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Tom Coenye - One of the best experts on this subject based on the ideXlab platform.
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stimulation of superoxide production increases fungicidal action of Miconazole against candida albicans biofilms
Scientific Reports, 2016Co-Authors: Kaat De Cremer, Tom Coenye, Bruno P A Cammue, Katrijn De Brucker, Ines Staes, Annelies Peeters, Freija Van Den Driessche, Karin ThevissenAbstract:We performed a whole-transcriptome analysis of Miconazole-treated Candida albicans biofilms, using RNA-sequencing. Our aim was to identify molecular pathways employed by biofilm cells of this pathogen to resist action of the commonly used antifungal Miconazole. As expected, genes involved in sterol biosynthesis and genes encoding drug efflux pumps were highly induced in biofilm cells upon Miconazole treatment. Other processes were affected as well, including the electron transport chain (ETC), of which eight components were transcriptionally downregulated. Within a diverse set of 17 inhibitors/inducers of the transcriptionally affected pathways, the ETC inhibitors acted most synergistically with Miconazole against C. albicans biofilm cells. Synergy was not observed for planktonically growing C. albicans cultures or when biofilms were treated in oxygen-deprived conditions, pointing to a biofilm-specific oxygen-dependent tolerance mechanism. In line, a correlation between Miconazole's fungicidal action against C. albicans biofilm cells and the levels of superoxide radicals was observed, and confirmed both genetically and pharmacologically using a triple superoxide dismutase mutant and a superoxide dismutase inhibitor N-N'-diethyldithiocarbamate, respectively. Consequently, ETC inhibitors that result in mitochondrial dysfunction and affect production of reactive oxygen species can increase Miconazole's fungicidal activity against C. albicans biofilm cells.
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genomewide screening for genes involved in biofilm formation and Miconazole susceptibility in saccharomyces cerevisiae
Fems Yeast Research, 2013Co-Authors: Davy Vandenbosch, Hans Nelis, Evelien De Canck, Inne Dhondt, Petra Rigole, Tom CoenyeAbstract:Infections related to fungal biofilms are difficult to treat due to the reduced susceptibility of sessile cells to most antifungal agents. Previous research has shown that 1-10% of sessile Candida cells survive treatment with high doses of Miconazole (a fungicidal imidazole). The aim of this study was to identify genes involved in fungal biofilm formation and to unravel the mechanisms of resistance of these biofilms to Miconazole. To this end, a screening of a Saccharomyces cerevisiae deletion mutant bank was carried out. Our results revealed that genes involved in peroxisomal transport and the biogenesis of the respiratory chain complex IV play an essential role in biofilm formation. On the other hand, genes involved in transcription and peroxisomal and mitochondrial organization seem to highly influence the susceptibility to Miconazole of yeast biofilms. Additionally, our data confirm previous findings on genes involved in biofilm formation and in general stress responses. Our data suggest the involvement of peroxisomes in biofilm formation and Miconazole resistance in fungal biofilms.
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superoxide dismutases are involved in candida albicans biofilm persistence against Miconazole
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Anna Bink, Davy Vandenbosch, Hans Nelis, Tom Coenye, Bruno P A Cammue, Karin ThevissenAbstract:We investigated the cellular mechanisms responsible for the occurrence of Miconazole-tolerant persisters in Candida albicans biofilms. Miconazole induced about 30% killing of sessile C. albicans cells at 75 μM. The fraction of Miconazole-tolerant persisters, i.e., cells that can survive high doses of Miconazole (0.6 to 2.4 mM), in these biofilms was 1 to 2%. Since Miconazole induces reactive oxygen species (ROS) in sessile C. albicans cells, we focused on a role for superoxide dismutases (Sods) in persistence and found the expression of Sod-encoding genes in sessile C. albicans cells induced by Miconazole compared to the expression levels in untreated sessile C. albicans cells. Moreover, addition of the superoxide dismutase inhibitor N,N′-diethyldithiocarbamate (DDC) to C. albicans biofilms resulted in an 18-fold reduction of the Miconazole-tolerant persister fraction and in increased endogenous ROS levels in these cells. Treatment of biofilms of C. albicans clinical isolates with DDC resulted in an 18-fold to more than 200-fold reduction of their Miconazole-tolerant persister fraction. To further confirm the important role for Sods in C. albicans biofilm persistence, we used a Δsod4 Δsod5 mutant lacking Sods 4 and 5. Biofilms of the Δsod4 Δsod5 mutant contained at least 3-fold less of the Miconazole-tolerant persisters and had increased ROS levels compared to biofilms of the isogenic wild type (WT). In conclusion, the occurrence of Miconazole-tolerant persisters in C. albicans biofilms is linked to the ROS-detoxifying activity of Sods. Moreover, Sod inhibitors can be used to potentiate the activity of Miconazole against C. albicans biofilms.
