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:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to assess a possible role of the natural glutathione defense system in the pathogenesis of rheumatoid arthritis (RA), serum reduced glutathione levels (GSH), glutathione reductase (GSR), glutathione S-transferase (GST), glutathione peroxidase (GSH-Px) and alkaline phosphatase (ALP) activities, lipid peroxidation (MDA content) and indexes of inflammation were evaluated in 58 rheumatic patients. Rheumatoid athritis was associated with significant depletion (ca. 50%) in GSH levels compared with normal control subjects. Serum levels of the detoxifying enzymes GSR and GSH-Px decreased by ca. 50% and 45%, respectively, whereas a threefold increase in the activity of GST was observed. A 1.2-fold increase in ALP was observed in patients with RA. These effects were accompanied by a 3.1-fold increase in serum MDA content. The MDA content was higher in RA patients who were seropositive for rheumatoid factor as well as positive for C-reactive proteins. The erythrocyte sedimentation rate for all patients with RA was approximately 13.8-fold higher than for the control group, and was higher among RA patients who were positive for C-reactive proteins and exhibited seropositivity for rheumatoid factor. Patients with RA receiving gold therapy exhibited significantly lower MDA levels whereas all other factors that were measured were not effected. The results support a hypothesis that defense mechanisms against reactive oxygen species are impaired in RA.
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PMID:The glutathione defense system in the pathogenesis of rheumatoid arthritis. 1118 Feb 82

Picroliv, an iridoid glycoside mixture prepared from the roots and rhizomes of Picrorhiza kurroa was found to be an effective inhibitor of hepatocarcinogenesis induced by N-Nitrosodiethylamine (NDEA) in rats. Animals administered with NDEA had large hepatic nodules and the liver weight was increased to 6.17 +/- 1.0 g/100 g.b.wt. as compared to the normal liver weight 2.84 +/- 0.08 g/100 g.b.wt. Picroliv administration (200 mg/Kg.b.wt) reduced the liver weight to 3.30 +/- 0.23 g/100 g.b.wt. Oral administration of Picroliv reduced NDEA-induced elevation of gamma-glutamyltranspeptidase (gamma-GT) in serum and liver to that of normal rats. Moreover, elevated levels of bilirubin, alkaline phosphatase (ALP), glutamatepyruvate transaminase (GPT) and serum peroxides were also found to be significantly reduced by Picroliv administration. Similar observations were noticed in glutathione (GSH) and glutathione S-transferase (GST) levels. Histopathological analysis of the Picroliv treated rat liver resembles that of a normal liver except for a few alterations such as hepatocytomegalia and karyomegalia in some focii. The results are indicative of the chemopreventive potential of Picroliv against chemically-induced liver tumours.
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PMID:Inhibition of N-nitrosodiethylamine-induced hepatocarcinogenesis by Picroliv. 1127 23

The intracellular signaling pathways responsible for cell cycle arrest and differentiation along the crypt-villus axis of the human small intestine remain largely unknown. p38 mitogen-activated protein kinases (MAPKs) have recently emerged as key modulators of various vertebrate cell differentiation processes. In order to elucidate further the mechanism(s) responsible for the loss of proliferative potential once committed intestinal cells begin to differentiate, the role and regulation of p38 MAPK with regard to differentiation were analyzed in both intact epithelium as well as in well established intestinal cell models recapitulating the crypt-villus axis in vitro. Results show that phosphorylated and active forms of p38 were detected primarily in the nuclei of differentiated villus cells. Inhibition of p38 MAPK signaling by 2-20 microm SB203580 did not affect E2F-dependent transcriptional activity in subconfluent Caco-2/15 or HIEC cells. p38 MAPK activity dramatically increased as soon as Caco-2/15 cells reached confluence, whereas addition of SB203580 during differentiation of Caco-2/15 cells strongly attenuated sucrase-isomaltase gene and protein expression as well as protein expression of villin and alkaline phosphatase. The binding of CDX2 to the sucrase-isomaltase promoter and its transcriptional activity were significantly reduced by SB203580. Pull-down glutathione S-transferase and immunoprecipitation experiments demonstrated a direct interaction of CDX3 with p38. Finally, p38-dependent phosphorylation of CDX3 was observed in differentiating Caco-2/15 cells. Taken together, our results indicate that p38 MAPK may be involved in the regulation of CDX2/3 function and intestinal cell differentiation.
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PMID:Intestinal epithelial cell differentiation involves activation of p38 mitogen-activated protein kinase that regulates the homeobox transcription factor CDX2. 1128 19

