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)

Natural killer (NK) cytotoxicity was assayed with P3-X63-Ag8-U1 (P3U-1) target cells which had been previously demonstrated to release endogenous alkaline phosphatase (AlP) on the attack of lymphocyte-activated killer cells). P3U-1 cells showed a definite sensitivity to the AlP-release test, but no response in the Cr-release test at all. The AlP-release was not inhibited by anti-perforin antibody, benzoate, phenyl-methyl-sulfonyl-fluoride, soybean trypsin inhibitor, Succinyl-Gly-Pro-Leu-Gly-Pro-amino-methyl-coumarin, or gamma-radiation to effector cells, but was inhibited by o-phenanthroline, anti-CD13 antibody, and anti-LFA-1 alpha antibody. The AlP-release from P3U-1, therefore, did not appear to be brought on by the NK cell-derived perforin, hydroxy-radical, granzymes or cytosolic proteases. The inhibition by o-phenanthroline and the antibody for CD13 (aminopeptidase N) or the adhesion factor in NK cells, however, indicated that the membrane of such cells with adhesion ligand to NK cells was probably susceptible to NK cell surface-associated metaloprotease in an adhesion dependent manner to the extent of some injury without complete perforation through the membrane.
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PMID:[An adhesion dependent injury of target cell membrane by NK cell surface associated metaloprotease]. 856 38

Several peroxisome proliferators have been shown to produce pancreatic acinar cell hyperplasia/adenocarcinomas in 2-year bioassays with rats: ammonium perfluorooctanoate (C8), clofibrate, methylclofenapate, HCFC-123, and Wyeth-14,643 (WY). We have used in vitro (C8, WY) and in vivo (WY) approaches to examine several possible mechanisms of pancreatic tumorigenesis by peroxisome proliferating compounds. These mechanisms include cholecystokinin receptor agonism (CCK(A)), trypsin inhibition, alterations in gut fat content, cholestasis, and altered bile flow/composition. All of these mechanisms enhance pancreatic growth either by binding to the CCK(A) receptor or by increasing plasma CCK levels. In vitro experiments using a receptor competition binding assay demonstrated that WY and C8 do not bind directly to the CCK(A) receptor. In a continuous spectrophotometric assay, WY and C8 also failed to inhibit trypsin, a common mechanism for increasing plasma CCK levels. These in vitro results suggested that WY was not acting via the two most common mechanisms for modulation of pancreas growth. Two types of in vivo experiments were conducted. The subchronic study (2-month duration) was designed primarily to detect early changes in pancreatic growth such as those mediated by compounds that inhibit trypsin or act as CCK(A) receptor agonists. The chronic study (6 months) was designed primarily to evaluate whether the pancreatic lesions were secondary to hepatic changes such as cholestasis and/or altered bile flow/composition. In the in vivo experiments, male Crl:CDBR rats were fed diets containing 0 or 100 ppm WY. In the subchronic study WY-treated rats had a twofold increase in mean relative liver weights, an eightfold increase in hepatic peroxisomal proliferation, and a fourfold increase in hepatocyte cell proliferation after 1 week which remained elevated throughout the 2 months of treatment. In contrast, no pancreatic weight effects, increases in plasma CCK, or acinar cell proliferation was seen through 2 months in the WY group when compared to the control group. Fecal fat concentrations were also measured at 2 months and demonstrated no difference between control and WY-treated animals. The absence of any early pancreas changes in the subchronic study is consistent with the in vitro data which demonstrated that WY is not a CCK(A) agonist or a trypsin inhibitor. The chronic study demonstrated increases in pancreatic weights at 3 months (6% above control) and 6 months (17% above control), as well as increased CCK plasma levels in the WY-treated group. Liver effects in the chronic study paralleled those of the subchronic time points. Clinical pathology endpoints including increased serum concentrations of bile acids, alkaline phosphatase, and bilirubin were indicative of cholestasis in the chronic WY-treated group. The cholestasis may be responsible for the downward trend in total bile acid output, both of which may contribute to the modest increases in plasma CCK levels. These results indicate that chronic exposure to WY causes liver alterations such as cholestasis, which may increase plasma concentrations of CCK. Hence, WY may induce pancreatic acinar cell adenomas/adenocarcinomas via a mild but sustained increase in CCK levels secondary to hepatic cholestasis.
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PMID:Mechanisms for the pancreatic oncogenic effects of the peroxisome proliferator Wyeth-14,643. 926 17

