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)

The effects of hexachlorocyclohexane (HCH) on growth performance and immune and oxidative stress in growing/finishing pigs were studied. Seventy-two pigs, with equal numbers of barrows and gilts, of the same genotype (Duroc x Landrace x Large White), were randomly assigned to three groups receiving the same basal diet, exposed to 0, 0.4 and 0.8 mg/kg technical HCH, respectively, for 90 days. Six pigs from each group were randomly picked out and slaughtered on a finishing feeding trial. The result showed that addition of HCH did not affect the growth performance significantly but increased the weight of kidney and thymus significantly. Total serum IgG and IgM were elevated significantly, but there were no significant differences in serum IgA, C3 and C4 among the groups. Addition of HCH to feedstuff reduced superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GSH-Px) activities in liver, reduced serum catalase (CAT) activity, and increased serum malondialehyde (MDA). Moreover, the activities of serum alanine aminotransferase and alkaline phosphatase were increased significantly. Addition of 0.4 mg/kg or 0.8 mg/kg HCH did not affect the growth performance but affected the immune and antioxidant potential.
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PMID:Effect of HCH contamination of diet on the growth performance and immune and antioxidant ability in growing/finishing pigs. 1683 6

In this chapter, we describe the methods we have used to show that chicken leukemia inhibitory factor (LIF) maintains chicken embryonic stem (ES) cells in an undifferentiated state in culture. Recombinant chicken LIF (rchLIF) was expressed as a fusion protein linked to glutathione S-transferase (GST) and purified to greater than 90% purity in two chromatography stages, the first an affinity step using the GST tail, which was cleaved before further purification by gel chromatography. Chicken ES cells were obtained by culturing chicken blastodermal cells isolated from stage X embryos of freshly laid chicken eggs. These cells can be maintained in media containing rchLIF for at least 9 d without any other cytokines or feeder cells. Chicken ES cells were characterized by the expression of alkaline phosphatase activity, stage-specific embryonic antigen (SSEA)-1 and embryonal carcinoma cell monoclonal antibody-1. In addition, the phosphorylation of signal transducers and activators of transcription-3 by LIF, which is sufficient to maintain the undifferentiated state of ES cells, was detected by Western blotting analysis.
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PMID:Maintenance of chicken embryonic stem cells in vitro. 1684 81

Acute renal failure (ARF) is a frequent problem in the intensive care unit and is associated with a high mortality. Early recognition could help clinical management, but current indices lack sufficient predictive value for ARF. Therefore, there might be a need for biomarkers in detecting renal tubular injury and/or dysfunction at an early stage before a decline in glomerular filtration rate is noted by an increased serum creatinine. A MEDLINE/PubMed search was performed, including all articles about biomarkers for ARF. All publication types, human and animal studies, or subsets were searched in English language. An extraction of relevant articles was made for the purpose of this narrative review. These biomarkers include tubular enzymes (alpha- and pi-glutathione S-transferase, N-acetyl-glucosaminidase, alkaline phosphatase, gamma-glutamyl transpeptidase, Ala-(Leu-Gly)-aminopeptidase, and fructose-1,6-biphosphatase), low-molecular weight urinary proteins (alpha1- and beta2-microglobulin, retinol-binding protein, adenosine deaminase-binding protein, and cystatin C), Na+/H+ exchanger, neutrophil gelatinase-associated lipocalin, cysteine-rich protein 61, kidney injury molecule 1, urinary interleukins/adhesion molecules, and markers of glomerular filtration such as proatrial natriuretic peptide (1-98) and cystatin C. These biomarkers, detected in urine or serum shortly after tubular injury, have been suggested to contribute to prediction of ARF and need for renal replacement therapy. However, excretion of these biomarkers may also increase after reversible and mild dysfunction and may not necessarily be associated with persistent or irreversible damage. Large prospective studies in human are needed to demonstrate an improved outcome of biomarker-driven management of the patient at risk for ARF.
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PMID:Biomarkers of acute renal injury and renal failure. 1691 49

