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Statements

Subject Item
n2:RIV%2F00216208%3A11160%2F14%3A10282201%21RIV15-MSM-11160___
rdf:type
skos:Concept n19:Vysledek
rdfs:seeAlso
http://aac.asm.org/content/58/10/5650.full
dcterms:description
Amphotericin B (AmB) is excreted via the renal excretion route. This excretion process may result in nephrotoxicity. However, relevant information on the precise renal excretion mechanisms is not available. The aim of the study was to analyze the possible interaction of AmB or its prodrug AmB deoxycholate (AmB-DOC) with the typical renal organic anion transporters (OATs) and organic cation transporters (OCTs), using cellular and organ models. The relevant transport systems were then investigated in terms of the drug-drug interactions of AmB-DOC with antivirals that might potentially be used concomitantly. To analyze the renal excretion mechanisms of [(3)H]AmB, perfused rat kidney was employed. HeLa and MDCK II cells transiently transfected with human OAT1 (hOAT1) or hOCT2 were used as the cellular models. A significant tubular secretion of AmB was demonstrated in the perfused rat kidney. The cellular studies performed confirmed the active transport of AmB into cells. AmB did not interact with hOAT1 but strongly inhibited hOCT2. In contrast, AmB-DOC inhibited both hOAT1 and hOCT2. However, [(3)H]AmB cellular uptake by hOAT1 and hOCT2 was not found. AmB-DOC interacted significantly with adefovir, tenofovir, and cidofovir in hOAT1-transfected cells at supratherapeutic concentrations. In conclusion, the significant potency of AmB and AmB-DOC for inhibiting the transporters was demonstrated in this study. The secretion of AmB in the renal tubules is likely not related to the transporters here, since the drug was not proven to be a substrate for them. Drug-drug interactions of AmB and the antivirals used in this study on the investigated transporters are not probable. Amphotericin B (AmB) is excreted via the renal excretion route. This excretion process may result in nephrotoxicity. However, relevant information on the precise renal excretion mechanisms is not available. The aim of the study was to analyze the possible interaction of AmB or its prodrug AmB deoxycholate (AmB-DOC) with the typical renal organic anion transporters (OATs) and organic cation transporters (OCTs), using cellular and organ models. The relevant transport systems were then investigated in terms of the drug-drug interactions of AmB-DOC with antivirals that might potentially be used concomitantly. To analyze the renal excretion mechanisms of [(3)H]AmB, perfused rat kidney was employed. HeLa and MDCK II cells transiently transfected with human OAT1 (hOAT1) or hOCT2 were used as the cellular models. A significant tubular secretion of AmB was demonstrated in the perfused rat kidney. The cellular studies performed confirmed the active transport of AmB into cells. AmB did not interact with hOAT1 but strongly inhibited hOCT2. In contrast, AmB-DOC inhibited both hOAT1 and hOCT2. However, [(3)H]AmB cellular uptake by hOAT1 and hOCT2 was not found. AmB-DOC interacted significantly with adefovir, tenofovir, and cidofovir in hOAT1-transfected cells at supratherapeutic concentrations. In conclusion, the significant potency of AmB and AmB-DOC for inhibiting the transporters was demonstrated in this study. The secretion of AmB in the renal tubules is likely not related to the transporters here, since the drug was not proven to be a substrate for them. Drug-drug interactions of AmB and the antivirals used in this study on the investigated transporters are not probable.
dcterms:title
Renal handling of amphotericin B and amphotericin B-deoxycholate and potential renal drug-drug interactions with selected antivirals Renal handling of amphotericin B and amphotericin B-deoxycholate and potential renal drug-drug interactions with selected antivirals
skos:prefLabel
Renal handling of amphotericin B and amphotericin B-deoxycholate and potential renal drug-drug interactions with selected antivirals Renal handling of amphotericin B and amphotericin B-deoxycholate and potential renal drug-drug interactions with selected antivirals
skos:notation
RIV/00216208:11160/14:10282201!RIV15-MSM-11160___
n3:aktivita
n8:S n8:P n8:I
n3:aktivity
I, P(EE2.3.30.0022), S
n3:cisloPeriodika
10
n3:dodaniDat
n18:2015
n3:domaciTvurceVysledku
n5:6128998 n5:8634351 n5:1731319 n5:3161579
n3:druhVysledku
n10:J
n3:duvernostUdaju
n20:S
n3:entitaPredkladatele
n17:predkladatel
n3:idSjednocenehoVysledku
42170
n3:idVysledku
RIV/00216208:11160/14:10282201
n3:jazykVysledku
n13:eng
n3:klicovaSlova
plasma; tenofovir; adefovir; pharmacokinetics; antifungal agents; anion transporters; lipid complex; perfused rat-kidney; nucleotide analogs cidofovir; organic cation transporters
n3:klicoveSlovo
n9:lipid%20complex n9:pharmacokinetics n9:tenofovir n9:perfused%20rat-kidney n9:nucleotide%20analogs%20cidofovir n9:adefovir n9:antifungal%20agents n9:plasma n9:organic%20cation%20transporters n9:anion%20transporters
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[A575C5DCBCEA]
n3:nazevZdroje
Antimicrobial Agents and Chemotherapy
n3:obor
n14:FR
n3:pocetDomacichTvurcuVysledku
4
n3:pocetTvurcuVysledku
4
n3:projekt
n12:EE2.3.30.0022
n3:rokUplatneniVysledku
n18:2014
n3:svazekPeriodika
58
n3:tvurceVysledku
Volková, Marie Mandíková, Jana Trejtnar, František Kočíncová, Jana
n3:wos
000344157500002
s:issn
0066-4804
s:numberOfPages
8
n4:doi
10.1128/AAC.02829-14
n15:organizacniJednotka
11160