Does microwave and hydrogen peroxide disinfection reduce Candida albicans biofilm on polymethyl methacrylate denture surfaces?

Author(s):  
Ilse Verónica Martínez-Serna ◽  
Marine Ortiz Magdaleno ◽  
Juan Antonio Cepeda-Bravo ◽  
Gabriel Fernando Romo-Ramírez ◽  
Luis Octavio Sánchez-Vargas
2008 ◽  
Vol 7 (11) ◽  
pp. 2008-2011 ◽  
Author(s):  
Olviyani Nasution ◽  
Kavitha Srinivasa ◽  
Minsun Kim ◽  
Yeo-Jung Kim ◽  
Wankee Kim ◽  
...  

ABSTRACT In this study, we demonstrate that hyphal differentiation is induced by the subtoxic concentration of exogenous H2O2 in Candida albicans. This finding is confirmed by the changing intracellular concentration of H2O2. In order to induce the same level of differentiation, low concentrations of exogenous H2O2 are required for the null mutants of the thiol-specific antioxidant and catalase, while higher concentrations are needed for cells treated with ascorbic acid, an antioxidant chemical.


2019 ◽  
Vol 58 (3) ◽  
pp. 341-350
Author(s):  
Bruna Gonçalves ◽  
Nuno Miguel Azevedo ◽  
Mariana Henriques ◽  
Sónia Silva

Abstract Vulvovaginal candidiasis (VVC) is an infection usually caused by Candida albicans and increasingly by Candida glabrata, which has an intrinsically high resistance to commonly used antifungals. Candida species possess virulence factors that contribute to VVC development, as the ability to form biofilms in vaginal walls and intrauterine devices. It is known that VVC is promoted by conditions that increase the hormones levels, during pregnancy, however, the effects of hormones on Candida cells are poorly studied, especially in C. glabrata. Thus, the influence of progesterone and β-estradiol, at normal cycle and pregnancy concentrations, on biofilm formation and resistance of C. albicans and C. glabrata vaginal isolates, was analyzed using acidic conditions (pH 4). Biofilms of C. albicans developed in the presence of hormones presented reduced biomass (up to 65%) and impaired cells ability to produce filamentous forms. On the other hand, C. glabrata presented high adaptation to the presence of hormones, which did not affect its biofilm formation. Additionally, hormones impaired the susceptibility of C. albicans and C. glabrata cells to azoles, with potential clinical significance in the presence of pregnancy hormone levels. A similar result was obtained for the susceptibility to hydrogen peroxide, a biological vaginal barrier against Candida growth. Overall, the results of this study suggest that hormones may act as environmental cues promoting Candida protection from vaginal defenses and harmful conditions, what may have implications in Candida vaginal pathogenicity and treatment of VVC, especially in C. glabrata infections due to its high adaptability to vaginal conditions.


2011 ◽  
Vol 2 (3) ◽  
pp. 237-242
Author(s):  
Achut R Devarhubli ◽  
VK Subbarao ◽  
NP Patil

ABSTRACT Over the years researchers have reported on the frequency and distribution of yeast in the oropharynx of apparently normal individuals and those with systemic or mycotic diseases wearing dentures. Few workers have taken into consideration the role played by the legion of denture base materials on the occurrence and progression of denture stomatitis. Hence this study was undertaken with the objective of evaluating the in vitro adherence of Candida albicans to different denture base materials namely reinforced polymethyl methacrylate, Nonreinforced polymethyl methacrylate and Cobalt chrome alloy of which chrome cobalt alloy showed less adherence to candidal cells compared to the two polymethyl methacrylate resins.


2005 ◽  
Vol 4 (12) ◽  
pp. 2160-2169 ◽  
Author(s):  
K. Sohn ◽  
M. Roehm ◽  
C. Urban ◽  
N. Saunders ◽  
D. Rothenstein ◽  
...  