Chemoprevention is an important alternative approach to control cancer. Chemical substances with multiple inhibitory properties would be a welcome addition to the class of chemopreventive drugs. In this study, we investigated the antioxidant, anti-inflammatory, antimutagenic and cancer preventive activities of aqueous extract of a macrofungus Phellinus rimosus (Berk) Pilat. The extract exhibited superoxide anion (O2-), hydroxyl radical (*OH), nitric oxide (NO*) scavenging and lipid peroxidation inhibiting activities. The inhibitory concentrations required by the extract to scavenge 50% (IC50) of the superoxide anion, hydroxyl radical and nitric oxide generated were 126 +/- 5.1, 71 +/- 4.7 and 31 +/- 4.5 microg/ml respectively. The concentration required to inhibit 50% of Fe2+ induced lipid peroxidation in rat liver homogenate was 318 +/- 2.4 microg/ml. The extract showed significant (P<0.05) anti-inflammatory activity in a dose dependent manner. Extract (100 mg/kg body wt, p.o) inhibited 44.5, 45.4 and 47% carrageenen, dextran and formalin induced inflammations respectively. The antimutagenic activity was determined by the Ames' Salmonella mutagenecity assay using histidine mutant Salmonella typhimurium strains. The extract at concentration of 5 mg/plate showed antimutagenecity against benzo[a]pyrene (B[a]P) and 4-nitro-o-pheneylenediamine (NPDA) induced mutations of TA98 and TA100 respectively. Anticarcinogenic activity was evaluated using N-nitrosodiethylamine (NDEA) induced hepatocellular carcinoma (HCC) in rats. Serum gamma glutamyl transpeptidase (GGT), glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) activities and lipid peroxidation level (MDA) were elevated significantly (P<0.05) in the NDEA alone treated group of animals. Treatment of the extract (25 and 50 mg/kg body wt, p.o.) prior to the NDEA administration decreased the serum GGT, GOT, GPT and ALP activities and MDA level in a dose dependent manner. The NDEA alone treated animals showed altered serum albumin/globulin ratio (A:G ratio), hyperfibrinogenaemia, increased hepatic glutathione S-transferase (GST) activity, glutathione-peroxidsae (GPx) activity and reduced glutathione (GSH) level compared to the extract plus NDEA treated group. The extract also inhibited in vitro aniline hydroxylase (AH) activity of rat liver induced by phenobarbitone in a dose dependent manner. The results, thus suggest the significant chemopreventive properties of the aqueous extract of the Phellinus rimosus against NDEA induced hepatocellular carcinoma by its antioxidant, anti-inflammatory and antimutagenic activities.
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PMID:Chemopreventive activity of a macrofungus Phellinus rimosus against N-nitrosodiethylamine induced hepatocellular carcinoma in rat. 1702 71

The effect of oxfendazole (OX), a benzimidazole anthelmintic, on hepatic gene expression was investigated in the liver of rats as a preliminary study to elucidate the possible mechanism of its non-genotoxic hepatocarcinogenesis. The liver from a male F344/N rat given a diet containing 500 ppm of OX for 3 weeks was examined by global gene expression analysis in comparison with an untreated rat. Microarray analysis revealed that phase I and phase II detoxifying enzymes were up-regulated in an OX-treated rat. In addition to these genes, the expressions of several upregulated genes related to xenobiotic metabolism and oxidative stress [e.g. Cyp1a1; NAD(P)H dehydrogenase, quinone 1 (Nqo1); glutathione peroxidase 2 (Gpx2); glutathione S-transferase Yc2 subunit (Yc2)], were confirmed by real-time reverse transcription polymerase chain reaction (RT-PCR). Furthermore, rats were administered 500 or 1,000 ppm of OX for 9 weeks, and the effect of OX on oxidative stress responses was evaluated by real-time RT-PCR along with conventional toxicological assays, including lipid peroxidation (thiobarbituric acid-reactive substance; TBARS). A longer treatment period and/or a higher dose of OX tended to increase the gene expressions of not only phase I (Cyp1a1 and Cyp1a2) but also phase II (Nqo1, Gpx2, Yc2, and Akr7a3) drug metabolizing enzymes. Toxicological parameters, such as TBARS, serum aspartate aminotransferase (AST), and serum alkaline phosphatase (ALP), showed slight but significant increases after treatment with OX for 9 weeks. These results indicate that OX elicits adaptive responses against oxidative stress in the liver and suggest that the imbalance in redox status might be one of the factors triggering the initial step of OX-induced non-genotoxic carcinogenesis in the liver of rats.
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PMID:Gene expression analyses of the liver in rats treated with oxfendazole. 1734 Jan 21

Stannous chloride (SnCl2) is a reducing chemical agent used in several man-made products. SnCl2 can generate reactive oxygen species (ROS). Therefore, the present study has been carried out to investigate the antioxidant action of l-ascorbic acid (AA) in minimizing SnCl2 toxicity on lipid peroxidation, antioxidant enzyme, and biochemical parameters in male New Zealand white rabbits. Animals were assigned to one of four treatment groups: 0mg AA and 0mg SnCl2/kg BW (control); 40 mg AA/kg BW; 20mg SnCl2/kg BW; 20mg SnCl2 plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Results obtained showed that SnCl2 significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma, while the activities of glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT), and the level of sulfhydryl groups (SH-group) were decreased (P<0.05) in blood plasma. Aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP) and lactate dehydrogenase (LDH) activities were decreased (P<0.05). Stannous chloride significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL), glucose, urea and total bilirubin. On the other hand, the level of plasma high-density lipoprotein (HDL), total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. Ascorbic acid alone significantly decreased the levels of TBARS, lipids and urea, and increased the activities of GST, SOD and CAT, and the levels of SH-group and proteins. While the rest of the tested parameters were not affected. Also, the presence of AA with SnCl2 alleviated its harmful effects on most of the tested parameters. Therefore, the present results revealed that treatment with AA could minimize the toxic effects of stannous chloride.
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PMID:Study of the protective effect of ascorbic acid against the toxicity of stannous chloride on oxidative damage, antioxidant enzymes and biochemical parameters in rabbits. 1743 20

