis in fisher 344 rats. 1809 47

High intakes of carotenoid-rich fruits and vegetables are associated with a reduced risk of various cancers including colon cancer. A human intervention study with carrot and tomato juice should show whether a diet rich in carotenoids, especially high in beta-carotene and lycopene, can modify luminal processes relevant to colon carcinogenesis. In a randomised cross-over trial, twenty-two healthy young men on a low-carotenoid diet consumed 330 ml tomato or carrot juice per d for 2 weeks. Intervention periods were preceded by 2-week depletion phases. At the end of each study period, faeces of twelve volunteers were collected for chemical analyses and use in cell-culture systems. Consumption of carrot juice led to a marked increase of beta-carotene and alpha-carotene in faeces and faecal water, as did lycopene after consumption of tomato juice. In the succeeding depletion phases, carotenoid contents in faeces and faecal water returned to their initial values. Faecal water showed high dose-dependent cytotoxic and anti-proliferative effects on colon adenocarcinoma cells (HT29). These effects were not markedly changed by carrot and tomato juice consumption. Neither bile acid concentrations nor activities of the bacterial enzymes beta-glucosidase and beta-glucuronidase in faecal water changed after carrot and tomato juice consumption. Faecal water pH decreased only after carrot juice consumption. SCFA were probably not responsible for this effect, as SCFA concentrations and profiles did not change significantly. In summary, in the present study, 2-week interventions with carotenoid-rich juices led only to minor changes in investigated luminal biomarkers relevant to colon carcinogenesis.
 ...
PMID:Effects of carrot and tomato juice consumption on faecal markers relevant to colon carcinogenesis in humans. 1825 85


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>