Sacchromyces cerevisiae protein disulfide isomerase (yPDI) was expressed in the E. coli periplasm by using plasmids encoding the OmpA-yPDI-(His)(6) fusion gene under the control of the araBAD, trc, or T7 promoter. The expression levels of yeast PDI under these promoters were compared. Our results showed that yeast PDI expressed into the periplasm could catalyze the formation of disulfide bonds in alkaline phosphatase, restoring the phoA(+) phenotype in dsbA(-) mutants. The yeast PDI was purified from the Escherichia coli periplasm and shown to exhibit catalytic properties comparable to those of the rat enzyme with reduced RNase as substrate. In vivo, coexpression of the yeast PDI increased the yield of bovine pancreatic trypsin inhibitor (BPTI) in E. coli by 2-fold, similar to the effect seen previously with the coexpression of the rat enzyme. However yeast PDI was more effective than rat PDI in facilitating the expression of active tissue plasminogen activator (tPA). These results point to differences in the substrate specificity of various PDI enzymes, at least in the context of the E. coli periplasm.
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PMID:Facilitating the formation of disulfide bonds in the Escherichia coli periplasm via coexpression of yeast protein disulfide isomerase. 1058 86

Rotavirus (RV) is considered to be one of the major causes of acute episodic diarrhoea throughout the world. This study was undertaken to investigate the effect of soybean trypsin inhibitor (TI) on brush-border enzymes during rotavirus infection in protein energy malnourished (PEM) infant mice. Animals were divided into 4 groups, namely controls, PEM, PEM+RV and PEM+RV+TI (n = 36 each). Group 1 and 2 animals were orally inoculated with 50 microl of normal saline each. Group 3 animals were orally inoculated with 50 microl of 100 ID50 dose of RV stock each. Group 4 animals were similarly inoculated with 0.6 mg TI/g body weight along with 50 microl of RV stock each. Animals were examined daily for diarrhoea and their body weight was recorded on alternate days postinoculation (dpi). Animals were killed by cervical dislocation after being given light chloroform anesthesia on 0, 1, 3, 5, 7 and 10 dpi. Small intestines were excised and homogenized in normal saline. Proteins, gammaglutamyl transpeptidase, alkaline phosphatase and disaccharidases were estimated in jejunum and ileum. Body weight was significantly reduced in PEM animals and with RV infection. Histologically, focal areas of vacuolar degeneration of lining epithelium were seen in RV-infected animals. Disaccharidases and other enzyme activities were decreased significantly in the PEM group compared to healthy controls and further depressed with RV infection in malnourished animals as compared to non-infected PEM. The enzyme activities were restored in animals receiving TI along with RV compared to the group receiving RV without TI. With the administration of soybean TI, the activities of disaccharidases, alkaline phosphatase, gammaglutamyl transpeptidase and intestinal architecture were restored showing a protective effect in PEM during RV infection.
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PMID:Influence of soybean trypsin inhibitor on small bowel enzyme activities during rotavirus infection in malnourished infant mice. 1114 24