Chlamydophila pneumoniae is an obligate intracellular bacterium that causes bronchitis, pharyngitis, and pneumonia and may be involved in atherogenesis and Alzheimer's disease. Genome sequencing has identified three eukaryote-type serine/threonine protein kinases, Pkn1, Pkn5, and PknD, that may be important signaling molecules in Chlamydia. Full-length PknD was cloned and expressed as a histidine-tagged protein in Escherichia coli. Differential centrifugation followed by sodium carbonate treatment of E. coli membranes demonstrated that His-PknD is an integral membrane protein. Fusions of overlapping PknD fragments to alkaline phosphatase revealed that PknD contains a single transmembrane domain and that the kinase domain is in the cytoplasm. To facilitate solubility, the kinase domain was cloned and expressed as a glutathione S-transferase (GST) fusion protein in E. coli. Purified GST-PknD kinase domain autophosphorylated, and catalytic mutants (K33G, D156G, and K33G-D156G mutants) and activation loop mutants (T185A and T193A) were inactive. PknD phosphorylated recombinant Cpn0712, a type III secretion YscD homolog that has two forkhead-associated domains. Thin-layer chromatography revealed that the PknD kinase domain autophosphorylated on threonine and tyrosine and phosphorylated the FHA-2 domain of Cpn0712 on serine and tyrosine. To our knowledge, this is the first demonstration of a bacterial protein kinase with amino acid specificity for both serine/threonine and tyrosine residues and this is the first study to show phosphorylation of a predicted type III secretion structural protein.
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PMID:Chlamydophila pneumoniae PknD exhibits dual amino acid specificity and phosphorylates Cpn0712, a putative type III secretion YscD homolog. 1776 19

Arsenic is one of the ubiquitous environmental pollutants, which affects nearly all organ systems. The present study has been carried out to investigate the hepatoprotective role of arjunolic acid, a triterpenoid saponin, against arsenic-induced oxidative damages in murine livers. Administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly reduced the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione S-transferase, glutathione reductase and glutathione peroxidase as well as depleted the level of reduced glutathione and total thiols. In addition, sodium arsenite also increased the activities of serum marker enzymes, alanine transaminase and alkaline phosphatase, enhanced DNA fragmentation, protein carbonyl content, lipid peroxidation end-products and the level of oxidized glutathione. Studies with arjunolic acid show that in vitro it possesses free radical-scavenging and in vivo antioxidant activities. Treatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days prior to arsenic administration prevents the alterations of the activities of all antioxidant indices and levels of the other parameters studied. Histological studies revealed less centrilobular necrosis in the liver treated with arjunolic acid prior to arsenic intoxication compared to the liver treated with the toxin alone. Effects of a known antioxidant, vitamin C, have been included in the study as a positive control. In conclusion, the results suggest that arjunolic acid possesses the ability to attenuate arsenic-induced oxidative stress in murine liver probably via its antioxidant activity.
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PMID:Protection of arsenic-induced hepatic disorder by arjunolic acid. 1791 Jun 17

Methanolic extract of Phyllanthus-polyphyllus was evaluated for hepatoprotective and antioxidant activities in rats. The plant extract (200 and 300 mg/kg, p.o.) showed a remarkable hepatoprotective and antioxidant activity against acetaminophen induced hepatotoxicity as judged from the serum marker enzymes and antioxidant levels in liver tissues. Acetaminophen induced a significant rise in aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase (LPO) with a reduction of total protein, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione S-transferase (GST). Treatment of rats with different doses of plant extract (200 and 300 mg/kg) significantly (P<0.001) altered serum marker enzymes and antioxidant levels to near normal against acetaminophen treated rats. The activity of the extract at dose of 300 mg/kg was comparable to the standard drug, silymarin (50 mg/kg, p.o.). Histopathological changes of liver sample were compared with respective control. Results indicate the hepatoprotective and antioxidant properties of Phyllanthus polyphyllus against acetaminophen-induced hepatotoxicity in rats.
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PMID:Protective effect of Phyllanthus polyphyllus on acetaminophen induced hepatotoxicity in rats. 1816 21

Multipotent mesenchymal stromal cells (MSCs) can be isolated from bone marrow or peripheral blood. To identify phenotypical and functional differences between MSCs derived from these sources, the human bone marrow-derived, fibroblast-like cell line L87/4 was compared with the peripheral blood-derived, fibroblast-like cell line V54/2. Both cell lines expressed similar levels of SH3+, CD45(-), CD68(-), CD133(-), and HLA-DR(-). The bone marrow-derived cells expressed higher surface levels of CD105, CD10, and CD117 and preferentially expressed alkaline phosphatase, glutathione S-transferase P, and cofilin-1. The peripheral blood-derived line showed a higher number of CD34+/CD105+ double-positive and side population (SP) cells. The results demonstrate the more multipotent, yet quiescent, stromal phenotype of bone marrow MSCs, whereas MSCs isolated from the circulation display more hematopoietic-lineage characteristics. Importantly, potential marker genes that distinguish the two stages of MSCs are defined.
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PMID:Alkaline phosphatase, glutathione-S-transferase-P, and cofilin-1 distinguish multipotent mesenchymal stromal cell lines derived from the bone marrow versus peripheral blood. 1823 66


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