02489nas a2200277   4500008004100000022001400041245016500055210006900220260006700289300001000356490000800366520147900374653001401853653002101867653001501888653001501903653001901918653002801937100001701965700002101982700001602003700001702019700002102036700002602057856012802083       2015                        eng d  a1364-507200aPossible mechanism of antifungal phenazine-1-carboxamide from pseudomonas sp against dimorphic fungi Benjaminiella poitrasii and human pathogen Candida albicans0 aPossible mechanism of antifungal phenazine1carboxamide from pseu  a111 RIVER ST, HOBOKEN 07030-5774, NJ USAbWILEY-BLACKWELLcJAN  a39-480 v1183 a<p>AimInvestigation of antifungal mechanism of phenazine 1-carboxamide (PC) produced by a Pseudomonas strain MCC2142. Methods and ResultsAn antifungal metabolite produced by a Pseudomonas was purified and identified as PC. Human pathogenic fungi such as Candida albicans, Candidaglabrata, Cryptococcus neoformans, Fusarium oxysporum, Aspergillus fumigatus and Aspergillus niger were found to be inhibited by PC (MIC90 32-64gml(-1)). Addition of PC (20gml(-1)) during yeast (Y)-hypha (H) transitions inhibited germ tube formation by &gt;90% and &gt;99% in C.albicans National Collection of Industrial Microorganisms (NCIM) 3471 and nonpathogenic model Benjaminiella poitrasii, respectively. After exposure to PC (20gml(-1)), 75-80% yeast cells of B.poitrasii and C.albicans NCIM 3471 showed rhodamine 123 fluorescence indicating high intracellular reactive oxygen species (ROS) production. ROS further led to hyperpolarization of mitochondrial membrane, subsequently induction of apoptosis as evident by externalization of phosphatidylserine, DNA fragmentation, chromatin condensation and finally death in B.poitrasii. In C.albicans NCIM 3471, PC (20gml(-1)) induced apoptosis. ConclusionsThe antifungal effect of PC in B.poitrasii and C.albicans may be due to ROS-mediated apoptotic death. Significance and Impact of the StudyInhibition of Y-H transition of B.poitrasii and C.albicans by PC indicates that it may prove useful in the control of dimorphic human pathogens.</p>10aApoptosis10aCandida albicans10adimorphism10aphenazines10aPseudomonas sp10areactive oxygen species1 aTupe, S., G.1 aKulkarni, R., R.1 aShirazi, F.1 aSant, D., G.1 aJoshi, Swati, P.1 aDeshpande, Mukund, V.  uhttps://library.ncl.res.in/content/possible-mechanism-antifungal-phenazine-1-carboxamide-pseudomonas-sp-against-dimorphic-001584nas a2200169   4500008004100000245007000041210006900111260000800180300001400188490000800202520101100210100001701221700002501238700002401263700002601287856010101313       2016                        eng d00aFungal cell membrane-promising drug target for antifungal therapy0 aFungal cell membranepromising drug target for antifungal therapy  cDEC  a1498-15100 v1213 aIncrease in invasive fungal infections over the past few years especially in immunocompromised patients prompted the search for new antifungal agents with improved efficacy. Current antifungal armoury includes very few effective drugs like Amphotericin B; new generation azoles, including voriconazole and posaconazole; echinocandins like caspofungin and micafungin to name a few. Azole class of antifungals which target the fungal cell membrane are the first choice of treatment for many years because of their effectiveness. As the fungal cell membrane is predominantly made up of sterols, glycerophospholipids and sphingolipids, the role of lipids in pathogenesis and target identification for improved therapeutics were largely pursued by researchers during the last few years. Present review focuses on cell membrane as an antifungal target with emphasis on membrane biogenesis, structure and function of cell membrane, cell membrane inhibitors, screening assays, recent advances and future prospects.1 aSant, D., G.1 aTupe, Santosh, Genba1 aRamana, Chepuri, V.1 aDeshpande, Mukund, V.  uhttps://library.ncl.res.in/content/fungal-cell-membrane-promising-drug-target-antifungal-therapy