Disease relevance of nystatin

• In women with presumed candidiasis hypersensitivity syndrome, nystatin does not reduce systemic or psychological symptoms significantly more than placebo [1].
• Nystatin prophylaxis in leukemia and lymphoma [2].
• Thirty-five symptomatic infections (five of which were bacteremias) occurred in patients receiving trimethoprim-sulfamethoxazole plus nystatin, whereas 31 infections (eight bacteremias) occurred in patients receiving gentamicin plus nystatin [3].
• Results show that 10 and 20 min of anoxia partially inhibited Nys-stimulated and mitochondrial respiration, and partially decreased the K contents, but all these effects were largely reversible after 20 min of reoxygenation [4].
• We have compared the effects of the complement membrane attack complex (MAC), nystatin, and melittin on the envelope of murine leukemia viruses to determine if channel formation alone is sufficient to cause membranolysis [5].

Psychiatry related information on nystatin

• A teratogenic potential of nystatin was seen in 1 CA-group (hypospadias) in 2 different approaches of the study (case-control and total control--CA groups comparison) during the critical period of this congenital abnormality [6].
• These imidazole agents have largely replaced nystatin as primary therapy because of greater antifungal activity and shorter treatment regimens, thereby enhancing patient compliance [7].

High impact information on nystatin

• The AMBr cell line also exhibited increased resistance to other polyene macrolide antibiotics such as nystatin and pentamycin [8].
• We show that previously known and new genes are necessary for optimal growth under six well-studied conditions: high salt, sorbitol, galactose, pH 8, minimal medium and nystatin treatment [9].
• The ouabain- and bumetanide-resistant K efflux from CC cells was volume and pH dependent: K efflux from CC cells rose from 5-6 to 20-25 mmol/liter of cells X h, when cell volume was increased by increasing cell solute content (nystatin method) or by exposure to hypotonic media [10].
• Cellular respiration was measured upon addition of nystatin (Nys) to maximally stimulate Na pump activity [4].
• This sensitivity was partially corrected by rehydrating xerocytic erythrocytes by means of the cation-ionophore nystatin in a high potassium buffer [11].

Chemical compound and disease context of nystatin

• An open study designed to compare the effectiveness and safety of clotrimazole troches with nystatin oral suspension in the prevention of oropharyngeal candidiasis was conducted [12].
• The nystatin group experienced nine local yeast infections (four thrush, three esophagitis, and two vaginitis); three patients receiving ketoconazole had thrush [13].
• Treatment of oral candidiasis: a study to determine the clinical response of sodium benzoate compared with nystatin suspension [14].
• Miconazole was more effective than nystatin in treating esophageal candidiasis and could be a valid alternative to more expensive azolic drugs in developing countries [15].
• Treatment with the inhibitors nystatin, methyl-beta-cyclodextrin, and genistein, as well as transfection of cells with dominant-negative caveolin-1, had no effect on influenza virus infection [16].

Biological context of nystatin

• Cyanohydrin acetonide alkylations were used to assemble the carbon skeleton, and a simple modification of the strategy allowed an advanced intermediate to be converted to either the candidin polyol or the nystatin polyol [17].
• The action was concentration dependent, with an IC50 of 0.7 +/- 0.4 nmol/L (n = 22), and was also observed using the nystatin method [18].
• Stimulation of the (Na+,K+)-ATPase produced as a result of nystatin-mediated dissipation of plasma membrane Na+ and K+ gradients results in increased respiration with an oxygen consumption rate characteristic of optimal ATP synthesis (state 3) [19].
• PKC sequestration and pericentrion formation were blocked by hypertonic sucrose as well as by potassium depletion (inhibitors of clathrin-dependent endocytosis) but not by nystatin or filipin, which inhibit clathrin-independent pathways [20].
• Decreasing [Cl-]i (without concomitant cell shrinkage) by incubating cultures with apical nystatin and reduced apical [Cl-] ([Cl-]alpha) likewise increases both cotransport activity and cotransport protein phosphorylation [21].

Anatomical context of nystatin

• Selective permeabilization of apical or basolateral membranes with the monovalent ionophore nystatin was used to isolate basolateral K+ and apical Cl- channel activity, respectively [22].
• METHODS: Guinea pig colon epithelium with the apical membrane perforated with nystatin in Ussing chambers is used to show a basolateral Cl(-) conductance [23].
• Apical addition of nystatin virtually abolished amiloride-sensitive apical sodium uptake in both groups, indicating that the ionophore formed channels in the apical membrane of noninflamed and diseased mucosa [24].
• Further, functional studies indicated that the localization of uPAR and its ligand in caveolae enhances pericellular plasminogen activation, since treatment of the cells with drugs that interfere with the structural integrity of caveolae, such as nystatin, markedly reduced cell surface plasmin generation [25].
• Here, we show that the GPI-anchored CD59 molecule on Jurkat T cells is internalized after cross-linking, a process inhibited by nystatin, a sterol chelating agent [26].

Associations of nystatin with other chemical compounds

• Inactivation of the Ca channel of Aplysia neurons was studied in the absence of potassium current in cells that were cesium-loaded with the aid of the ionophore nystatin [27].
• Hepatocytes were loaded with tetramethylammonium by briefly exposing liver slices to nystatin, a cation poreforming antibiotic [28].
• In addition, nystatin prevents cisplatin-induced transient increase in plasma membrane fluidity that could be required for CD95 translocation [29].
• Interestingly, nystatin prevents the translocation of the aSMase to the extracellular surface of plasma membrane and the production of ceramide, suggesting that these early events require raft integrity [29].
• In cultured mouse mpkCCDcl4 collecting duct cells, increasing [Na+]i either by cell membrane permeabilization with amphotericin B or nystatin, or by incubating cells in a K(+)-free medium, also increased Na,K-ATPase cell surface expression [30].

Gene context of nystatin

• Lipid raft integrity is essential for LPS-cellular activation, since raft-disrupting drugs, such as nystatin or MCD, inhibit LPS-induced TNF-alpha secretion [31].
• The inhibitory effect of EGF on Na(+) absorption was not due to inhibition of basolateral Na(+)-K(+)-ATPase, because the pump current elicited by permeabilization of apical membrane with nystatin was not reduced by EGF [32].
• Hence, a TLR-dependent mechanism could serve as the molecular basis for the proinflammatory properties of nystatin [33].
• A ras1 strain transformed with this plasmid was subjected to ethyl methanesulfonate mutagenesis and nystatin enrichment [34].
• The ERG5 gene from Saccharomyces cerevisiae was cloned by complementation of an erg5-1 mutation using a negative selection protocol involving screening for nystatin-sensitive transformants [35].

Analytical, diagnostic and therapeutic context of nystatin

• Membrane voltage (Vm) and ion currents of pod were examined with the patch clamp technique in fast whole cell and whole cell nystatin configuration [36].
• Uphill adenosine transport was not observed when extracellular Na+ was replaced by Li+, K+, Cs+, or N-methyl-D-glucammonium ions, or after treatment of the cells with nystatin, a Na+ ionophore [37].
• Site-specific mutagenesis of Ser-170 both in the wild-type NysA and in the hybrid loading module containing malonyl-specific acyltransferase domain from the extender module had no effect on nystatin biosynthesis [38].
• The changes of volume distribution curves of erythrocytes during and after lysis by complement or nystatin or in hypotonic buffers were measured by flow cytometry [39].
• 6. Use of nystatin permitted assessment of whether microelectrode impalement introduced a significant shunt conductance into the untreated apical membrane, with the conclusion that such a shunt was negligible in the present experiments [40].

References