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In vitro anti-Candida activity of selective serotonin reuptake inhibitors against fluconazole-resistant strains and their activity against biofilm-forming isolates

2017; Elsevier BV; Volume: 107; Linguagem: Inglês

10.1016/j.micpath.2017.04.008

1096-1208

Rose Anny Costa Silva, Cecília Rocha da Silva, João Batista de Andrade Neto, Anderson Ramos da Silva, Rosana Sousa Campos, Sandro Serpa, Francisca Bruna Stefany Aires do Nascimento, Brenda da Silva Gaspar, Said Gonçalves da Cruz Fonseca, Maria Aparecida Alexandre Josino, Thalles B. Grangeiro, Danielle S. Macêdo, David Freitas de Lucena, Manoel Odorico de Moraes, Bruno C. Cavalcanti, Hélio Vitoriano Nobre Júnior,

Phenothiazines and Benzothiazines Synthesis and Activities

Recent research has shown broad antifungal activity of the classic antidepressants selective serotonin reuptake inhibitors (SSRIs). This fact, combined with the increased cross-resistance frequency of the genre Candida regarding the main treatment today, fluconazole, requires the development of novel therapeutic strategies. In that context, this study aimed to assess the antifungal potential of fluoxetine, sertraline, and paroxetine against fluconazole-resistant Candida spp. planktonic cells, as well as to assess the mechanism of action and the viability of biofilms treated with fluoxetine. After 24 h, the fluconazole-resistant Candida spp. strains showed minimum inhibitory concentration (MIC) in the ranges of 20-160 μg/mL for fluoxetine, 10-20 μg/mL for sertraline, and 10-100.8 μg/mL for paroxetine by the broth microdilution method (M27-A3). According to our data by flow cytometry, each of the SSRIs cause fungal death after damaging the plasma and mitochondrial membrane, which activates apoptotic signaling pathways and leads to dose-dependant cell viability loss. Regarding biofilm-forming isolates, the fluoxetine reduce mature biofilm of all the species tested. Therefore, it is concluded that SSRIs are capable of inhibit the growth in vitro of Candida spp., both in planktonic form, as biofilm, inducing cellular death by apoptosis.