Administration of tamoxifen (TAM) has been shown to induce hepatocellular carcinogenesis and TAM-DNA adduct formation in rat liver. Here we present TAM-DNA adduct localization and semi-quantitation in hepatic tissue of rats by immunohistochemical staining followed by image analysis. We have also used a quantitative immunoassay to provide a validation for the immunohistochemical values. Rats were fed diets containing 0, 5, 50, 150 or 500 p.p.m. TAM for 45 weeks. Serial sections of paraffin-embedded liver were stained for TAM-DNA adducts using a polyclonal TAM-DNA antiserum. Subsequently, visualization of TAM-DNA adducts was performed by peroxidase-conjugated secondary antibody-mediated signal amplification using biotinyl tyramide followed by streptavidin-alkaline phosphatase and fast red. Semi-quantitation of nuclear color intensity was achieved with an Automated Cellular Imaging System (ACIS), with a detection limit of 1 TAM-DNA adduct per 10(7) nt for these experiments. In parenchymal cells of liver sections from TAM-exposed animals a dose-dependent increase in nuclear staining was observed by ACIS and the TAM-DNA adduct levels determined by ACIS were validated in liver DNA by quantitative chemiluminescence immunoassay (CIA). Comparison of semi-quantitative values determined by ACIS with quantitative values determined by CIA showed a strong correlation (r = 0.924) between the two methods. At 45 weeks of TAM exposure the liver cytoplasm contained placental glutathione S-transferase (GST-p)-positive foci, as indicated by new fuchsin staining. Staining of serial sections revealed a relative lack of TAM-DNA adducts within these enzyme-altered foci. In addition, some GST-p foci contained islands of cells that did not stain for GST-p but were positive for TAM-DNA adduct formation. This study validates the use of ACIS for TAM-DNA adduct formation and demonstrates that steady-state TAM-DNA adduct levels observed in livers of rats chronically fed TAM for several months increase in relation to dose. In addition, unlike the normal surrounding liver, preneoplastic GST-p-positive foci have virtually no TAM-DNA adducts.
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PMID:Immunohistochemical localization and semi-quantitation of hepatic tamoxifen-DNA adducts in rats exposed orally to tamoxifen. 1157 11

Cancer chemopreventive potential of Cancare, a multi-herbal formulation on chemically induced tumours was studied by N-nitrosodiethylamine (NDEA) induced hepatocarcinogenesis in rats and 20-methylcholanthrene (20-MC) induced sarcoma development in mice. Oral administration of Cancare was found to inhibit the liver tumour development induced by N-nitrosodiethylamine. Animals administered with NDEA had visible liver tumours by the end of 30th weeks and the liver weight was raised to 6.1 +/- 1.4 g/ 100 g body wt. None of the animals treated with Cancare (150 mg/ kg) developed any visible liver tumours by this period and the liver weight was 3.0 +/- 0.6 g/ 100 g body wt. Gamma-Glutamyl transpeptidase, a marker of hepatocellularcarcinoma, which was raised to 83.7 +/- 8. 9 U/l in serum of NDEA treated group was reduced to 35.2 +/- 6.1 U/l by simultaneous administration of Cancare. Elevated levels of serum alkaline phosphatase, glutamate pyruvate transaminase, bilirubin, liver glutathione S-transferase, glutathione and gamma-Glutamyl transpeptidase in the NDEA administered group was significantly reduced by Cancare administration. Cancare administration inhibited the sarcoma development and increased the life span of mice administered with 20-MC dose dependently. All animals in the control group developed sarcomas by 150th day and dead by 174th day after 20-MC administration. Cancare administration (30 mg and 150 mg/kg) inhibited the sarcoma development (46.7 and 60%) as well as increased the life span (53.3 and 66.7%) as estimated on 240th day after 20-MC administration. The results are indicative of the chemopreventive potential of Cancare against chemically induced neoplasmas.
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PMID:Cancare-a herbal formulation inhibits chemically induced tumours in experimental animals. 1201 58

