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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1986-9-16
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pubmed:abstractText |
The sodium pump, (Na+ + K+)-ATPase, which is involved in the transport of cations and water movement by the colonic mucosa, may be decreased in various diarrhoeal states. In this study, we have measured 3H-ouabain binding and (Na+ + K+)-ATPase activity in human colonic biopsy homogenates and the influence of various inflammatory and antiinflammatory compounds on these parameters. 3H-ouabain binds to one site of high affinity (KD 1.9 +/- 0.2 X 10(-9) mol/l) with a maximal binding capacity of 7.5 +/- 0.8 X 10(14) binding sites/g protein. Both arachidonic and linoleic acid inhibited (Na+ + K+)-ATPase activity (IC50 arachidonic acid: 7.5 X 10(-5) mol/l, linoleic acid: 6.5 X 10(-5) mol/l) and Mg2+-ATPase activity (IC50 arachidonic acid: 9 X 10(-5) mol/l, linoleic acid: 4 X 10(-5) mol/l). Arachidonic acid inhibited 3H-ouabain binding, (IC50 3.2 X 10(-5) mol/l). The following antiinflammatory compounds, at concentrations up to 1 X 10(-3) mol/l, did not influence ATPase activity directly nor reverse the arachidonic acid-induced inhibition: indomethacin (cyclooxygenase inhibitor), nordihydroguaiaretic acid (lipoxygenase inhibitor), sulphasalazine and its metabolites: 5-aminosalicylic acid, N-acetylaminosalicylic acid and sulphapyridine. These results indicate that human colonic (Na+ + K+)-ATPase is inhibited by the prostanoid precursors, arachidonic and linoleic acid. From a therapeutic point of view (effect on colonic (Na+ + K+)-ATPase and perhaps diarrhoea), the suppression of the production of these prostanoid precursors by drugs may, therefore, be beneficial in the treatment of inflammatory bowel disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Linoleic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Linoleic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Ouabain,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0028-1298
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
332
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
398-402
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:3016558-Anti-Inflammatory Agents,
pubmed-meshheading:3016558-Arachidonic Acid,
pubmed-meshheading:3016558-Arachidonic Acids,
pubmed-meshheading:3016558-Colon, Sigmoid,
pubmed-meshheading:3016558-Humans,
pubmed-meshheading:3016558-Intestinal Mucosa,
pubmed-meshheading:3016558-Linoleic Acid,
pubmed-meshheading:3016558-Linoleic Acids,
pubmed-meshheading:3016558-Ouabain,
pubmed-meshheading:3016558-Sodium-Potassium-Exchanging ATPase
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pubmed:year |
1986
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pubmed:articleTitle |
Inhibition of human colonic (Na+ + K+)-ATPase by arachidonic and linoleic acid.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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