Superoxide dismutases and glutaredoxins have a distinct role in the response of Candida albicans to oxidative stress generated by the chemical compounds menadione and diamide.
Identifieur interne : 000809 ( Main/Exploration ); précédent : 000808; suivant : 000810Superoxide dismutases and glutaredoxins have a distinct role in the response of Candida albicans to oxidative stress generated by the chemical compounds menadione and diamide.
Auteurs : Guilherme Maranhão Chaves [Brésil] ; Walicyranison Plinio Da SilvaSource :
- Memorias do Instituto Oswaldo Cruz [ 1678-8060 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Candida albicans (effets des médicaments et des substances chimiques), Candida albicans (enzymologie), Candida albicans (génétique), Candidose (microbiologie), Femelle (MeSH), Glutarédoxines (génétique), Glutarédoxines (physiologie), Génotype (MeSH), Modèles animaux de maladie humaine (MeSH), Mutation (MeSH), Ménadione (pharmacologie), Phénotype (MeSH), Résistance des champignons aux médicaments (génétique), Souris (MeSH), Souris de lignée BALB C (MeSH), Stress oxydatif (effets des médicaments et des substances chimiques), Superoxide dismutase (génétique), Superoxide dismutase (physiologie), Tétraméthyl-diazènedicarboxamide (pharmacologie), Virulence (MeSH).
- MESH :
- effets des médicaments et des substances chimiques : Candida albicans, Stress oxydatif.
- enzymologie : Candida albicans.
- génétique : Candida albicans, Glutarédoxines, Résistance des champignons aux médicaments, Superoxide dismutase.
- microbiologie : Candidose.
- pharmacologie : Ménadione, Tétraméthyl-diazènedicarboxamide.
- physiologie : Glutarédoxines, Superoxide dismutase.
- Animaux, Femelle, Génotype, Modèles animaux de maladie humaine, Mutation, Phénotype, Souris, Souris de lignée BALB C, Virulence.
English descriptors
- KwdEn :
- Animals (MeSH), Candida albicans (drug effects), Candida albicans (enzymology), Candida albicans (genetics), Candidiasis (microbiology), Diamide (pharmacology), Disease Models, Animal (MeSH), Drug Resistance, Fungal (genetics), Female (MeSH), Genotype (MeSH), Glutaredoxins (genetics), Glutaredoxins (physiology), Mice (MeSH), Mice, Inbred BALB C (MeSH), Mutation (MeSH), Oxidative Stress (drug effects), Phenotype (MeSH), Superoxide Dismutase (genetics), Superoxide Dismutase (physiology), Virulence (MeSH), Vitamin K 3 (pharmacology).
- MESH :
- chemical , genetics : Glutaredoxins, Superoxide Dismutase.
- chemical , pharmacology : Diamide, Vitamin K 3.
- drug effects : Candida albicans, Oxidative Stress.
- enzymology : Candida albicans.
- genetics : Candida albicans, Drug Resistance, Fungal.
- microbiology : Candidiasis.
- chemical , physiology : Glutaredoxins, Superoxide Dismutase.
- Animals, Disease Models, Animal, Female, Genotype, Mice, Mice, Inbred BALB C, Mutation, Phenotype, Virulence.
Abstract
To cope with oxidative stress, Candida albicans possesses several enzymes involved in a number of biological processes, including superoxide dismutases (Sods) and glutaredoxins (Grxs). The resistance of C. albicans to reactive oxygen species is thought to act as a virulence factor. Genes such as SOD1 and GRX2, which encode for a Sod and Grx, respectively, in C. albicans are widely recognised to be important for pathogenesis. We generated a double mutant, Δgrx2/sod1, for both genes. This strain is very defective in hyphae formation and is susceptible to killing by neutrophils. When exposed to two compounds that generate reactive oxygen species, the double null mutant was susceptible to menadione and resistant to diamide. The reintegration of the SOD1 gene in the null mutant led to recovery in resistance to menadione, whereas reintegration of the GRX2 gene made the null mutant sensitive to diamide. Despite having two different roles in the responses to oxidative stress generated by chemical compounds, GRX2 and SOD1 are important for C. albicans pathogenesis because the double mutant Δgrx2/sod1 was very susceptible to neutrophil killing and was defective in hyphae formation in addition to having a lower virulence in an animal model of systemic infection.