Zinc (Zn) is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth and reproduction. The present study was conducted to investigate the effects of adequate Zn level (38 mg/kg diet, as a control) and two low levels that create Zn deficiencies (19 mg/kg diet, 1/2 of the control and 3.8 mg/kg diet, 1/10 of the control) in growing male and female rats for 10 weeks. To evaluate the effects of these levels, the concentrations of thiobarbituric acid-reactive substances (TBARS), biochemical parameters and protein pattern were studied. Lipid peroxidation in liver, brain and testes of rats fed Zn-deficient diet was indicated by increased TBARS. Serum, liver, brain and testes glutathione S-transferase (GST) activities were significantly (P<0.05) increased in Zn-deficient rats, the effect was pronounced in rats fed the lowest level of Zn (1/10 of control). The activity of lactate dehydrogenase (LDH) was significantly (P<0.05) increased in liver, brain and testes, but decreased in serum in a dose-dependent manner. Zinc deficiency increased (P<0.05) liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in a dose-dependent manner, while there was no effect on the activity of these enzymes in testes. Zinc deficiency resulted in a significant (P<0.05) decrease in the activity of alkaline phosphatase (AlP) in serum and liver in a dose-dependent manner, but no effect in testes was found. The activity of acid phosphatase (AcP) was not affected in serum, liver and testes. Zn-deficient rats had higher liver concentrations of total lipids (TL), cholesterol, triglyceride (TG), and low density lipoprotein (LDL), while high density lipoprotein (HDL) was significantly (P<0.05) declined in a dose-dependent manner. Brain and serum acetylcholinesterase (AChE) activities were, however, not affected (P<0.05) by Zn deficiency. Protein content in liver, brain and testes showed a significant (P<0.05) decrease in rats fed the lowest level of Zn (1/10 of control). Polyacrylamide gel electrophoresis (native-PAGE) of serum proteins revealed that the intensity of immunoglobulins, serum albumin as well as several peptide bands were decreased in rats fed 1/2 or 1/10 of Zn adequate, i.e. their synthesis was affected and it was pronounced with the lowest level of Zn deficiency (1/10 of control). However, no clear effect on the transferrin was observed in both cases compared to controls. From the results of this study it can be concluded that Zn deficiency exerts numerous alterations in the studied biochemical parameters, protein pattern, and increased lipid peroxidation.
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PMID:Dietary zinc deficiency induced-changes in the activity of enzymes and the levels of free radicals, lipids and protein electrophoretic behavior in growing rats. 1204 50

Acute and sub-acute toxic effects of a novel phosphorothionate coded as RPR-II on testis of albino rats were studied. In acute study rats received a single dose of 12.3 mg/kg of RPR-II and sacrificed after 24 hr. For sub-acute study 0.58 mg/kg/day was administered orally to rats for 10 and 21 days. Acute exposure of rats to RPR-II brought no change either in the gonadosomatic index (GSI) or in the structure of testis or in the serum levels of testosterone. Testis glutathione (GSH) level and glutathione S-transferase (GST) activity was significantly decreased whereas, acid phosphatase (AcP) levels increased significantly at 24 hr post-treatment. On 7th day (withdrawal period) after the cessation of the treatment the GSH, GST, AcP, and AkP levels reached to near control. The sub-acute study revealed a significant decrease in GSI on 10th and 21st day of the treatment. In contrast, a time-dependent and significant increased in GSH level and GST activity was observed on 100th and 21st day of post-treatment, except GSH level on 10th day, which was declined. Due to RPR-II treatment the testis AcP and alkaline phosphatase (AkP) levels were significant at both 10th and 21st day of medication but AcP levels were increased whereas AkP levels decreased. The histopathological studies on day 10th showed considerable loss of spermatozoids in testis and at 21st day complete derangement of cellular organization was observed. Testosterone levels decreased significantly on 10th day and remained significantly low at 21st day. However, withdrawal studies showed a recovery in testis of rat treated with RPR-II. GST, GSH, GSI, AcP and AkP values recovered, testosterone levels were also well recovered but recovery in testis structure remained at a low profile. The present study suggests that RPR-II may cause testicular toxicity in rats affecting the normal functioning of testis and it also gave some new information in withdrawal studies.
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PMID:Acute and sub-acute effects of 2-butenoic acid-3-(diethoxy phosphinothioyl) methyl ester (RPR-II) on testis of albino rat. 1262 78

