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 continuation of our previous studies, which demonstrated a decreased glutathione peroxidase (GSH-Px) activity of erythrocytes from multiple sclerosis (MS) patients the activity of some enzymes regulating the peroxide level (GSH-PX and glutathione reductase (GSSG-Rd)) in leucocytes and erythrocytes respectively, the selenium level of whole blood and the beta-glucuronidase activity of serum (marker of lysosomal membrane damage) were assayed in this group of patients. GSH-Px activity in lymphocytes and granulocytes from MS patients was significantly (2 alpha smaller than or equal to 0.01) decreased by 35-50%. Erythrocyte glutathione reductase activity was only insignificantly decreased in MS patients. Erythrocyte GSH-Px : GSSG-Rd ratio was 11.0 for the control group, but 8.0 for the MS group. The selenium content of whole blood and serum from Danish MS patients was normal. The selenium level in erythrocytes from Danish MS patients was however higher than the selenium level in erythrocytes from controls.
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PMID:Leucocyte glutathione peroxidase activity and selenium level in multiple sclerosis. 742 Jan 26

Mouse colon adenocarcinoma Co38 is widely used as a screening model for human colon tumors. To understand better the influence of tumor size on the main drug-metabolizing enzyme systems, we tested 15 mouse Co38 tumors at different sizes. The average weight was 917 +/- 444 mg (range, 300-1,400 mg). Cytochromes P-450 (1A1/1A2, 2B1/B2, 2C8-10, 2E1, 3A4), epoxide hydrolase (EH), and glutathione-S-transferases (GST-alpha, -mu, and -pi) were assayed by immunoblotting. The activities of the following enzymes or cofactors were determined by spectrophotometric or fluorometric assays: 1-chloro-2,4-dinitrobenzene-GST (CDNB-GST), selenium-independent glutathione peroxidase (GPX), 3,4-dichloronitrobenzene-GST (DCNB-GST), ethacrynic acid-GST (EA-GST), total glutathione (GSH), uridine diphosphate-glucuronosyltransferase (UDP-GT), beta-glucuronidase (beta G), sulfotransferase (ST), and sulfatase (S). Our results showed the absence of all probed P-450s and EH in Co38 tumors. No relationship was found between the Co38 tumor weights and GPX, GST-alpha, and EA-GST (regression analysis). However, a significant correlation was found between the tumor weights and all other enzymes investigated. For certain enzymes or cofactors, a linear decrease (P < 0.05) was observed as a function of tumor weight (CDNB-GST, DCNB-GST, GST-mu, GST-pi, GSH, and beta G). Other enzymatic activities (UDP-GT, S, and ST) were found to decrease in medium-size tumors and to increase in large tumors (P < 0.05; quadratic correlation). These data demonstrate that the expression of many drug-metabolizing enzyme systems is altered during tumor growth and suggest that tumoral response to chemotherapy could be altered as a function of tumor size.
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PMID:Influence of tumor size on the main drug-metabolizing enzyme systems in mouse colon adenocarcinoma Co38. 792 60