DOI: 10.1590/s0074-02762012000800006
PubMed: 23295749
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Candida albicans (genetics)</term>
<term>Candidiasis (microbiology)</term>
<term>Diamide (pharmacology)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Drug Resistance, Fungal (genetics)</term>
<term>Female (MeSH)</term>
<term>Genotype (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (physiology)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Oxidative Stress (drug effects)</term>
<term>Phenotype (MeSH)</term>
<term>Superoxide Dismutase (genetics)</term>
<term>Superoxide Dismutase (physiology)</term>
<term>Virulence (MeSH)</term>
<term>Vitamin K 3 (pharmacology)</term>
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<term>Candida albicans (effets des médicaments et des substances chimiques)</term>
<term>Candida albicans (enzymologie)</term>
<term>Candida albicans (génétique)</term>
<term>Candidose (microbiologie)</term>
<term>Femelle (MeSH)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (physiologie)</term>
<term>Génotype (MeSH)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Ménadione (pharmacologie)</term>
<term>Phénotype (MeSH)</term>
<term>Résistance des champignons aux médicaments (génétique)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée BALB C (MeSH)</term>
<term>Stress oxydatif (effets des médicaments et des substances chimiques)</term>
<term>Superoxide dismutase (génétique)</term>
<term>Superoxide dismutase (physiologie)</term>
<term>Tétraméthyl-diazènedicarboxamide (pharmacologie)</term>
<term>Virulence (MeSH)</term>
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<term>Superoxide Dismutase</term>
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<term>Vitamin K 3</term>
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<term>Oxidative Stress</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Candida albicans</term>
<term>Drug Resistance, Fungal</term>
</keywords>
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<term>Glutarédoxines</term>
<term>Résistance des champignons aux médicaments</term>
<term>Superoxide dismutase</term>
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<term>Mutation</term>
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<front><div type="abstract" xml:lang="en">To cope with oxidative stress, Candida albicans possesses several enzymes involved in a number of biological processes, including superoxide dismutases (Sods) and glutaredoxins (Grxs). The resistance of C. albicans to reactive oxygen species is thought to act as a virulence factor. Genes such as SOD1 and GRX2, which encode for a Sod and Grx, respectively, in C. albicans are widely recognised to be important for pathogenesis. We generated a double mutant, Δgrx2/sod1, for both genes. This strain is very defective in hyphae formation and is susceptible to killing by neutrophils. When exposed to two compounds that generate reactive oxygen species, the double null mutant was susceptible to menadione and resistant to diamide. The reintegration of the SOD1 gene in the null mutant led to recovery in resistance to menadione, whereas reintegration of the GRX2 gene made the null mutant sensitive to diamide. Despite having two different roles in the responses to oxidative stress generated by chemical compounds, GRX2 and SOD1 are important for C. albicans pathogenesis because the double mutant Δgrx2/sod1 was very susceptible to neutrophil killing and was defective in hyphae formation in addition to having a lower virulence in an animal model of systemic infection.</div>
</front>
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<Abstract><AbstractText>To cope with oxidative stress, Candida albicans possesses several enzymes involved in a number of biological processes, including superoxide dismutases (Sods) and glutaredoxins (Grxs). The resistance of C. albicans to reactive oxygen species is thought to act as a virulence factor. Genes such as SOD1 and GRX2, which encode for a Sod and Grx, respectively, in C. albicans are widely recognised to be important for pathogenesis. We generated a double mutant, Δgrx2/sod1, for both genes. This strain is very defective in hyphae formation and is susceptible to killing by neutrophils. When exposed to two compounds that generate reactive oxygen species, the double null mutant was susceptible to menadione and resistant to diamide. The reintegration of the SOD1 gene in the null mutant led to recovery in resistance to menadione, whereas reintegration of the GRX2 gene made the null mutant sensitive to diamide. Despite having two different roles in the responses to oxidative stress generated by chemical compounds, GRX2 and SOD1 are important for C. albicans pathogenesis because the double mutant Δgrx2/sod1 was very susceptible to neutrophil killing and was defective in hyphae formation in addition to having a lower virulence in an animal model of systemic infection.</AbstractText>
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