Effect of isoflavone on cypermethrin-induced changes in enzyme activities and free radicals was studied in plasma, liver, brain and testes of male New Zealand White rabbits. Rabbits were orally given sublethal dose of cypermethrin (24 mg/kg BW; 1/100 LD50), while isoflavone (2 mg/kg BW) was given alone or in combination with cypermethrin. The tested doses were given to rabbits every other day for 12 weeks. Results obtained showed that cypermethrin significantly (P < 0.05) induced free radicals in plasma, liver, brain and testes. The activities of glutathione S-transferase (GST) (liver, brain and testes), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (liver and testes), and alkaline phosphatase (AlP) (liver) were significantly (P < 0.05) decreased due to cypermethrin administration. Contrariwise, the activities of GST, AST, ALT and AIP were increased in plasma. The activity of acetylcholinesterase (AChE) did not change in plasma and brain of treated rabbits with cypermethrin. Isoflavone alone significantly (p < 0.05) decreased the levels of free radicals in plasma, liver, brain and testes, while did not produce any significant effect on the investigated enzymes. However, isoflavone is able to reverse the changes in enzyme activities due to the effect of cypermethrin. Results concluded that isoflavone confers marked protection against cypermethrin-induced oxidative stress in rabbit's plasma, liver, brain and testes.
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PMID:Protective effects of isoflavone on some biochemical parameters affected by cypermethrin in male rabbits. 1271 53

The aim of the study was to evaluate serum a-glutathione S-transferase (s-GSTA) levels in patients with cystic fibrosis (CF) and to compare s-GSTA with other liver function tests and with a hepatic ultrasound scan (US). The cytosolic enzyme, alpha-glutathione S-transferase is predominantly found in the liver and is distributed uniformly in the liver tissue. In our study s-GSTA levels were measured in 37 CF patients aged 1 to 28 years (mean age 10.4 years, 24 males). The control group consisted of 27 patients aged 2 to 17 years (mean age 8.5 years, 18 males). The presence of hepatobiliary abnormalities was assessed by clinical examination, ultrasound scan, s-GSTA, and conventional liver enzymes: alanine aminotransferase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST) and gama-glutamyl transferase (GMT). The calculated 5-95 % range of s-GSTA for the control group was 0.098-2.54 microg/l, for the CF group 0.43-9.76 microg/l. Mean s-GSTA level in the control group was 1.55 microg/l (S.D.=1.57), and 2.05 micro/l (S.D.=2.60) in the CF group. In the group of CF patients, the serum levels were significantly higher than in the control group (P<0.01). No significant correlation existed in the CF group between s-GSTA and conventional liver tests (ALT, AST, ALP and GMT). Four patients in the CF group had hepatobiliary abnormalities detectable by conventional liver tests, s-GSTA and US. Four patients had abnormal s-GSTA, while conventional liver tests and US were normal. One other patient had abnormal hepatic US, but normal standard liver tests and s-GSTA. The study has suggested that a raised s-GSTA level might be a marker of possible pathological changes of the hepatobiliar system in CF patients. Serum GSTA seems to be a more sensitive marker than transaminases for the monitoring of hepatocellular integrity and as an early predictor of hepatic damage.
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PMID:Serum alpha-glutathione S-transferase as a sensitive marker of hepatocellular damage in patients with cystic fibrosis. 1279 Jul 69

Curcumin, a yellow pigment of turmeric (Curcuma longa), is a commonly used spice and a coloring agent in foods, drugs, and cosmetics. Curcumin is known to possess chemopreventive properties in various animal tumor models. In the present study the effect of curcumin on the development of altered hepatic foci (AHF), by using a medium term liver bioassay, has been evaluated. AHF were analyzed by quantitative stereology using the Leica Qwin Image Analysis system from frozen liver sections stained for g-glutamyl transferase, adenosine triphosphatase, glucose-6-phosphatase, alkaline phosphatase, and placental isozyme of glutathione S-transferase. A significant protection on diethylnitrosamine (DEN) initiated and 2-acetylaminofluorene (AAF) promoted AHF by curcumin was observed on these biological markers. The curcumin administration was found to restore the normal levels of the enzymes glutathione S-transferase and g-glutamyl transferase in rat liver following DEN-AAF exposure. Similarly, a significant protection was provided by curcumin in the enzyme-deficient foci for the adenosine triphosphatase-, alkaline phosphatase-, and glucose-6-phosphatase-treated groups in comparison to the DEN-AAF-treated group. These results show that curcumin can effectively suppress the DEN-induced development of AHF in rat liver.
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PMID:Suppression of altered hepatic foci development by curcumin in wistar rats. 1279 5


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