| pubmed-article:10383383 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0006837 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0001480 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0062743 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C1522538 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:10383383 | lifeskim:mentions | umls-concept:C0442040 | lld:lifeskim |
| pubmed-article:10383383 | pubmed:issue | 27 | lld:pubmed |
| pubmed-article:10383383 | pubmed:dateCreated | 1999-7-27 | lld:pubmed |
| pubmed-article:10383383 | pubmed:abstractText | Salivary histatins are potent in vitro antifungal proteins and have promise as therapeutic agents against oral candidiasis. We performed pharmacological studies directed at understanding the biochemical basis of Hst 5 candidacidal activity. Three inhibitors of mitochondrial metabolism: carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5 killing of Candida albicans, while not inhibiting cellular ATP production. In contrast, Hst 5 caused a drastic reduction of C. albicans intracellular ATP content, which was a result of an efflux of ATP. Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5-induced ATP efflux, thus establishing a correlation between ATP release and cell killing. Furthermore, C. albicans cells were respiring and had polarized membranes at least 80 min after ATP release, thus implying a non-lytic exit of cellular ATP in response to Hst 5. Based on evidence that transmembrane ATP efflux can occur in the absence of cytolysis through a channel-like pathway and that released ATP can act as a cytotoxic mediator by binding to membrane purinergic receptors, we evaluated whether extracellular ATP released by Hst 5 may have further functional role in cell killing. Consistent with this hypothesis, purinergic agonists BzATP and adenosine 5'O-(thiotriphosphate) induced loss of C. albicans cell viability and purinergic antagonists prevented Hst 5 killing. | lld:pubmed |
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| pubmed-article:10383383 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10383383 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10383383 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10383383 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10383383 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:10383383 | pubmed:author | pubmed-author:LloydT LTL | lld:pubmed |
| pubmed-article:10383383 | pubmed:author | pubmed-author:EdgertonMM | lld:pubmed |
| pubmed-article:10383383 | pubmed:author | pubmed-author:KoshlukovaS... | lld:pubmed |
| pubmed-article:10383383 | pubmed:author | pubmed-author:AraujoM WMW | lld:pubmed |
| pubmed-article:10383383 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10383383 | pubmed:day | 2 | lld:pubmed |
| pubmed-article:10383383 | pubmed:volume | 274 | lld:pubmed |
| pubmed-article:10383383 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10383383 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10383383 | pubmed:pagination | 18872-9 | lld:pubmed |
| pubmed-article:10383383 | pubmed:dateRevised | 2011-3-22 | lld:pubmed |
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| pubmed-article:10383383 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10383383 | pubmed:articleTitle | Salivary histatin 5 induces non-lytic release of ATP from Candida albicans leading to cell death. | lld:pubmed |
| pubmed-article:10383383 | pubmed:affiliation | Department of Oral Biology, School of Dental Medicine, State University of New York at Buffalo, Buffalo, New York 14214, USA. | lld:pubmed |
| pubmed-article:10383383 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10383383 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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