Antifungal mechanism of [RuIII(NH3)4catechol]+ complex on fluconazole-resistant Candida tropicalis

dc.creatorGomes Junior, Rafael Araújo
dc.creatorSilva, Roberto Santana da
dc.creatorLima, Renata Galvão de
dc.creatorSantos, Marcos André Vannier dos
dc.date2017-11-17T16:34:32Z
dc.date2017-11-17T16:34:32Z
dc.date2017
dc.date.accessioned2023-09-26T23:12:42Z
dc.date.available2023-09-26T23:12:42Z
dc.identifierGOMES JUNIOR, R. A. et al. Antifungal mechanism of [RuIII(NH3)4catechol]+ complex on fluconazole-resistant Candida tropicalis. FEMS Microbiology Letters, v. 364, n. 9, 2017
dc.identifier0378-1097
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/23262
dc.identifier10.1093/femsle/fnx073
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8888065
dc.descriptionCandidiasis, a major opportunistic mycosis caused by Candida sp., may comprise life-threatening systemic infections. The incidence of non-albicans species is rising, particularly in South America and they are frequently drug resistant, causing unresponsive cases. Thus, novel antimycotic agents are required. Here we tested the antifungal activity of [RuIII(NH3)4catechol]+ complex (RuCat), approaching possible action mechanisms on fluconazole-resistant Candida tropicalis. RuCat significantly (P < 0.05) inhibited the growth and viability of C. tropicalis dose-dependently (IC50 20.3 μM). Cytotoxicity of RuCat upon murine splenocytes was lower (Selectivity Index = 16). Scanning electron microscopy analysis showed pseudohyphae formation, yeast aggregation and surface damage. RuCat-treated samples investigated by transmission electron microscopy showed melanin granule trafficking to cell surfaces and extracellular milieu. Surface-adherent membrane fragments and extracellular debris were also observed. RuCat treatment produced intense H2DCFDA labeling, indicating reactive oxygen species (ROS) production which caused increased lipoperoxidation. ROS are involved in the fungicidal effect as N-acetyl-L-cysteine completely restored cell viability. Calcofluor White chitin staining suggests that 70 or 140 μM RuCat treatment for 2 h affected cell-wall structure. PI labeling indicated necrotic cell death. The present data indicate that RuCat triggers ROS production, lipoperoxidation and cell surface damage, culminating in selective necrotic death of drug-resistant C. tropicalis.
dc.formatapplication/pdf
dc.languageeng
dc.publisherOxford University Press
dc.rightsopen access
dc.subjectCandida tropicalis
dc.subjectResistente ao fluconazol
dc.subjectComplexo de rutênio
dc.subjectcatecol, agentes antifúngicos, candidíase
dc.subjectCandida tropicalis
dc.subjectfluconazole-resistant
dc.subjectRuthenium complex
dc.subjectcatechol, antifungal agents, candidiasis
dc.titleAntifungal mechanism of [RuIII(NH3)4catechol]+ complex on fluconazole-resistant Candida tropicalis
dc.typeArticle


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