The objective of this study was to assess any similarities between ovine intervertebral disc (IVD) serine proteinase inhibitory proteins (SPIs) and known mammalian IVD SPIs. Ovine IVDs were dissected into the annulus fibrosus and nucleus pulposus and the tissue finely diced then extracted with 4 M guanidine hydrochloride. The tissue extracts were subjected to caesium chloride density gradient ultracentrifugation to separate the large high buoyant density (rho > 1.5 g/mL) proteoglycans from the SPI proteins of low buoyant density (rho < 1.33 g/mL). The top two ultracentrifuge fractions containing the SPIs of interest were subjected to enzyme linked immunosorbent analysis (ELISA) and also examined by Western and Affinity blotting using an antibody to bovine pancreatic trypsin inhibitor and biotinylated trypsin respectively for detection and an alkaline phosphatase 5-bromo-4-chloro-3-indolyl phosphate/nitro blue tetrazolium system for visualisation. The major SPI proteins present in the Western and Affinity blots were 34-36 kDa species, minor 12 and 16, and 85 and 120 kDa species were also present. Qualitatively similar results were obtained for each respective tissue zone of the lumbar and lumbosacral disc specimens examined. Densitometric analysis of the major 34-36 kDa SPI bands visualised on Western and Affinity blots using NIH 1.61.1 image analysis software indicated that lumbar IVD samples contained higher levels of this SPI species than lumbosacral IVD samples. ELISA confirmed that lumbar IVD extracts contained quantitatively higher levels of BPTI equivalents per g of tissue extracted than lumbosacral IVDs. This study therefore has demonstrated that the ovine disc contains a range of SPI species which share some homology with bovine pancreatic trypsin inhibitor and in this respect are similar to SPIs previously demonstrated in canine IVDs.
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PMID:Affinity and Western blotting reveal homologies between ovine intervertebral disc serine proteinase inhibitory proteins and bovine pancreatic trypsin inhibitor. 1174 12

To investigate the role of soyabean trypsin inhibitor (TI) during rotavirus (RV) diarrhoea, changes in enzyme activities of six relevant mucosal enzymes (lactase, sucrase, maltase, trehalase, glucoamylase and alkaline phosphatase) were assayed following inoculation of suckling mice with EB rotavirus (serotype 3) along with the TI and compared with the age-matched healthy control mice. The animals were divided into three groups i.e. group 1 (controls), group 2 (RV inoculated) and group 3 (RV + TI inoculated and sacrificed under light anaesthesia on 0, 1, 3, 5, 7 and 10 day post inoculation (dpi). Then intestines were excised and divided into two parts (jejunum and ileum). They were separately homogenized in 0.9% cold normal saline and activities of mucosal enzyme were measured. Alkaline phosphatase and disaccharidases were found to be decreased significantly in RV inoculated animals in both the anatomical portions of small intestine of mice. These enzyme levels were restored with the administration of TI i.e. in group 3 and became comparable to the controls in both intestinal portions. These studies suggest that activity of intestinal enzymes which are important in digestive absorptive functions of small intestine were restored with the addition of TI whengiven to infant mice showing its protective efficacy during rotavirus infection.
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PMID:Protection against rotavirus diarrhoea in mice by trypsin inhibitor. 1256 17

Reactive polymers have been prepared by copolymeriz-ing N-isopropyl acrylamide (NIPAM) with N-acryloxy-succinimide (NASI) or glycidyl methacrylate (GMA). The amino groups of ligands could react with the residues of NASI or GMA and the polymers could be precipitated by temperature and/or salinity variation, since they contained the NIPAM residues. As a model, p-aminobenza-midine, a trypsin inhibitor, was attached to the polymers to form water-soluble macroligands, capable of selectively binding trypsin from a trypsin-chymotrypsin solution. After precipitation of the macroligand-trypsin complex, followed by dissociation, approximately 82% trypsin was isolated. The NIPAM-GMA copolymer was also reacted with immunogammaglobulin (IgG) and alkaline phosphatase (AP). It was demonstrated that the IgG bearing polymer was able to bind protein A and the whole complex was precipitable. The reactive polymer was also used for direct immobilization of AP which was active in repeated reactions.
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PMID:Syntheses and applications of water-soluble reactive polymers for purification and immobilization of biomolecules. 1858 16


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