ABSTRACT We applied two-dimensional gel electrophoresis to identify downstream effectors of CPH1 and EFG1 under hypha-inducing conditions in Candida albicans. Among the proteins that were expressed in wild-type cells but were strongly downregulated in a cph1Δ/efg1Δ double mutant in α-minimal essential medium at 37°C, we could identify not-yet-characterized proteins, including Cor33-1p and Cor33-2p. The two proteins are almost identical (97% identity) and represent products of allelic isoforms of the same gene. Cor33p is highly similar to Cip1p from Candida sp. but lacks any significant homology to proteins from Saccharomyces cerevisiae. Strikingly, both proteins share homology with phenylcoumaran benzylic ether reductases and isoflavone reductases from plants. For other hypha-inducing media, like yeast-peptone-dextrose (YPD) plus serum at 37°C, we could not detect any transcription for COR33 in wild-type cells, indicating that Cor33p is not hypha specific. In contrast, we found a strong induction for COR33 when cells were treated with 5 mM hydrogen peroxide. However, under oxidative conditions, transcription of COR33 was not dependent on EFG1, indicating that other regulatory factors are involved. In fact, upregulation depends on CAP1 at least, as transcript levels were clearly reduced in a Δcap1 mutant strain under oxidative conditions. Unlike in wild-type cells, transcription of COR33 in a tsa1Δ mutant can be induced by treatment with 0.1 mM hydrogen peroxide. This suggests a functional link between COR33 and thiol-specific antioxidant-like proteins that are important in the oxidative-stress response in yeasts. Concordantly, cor33Δ deletion mutants show retarded growth on YPD plates supplemented with hydrogen peroxide, indicating that COR33 in general is implicated in conferring tolerance toward oxidative stress on Candida albicans.


2010 ◽  
Vol 9 (4) ◽  
pp. 569-577 ◽  
Author(s):  
Aurélie Deveau ◽  
Amy E. Piispanen ◽  
Angelyca A. Jackson ◽  
Deborah A. Hogan

ABSTRACT Farnesol, a Candida albicans cell-cell signaling molecule that participates in the control of morphology, has an additional role in protection of the fungus against oxidative stress. In this report, we show that although farnesol induces the accumulation of intracellular reactive oxygen species (ROS), ROS generation is not necessary for the induction of catalase (Cat1)-mediated oxidative-stress resistance. Two antioxidants, α-tocopherol and, to a lesser extent, ascorbic acid effectively reduced intracellular ROS generation by farnesol but did not alter farnesol-induced oxidative-stress resistance. Farnesol inhibits the Ras1-adenylate cyclase (Cyr1) signaling pathway to achieve its effects on morphology under hypha-inducing conditions, and we demonstrate that farnesol induces oxidative-stress resistance by a similar mechanism. Strains lacking either Ras1 or Cyr1 no longer exhibited increased protection against hydrogen peroxide upon preincubation with farnesol. While we also observed the previously reported increase in the phosphorylation level of Hog1, a known regulator of oxidative-stress resistance, in the presence of farnesol, the hog1/hog1 mutant did not differ from wild-type strains in terms of farnesol-induced oxidative-stress resistance. Analysis of Hog1 levels and its phosphorylation states in different mutant backgrounds indicated that mutation of the components of the Ras1-adenylate cyclase pathway was sufficient to cause an increase of Hog1 phosphorylation even in the absence of farnesol or other exogenous sources of oxidative stress. This finding indicates the presence of unknown links between these signaling pathways. Our results suggest that farnesol effects on the Ras-adenylate cyclase cascade are responsible for many of the observed activities of this fungal signaling molecule.


2005 ◽  
Vol 4 (10) ◽  
pp. 1654-1661 ◽  
Author(s):  
Caroline Westwater ◽  
Edward Balish ◽  
David A. Schofield

ABSTRACT Candida albicans, the most frequent fungal pathogen of humans, encounters high levels of oxidants following ingestion by professional phagocytes and through contact with hydrogen peroxide-producing bacteria. In this study, we provide evidence that C. albicans is able to coordinately regulate the oxidative stress response at the global cell population level by releasing protective molecules into the surrounding medium. We demonstrate that conditioned medium, which is defined as a filter-sterilized supernatant from a C. albicans stationary-phase culture, is able to protect yeast cells from both hydrogen peroxide and superoxide anion-generating agents. Exponential-phase yeast cells preexposed to conditioned medium were able to survive levels of oxidative stress that would normally kill actively growing yeast cells. Heat treatment, digestion with proteinase K, pH adjustment, or the addition of the oxidant scavenger alpha-tocopherol did not alter the ability of conditioned medium to induce a protective response. Farnesol, a heat-stable quorum-sensing molecule (QSM) that is insensitive to proteolytic enzymes and is unaffected by pH extremes, is partly responsible for this protective response. In contrast, the QSM tyrosol did not alter the sensitivity of C. albicans cells to oxidants. Relative reverse transcription-PCR analysis indicates that Candida-conditioned growth medium induces the expression of CAT1, SOD1, SOD2, and SOD4, suggesting that protection may be mediated through the transcriptional regulation of antioxidant-encoding genes. Together, these data suggest a link between the quorum-sensing molecule farnesol and the oxidative stress response in C. albicans.


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