Since drug-metabolizing enzymes may influence the toxic response of tissues or organs to drugs, we studied their expression in human and colon tumor tissues, in an attempt to find new targets for chemotherapy and also to explain the intrinsic drug-insensitivity of most colon tumors to anticancer drugs. In the present work, we compared human colorectal tumors and peritumoral tissues to a mouse colorectal tumor (Co38) and normal murine colon with regard to their main drug-metabolizing enzyme systems. We investigated cytochromes P-450 (1A1/1A2, 2B1/B2, 2C, 2E1, 3A) and epoxide hydrolase (EH) by immunoblotting. Total glutathione (GSH) and the activities of the following enzymes: total GST, selenium-independent glutathione peroxidase (GPX), 1,2-dichloro-4-nitrobenzene-GST (DCNB-GST), ethacrynic acid-GST (EA-GST), UDP-glucuronosyltransferase 1 (UDPGT), beta-glucuronidase (beta G), sulfotransferase (ST) and sulfatase (S) were investigated by fluorometric and spectrophotometric assays. Results obtained by immunoblotting showed that mouse colon tumor Co38 did not express any of the probed cytochromes P-450, whereas human tumors showed the presence of cytochrome P-450 3A. EH was not expressed in either mouse colon tumor Co38 or normal mouse colon, whereas it was expressed in human peritumoral and tumoral colon tissues at similar levels. GPX and EA-GST were detected in all tumoral and non tumoral tissues of both species. DCNB-GST was expressed in all murine tissues investigated, but was not found in human tissues. For human peritumoral and tumoral colorectal tissues there was no significant difference between GST isoenzymes levels, whereas mouse colon tumor Co38 had a lower expression of DCNB-GST and EA-GST compared to normal mouse colon. No significant difference was observed between human tumors and peritumoral tissues for total GST, UDPGT1, beta G, ST and S activities. For murine colon tissues, the conjugation pathways (total GST, UDPGT1 and ST) were lower in Co38, whereas the opposite was observed for the hydrolytic enzymes (beta G and S). In conclusion, despite similarities between human and murine colon tumors, mouse colon tumor Co38 appears different from human colon tumors for many drug-metabolizing enzyme systems. These interspecies differences may have implications with regard to drug screening methodologies and preclinical evaluation of candidate anticancer drugs useful in the chemotherapy of human colorectal tumors.
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PMID:[Screening of principal enzymes involved in the metabolism of anticancer drugs in human and murine colonic tumors]. 817 93

The effect of curcumin on the biochemical changes induced by isoproterenol (ISO) administration in rats was examined. ISO (300 mg Kg-1 administered subcutaneously twice at an interval of 24 h) caused a decrease in body weight and an increase in heart weight, water content as well as in the levels of serum marker enzymes viz creatine kinase (CK), lactate dehydrogenase (LDH) and LDH1 isozyme. It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation. Curcumin at a concentration of 200 mg.Kg-1, when administered orally, showed a decrease in serum enzyme levels and the electrocardiographic changes got restored towards normalcy. Myocardial infarction was accompanied by the disintegration of membrane polyunsaturated fatty acids expressed by increase of thiobarbituric acid reactive substance (TBARS), a measure of lipid peroxides and by the impairment of natural scavenging, characterized by the decrease in the levels of superoxide dismutase, catalase, glutathione peroxidase, ceruloplasmin, alpha tocopherol, reduced glutathione (GSH) and ascorbic acid. The oral pretreatment with curcumin two days before and during ISO administration decreased the effect of lipid peroxidation. It was shown to have a membrane stabilizing action by inhibiting the release of beta-glucuronidase from nuclei, mitochondria, lysosome and microsome. Curcumin pre- and co-treatment decreased the severity of pathological changes and thus, could have a protective effect against the damage caused by myocardial infarction (MI).
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PMID:Protective role of curcumin against isoproterenol induced myocardial infarction in rats. 885 58

Portal hypertensive gastropathy is associated with a broad spectrum of gastric mucosal damage inspite of decreased gastric acid secretion, suggestive of compromised endogenous protective mechanisms. To determine the mechanisms of damage in portal hypertensive gastropathy we measured lipid peroxidation, glutathione, antioxidant and lysosomal enzymes in gastric mucosal homogenates from male Wistar rats with elevated intrasplenic pulp pressure, eighteen days after common bile duct ligation. Thiobarbituric acid-reactive substances and lysosomal enzymes (beta-glucuronidase and acid phosphatase) were increased in the common bile duct ligated group as compared to the sham-operated group. The levels of antioxidant defense enzymes, superoxide dismutase, glutathione peroxidase, catalase and glutathione were decreased as compared to the sham-operated controls. Pre-operative vitamin E administration decreased mucosal lipid peroxidation increased the levels of antioxidant defense enzymes and lowered the lysosomal enzymes. The plasma vitamin E levels in this group were lower when compared to animals receiving it post-operatively. In conclusion, free radical and lysosomal enzyme mediated damage may play a role in portal hypertensive gastropathy.
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PMID:Gastropathy and defense mechanisms in common bile duct ligated portal hypertensive rats. 1072 35

