Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11399
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dc.contributor.authorKovac, Suzanaen
dc.contributor.authorLoh, Su-Wenen
dc.contributor.authorLachal, Shamilahen
dc.contributor.authorShulkes, Arthuren
dc.contributor.authorBaldwin, Graham Sen
dc.date.accessioned2015-05-16T00:59:24Z
dc.date.available2015-05-16T00:59:24Z
dc.date.issued2011-12-08en
dc.identifier.citationBiochemical Pharmacology 2011; 83(4): 524-30en
dc.identifier.govdoc22172990en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11399en
dc.description.abstractThe peptide hormone gastrin binds two ferric ions with high affinity, and iron binding is essential for the biological activity of non-amidated gastrins in vitro and in vivo. Bi3+ ions also bind to glycine-extended gastrin17 (Ggly), but inhibit Ggly-induced cell proliferation and migration in gastrointestinal cell lines in vitro. The aims of the present study were firstly, to establish the mechanism by which Bi3+ ions inhibit the binding of Fe3+ ions to Ggly, and secondly, to test the effect of Bi3+ ions on the activity of non-amidated gastrins in vivo. The interaction between Bi3+ ions, Fe3+ ions and Ggly was investigated by ultraviolet spectroscopy. The effect of Bi3+ ions on colorectal mucosal proliferation was measured in three animal models. In vitro in the presence of Bi3+ ions the affinity of Fe3+ ions for Ggly was substantially reduced; the data was better fitted by a mixed, rather than a competitive, inhibition model. In rats treated with Ggly alone proliferation in the rectal mucosa was increased by 318%, but was reduced to control values (p < 0.001) in animals receiving oral bismuth plus Ggly. Proliferation in the colonic mucosa of mice overexpressing Ggly or progastrin was significantly greater than in wild-type mice, but was no greater than control (p < 0.01) in animals receiving oral bismuth. Thus a reduction in the binding of Fe3+ ions to Ggly and progastrin in the presence of Bi3+ ions is a likely explanation for the ability of oral bismuth to block the biological activity of non-amidated gastrins in vivo.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherColon.metabolismen
dc.subject.otherFemaleen
dc.subject.otherGastrins.antagonists & inhibitors.genetics.metabolismen
dc.subject.otherIron.metabolismen
dc.subject.otherKi-67 Antigen.metabolismen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Transgenicen
dc.subject.otherOrganometallic Compounds.pharmacologyen
dc.subject.otherProtein Bindingen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.titleBismuth ions inhibit the biological activity of non-amidated gastrins in vivo.en
dc.typeJournal Articleen
dc.identifier.journaltitleBiochemical pharmacologyen
dc.identifier.affiliationThe University of Melbourne Department of Surgery, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1016/j.bcp.2011.11.030en
dc.description.pages524-30en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/22172990en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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