Adriamycin, which is widely used in the treatment of various neoplastic conditions, exerts toxic effects in many organs. The present study was designed to investigate the effect of lipoic acid upon adriamycin induced peroxidative damages in rat kidney. The increase in peroxidated lipids on adriamycin administration was accompanied by alterations in the antioxidant defense systems. The extent of nephrotoxicity induced by adriamycin was evident from the decreased activities of the enzymes gamma-glutamyl transferase and beta-glucuronidase in the rat renal tissues. The study was carried out with adult male albino rats of Wistar strain, which comprised of one control and three experimental groups. Group I rats served as controls. Group II rats received adriamycin (1 mg kg(-1) body wt day(-1)) intravenously through the tail vein. Group III rats were given lipoic acid (35 mg kg(-1) body wt day(-1)) intraperitoneally. Group IV rats were given lipoic acid 24 h before the administration of adriamycin. Rats subjected to adriamycin administration showed a decline in the thiol capacity of the cell accompanied by high malondialdehyde levels along with lowered activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione metabolizing enzymes (glutathione reductase, glucose-6-phosphate dehydrogenase, glutathione-S-transferase). Lipoic acid pretreatment also restored the activities of gamma-glutamyl transferase and beta-glucuronidase nearly to control levels thereby suggesting nephroprotection. The study has highlighted the beneficial effects of lipoic acid pretreatment in reversing the damages caused by adriamycin and thereby bringing about an improvement in the oxidative stress parameters.
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PMID:Protective effect of lipoic acid on adriamycin induced lipid peroxidation in rat kidney. 1284 25

Inflammatory reactions to microbial infections may cause male infertility. The mechanisms of inhibition of spermatogenesis can be studied in vitro using rat Sertoli cells. Bacterial lipopolysaccharides (LPS) induce acute inflammations. So LPS treated Sertoli cells can be used to test for new therapeutic compounds. The present study aimed to investigate the protective efficacy of dl-alpha-lipoic acid (LA) on lipopolysaccharide (LPS)-induced oxidative stress in adult rat Sertoli cells. Sertoli cells were divided into 4 groups. Group I served as a control incubated with water (vehicle). Groups II and IV were incubated with 100 microM LA for 24h before incubating Groups III and IV with 50 microg/ml lipopolysaccharide (LPS) for 12h. In Group III cells (LPS-treated, no LA) the lactate concentration was decreased whereas hydrogen peroxide production and lipid peroxidation were significantly increased. Moreover, the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase, glutathione-S-transferase, glutathione reductase were reduced. The concentrations of antioxidant molecules such as reduced glutathione and vitamin C were significantly decreased. The activities of enzymes normally elevated in Sertoli cells, gamma-glutamyl transpeptidase and beta-glucuronidase, were significantly decreased. Treatment with LA (100 microM) for 24h before LPS-treatment (Group IV), prevented these changes in enzyme activities and metabolite concentrations. Therefore, LA may have a cyto-protective role during LPS-induced inflammation in adult rat Sertoli cells.
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PMID:Modulatory role of lipoic acid on lipopolysaccharide-induced oxidative stress in adult rat Sertoli cells in vitro. 1969 28

Inflammatory reactions that result from microbial infections, both localized and systemic, are reported to cause transient or permanent male infertility. The cellular mechanisms underlying the inhibitory effect of microbial infection on spermatogenesis is not fully understood. However, there is evidence that spermatogenesis is affected by bacterial lipopolysaccharides (LPS) that induce acute inflammatory responses. The aim here was to use LPS treatments to investigate the potential oxidative stress and toxicity in primary cultures of adult rat Sertoli cells. The Sertoli cells were established and incubated with different concentrations of LPS (5, 10 or 20 microg/ml) for 6, 12 and 24h. Lipid peroxidation (LPO) and hydrogen peroxide (H(2)O(2)) production, along with superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), reduced glutathione (GSH), lactate, lactic acid dehydrogenase (LDH), gamma-glutamyl transpeptidase (gamma-GT) and beta-glucuronidase were measured in these cells. LPO as well as H(2)O(2) production were significantly increased while antioxidant enzyme activities and GSH concentration were significantly depressed. Effects were dose and time-dependent at all incubation periods with 10 and 20 microg/ml LPS. Moreover, markers of Sertoli cell function such as lactate production, LDH, gamma-GT and beta-glucuronidase activities were decreased in a time and dose-dependent manner. Incubation of Sertoli cells with 5 microg/ml LPS for 12 and 24h significantly increased oxidative status but significantly decreased the antioxidant enzyme activities, GSH concentration and Sertoli cell markers. In contrast, the oxidative and antioxidant status and markers of Sertoli cell function did not show any significant change in treated Sertoli cells with 5 microg/ml LPS for 6h. Therefore, it may be concluded that LPS induces oxidative stress in Sertoli cells and adversely affects Sertoli cell functions.
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PMID:Bacterial lipopolysaccharide-induced oxidative stress in adult rat Sertoli cells in vitro. 2421 63

Cancer is a serious global public health problem. Cancer incidence and mortality have been steadily rising throughout the past century in most places of the world. There are several epidemiological evidences that support a protective role of probiotics against cancer. Lactic acid bacteria and their probioactive cellular substances exert many beneficial effects in the gastrointestinal tract, and also release various enzymes into the intestinal lumen and exert potential synergistic (LAB) effects on digestion and alleviate symptoms of intestinal malabsorption. Consumption of fermented dairy products with LAB may elicit anti-tumor effects. These effects are attributed to the inhibition of mutagenic activity, the decrease in several enzymes implicated in the generation of carcinogens, mutagens, or tumor-promoting agents, suppression of tumors, and epidemiology correlating dietary regimes and cancer. Specific cellular components in lactic acid bacteria seem to induce strong adjuvant effects including modulation of cell-mediated immune responses, activation of the reticulo-endothelial system, augmentation of cytokine pathways, and regulation of interleukins and tumor necrosis factors. Studies on the effect of probiotic consumption on cancer appear promising, since recent in vitro and in vivo studies have indicated that probiotic bacteria might reduce the risk, incidence and number of tumors of the colon, liver and bladder. The protective effect against cancer development may be ascribed to binding of mutagens by intestinal bacteria, may suppress the growth of bacteria that convert procarcinogens into carcinogens, thereby reducing the amount of carcinogens in the intestine, reduction of the enzymes beta-glucuronidase and beta-glucosidase and deconjugation of bile acids, or merely by enhancing the immune system of the host. There are isolated reports citing that administration of LAB results in increased activity of anti-oxidative enzymes or by modulating circulatory oxidative stress that protects cells against carcinogen-induced damage. These include glutathione-S-transferase, glutathione, glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase. However, there is no direct experimental evidence for cancer suppression in human subjects as a result of the consumption of probiotic cultures in fermented or unfermented dairy products, but there is a wealth of indirect evidence based largely on laboratory studies.
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PMID:Cancer-preventing attributes of probiotics: an update. 2018 14

The pathogenesis of periodontitis involves anaerobic oral bacteria as well as the host response to infection and several drugs have been developed which can curtail these deleterious effects. Proanthocyanidin, a novel flavanoid extracted from grape seeds, has been shown to provide a significant therapeutic effect on endotoxin (Escherichia coli) induced experimental periodontitis in rats. In this study, protective action of different doses of proanthocyanidins was investigated in blood by assaying the reactive oxygen species such as hydrogen peroxide, superoxide anion, myeloperoxidase and lipid peroxides, lysosomal enzyme activities such as cathepsin B, cathepsin D, beta-glucuronidase and acid phosphatase, nonenzymatic antioxidants such as ascorbic acid, alpha-tocopherol, ceruloplasmin, reduced glutathione and antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione-s-transferase. Experimental periodontitis rats showed a reduction in body weight and body weight gain could be noticed when they were administered proanthocyanidins. The levels of reactive oxygen species and lysosomal enzymes were found to increase whereas antioxidant levels were decreased significantly in experimental periodontitis. Proanthocyanidins at an effective dose of 30 mg/kg body weight, sc, for 30 days effected a decrease in serum reactive oxygen species, lipid peroxides, lysosomal enzymes, acute phase proteins and an increase in antioxidant levels. Histopathological evidence of experimental periodontitis showed cellular infiltration of inflammatory cells while proanthocyanidin treated groups demonstrated only scattered inflammatory cells and blood vessels. Thus, the results showed that dietary supplementation of proanthocyanidin enhanced the host resistance as well as the inhibition of the biological and mechanical irritants involved in the onset of gingivitis and the progression of periodontal disease.
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PMID:Protective effect of proanthocyanidins on endotoxin induced experimental periodontitis in rats. 2045 22


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