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fungicidal activity of Miconazole against candida spp biofilms
Journal of Antimicrobial Chemotherapy, 2010Co-Authors: Davy Vandenbosch, Hans Nelis, Kevin Braeckmans, Tom CoenyeAbstract:OBJECTIVES: Although azole antifungals are considered to be fungistatic, Miconazole has fungicidal activity against planktonic Candida albicans cells, presumably associated with the induction of reactive oxygen species (ROS) production. Only few data are available concerning the effect of Miconazole against sessile C. albicans cells. In the present study, the fungicidal activity of Miconazole against in vitro-grown mature Candida biofilms, and its relationship with the induction of ROS and ROS-dependent apoptosis were examined. METHODS: The effect of Miconazole on mature biofilms formed by 10 C. albicans strains and 5 strains from other Candida species was evaluated by plate counting and measuring the level of ROS induction. MIC tests were performed in the absence and presence of ascorbic acid, a quencher of ROS. The apoptotic population in C. albicans cells was determined using annexin-Cy3. RESULTS: Miconazole showed a significant fungicidal effect against all mature Candida biofilms tested and caused elevated ROS levels, both in planktonic and sessile cells. Addition of ascorbic acid drastically reduced these levels. While ROS quenching decreased the susceptibility to Miconazole of planktonic cells of most Candida strains, no reduced fungicidal activity of Miconazole against biofilms was observed. Miconazole did not cause a significant increase in apoptosis. CONCLUSIONS: ROS levels increased in all Candida biofilms upon addition of Miconazole. However, ROS induction was not the only factor that underlies its fungicidal activity, as quenching of ROS did not lead to an enhanced survival of biofilm cells. ROS-induced apoptosis was not observed in C. albicans cells after Miconazole treatment.
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fungicidal activity of Miconazole against candida spp biofilms
Journal of Antimicrobial Chemotherapy, 2010Co-Authors: Davy Vandenbosch, Hans Nelis, Kevin Braeckmans, Tom CoenyeAbstract:OBJECTIVES: Although azole antifungals are considered to be fungistatic, Miconazole has fungicidal activity against planktonic Candida albicans cells, presumably associated with the induction of reactive oxygen species (ROS) production. Only few data are available concerning the effect of Miconazole against sessile C. albicans cells. In the present study, the fungicidal activity of Miconazole against in vitro-grown mature Candida biofilms, and its relationship with the induction of ROS and ROS-dependent apoptosis were examined. METHODS: The effect of Miconazole on mature biofilms formed by 10 C. albicans strains and 5 strains from other Candida species was evaluated by plate counting and measuring the level of ROS induction. MIC tests were performed in the absence and presence of ascorbic acid, a quencher of ROS. The apoptotic population in C. albicans cells was determined using annexin-Cy3. RESULTS: Miconazole showed a significant fungicidal effect against all mature Candida biofilms tested and caused elevated ROS levels, both in planktonic and sessile cells. Addition of ascorbic acid drastically reduced these levels. While ROS quenching decreased the susceptibility to Miconazole of planktonic cells of most Candida strains, no reduced fungicidal activity of Miconazole against biofilms was observed. Miconazole did not cause a significant increase in apoptosis. CONCLUSIONS: ROS levels increased in all Candida biofilms upon addition of Miconazole. However, ROS induction was not the only factor that underlies its fungicidal activity, as quenching of ROS did not lead to an enhanced survival of biofilm cells. ROS-induced apoptosis was not observed in C. albicans cells after Miconazole treatment.
Karin Thevissen - One of the best experts on this subject based on the ideXlab platform.
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stimulation of superoxide production increases fungicidal action of Miconazole against candida albicans biofilms
Scientific Reports, 2016Co-Authors: Kaat De Cremer, Tom Coenye, Bruno P A Cammue, Katrijn De Brucker, Ines Staes, Annelies Peeters, Freija Van Den Driessche, Karin ThevissenAbstract:We performed a whole-transcriptome analysis of Miconazole-treated Candida albicans biofilms, using RNA-sequencing. Our aim was to identify molecular pathways employed by biofilm cells of this pathogen to resist action of the commonly used antifungal Miconazole. As expected, genes involved in sterol biosynthesis and genes encoding drug efflux pumps were highly induced in biofilm cells upon Miconazole treatment. Other processes were affected as well, including the electron transport chain (ETC), of which eight components were transcriptionally downregulated. Within a diverse set of 17 inhibitors/inducers of the transcriptionally affected pathways, the ETC inhibitors acted most synergistically with Miconazole against C. albicans biofilm cells. Synergy was not observed for planktonically growing C. albicans cultures or when biofilms were treated in oxygen-deprived conditions, pointing to a biofilm-specific oxygen-dependent tolerance mechanism. In line, a correlation between Miconazole's fungicidal action against C. albicans biofilm cells and the levels of superoxide radicals was observed, and confirmed both genetically and pharmacologically using a triple superoxide dismutase mutant and a superoxide dismutase inhibitor N-N'-diethyldithiocarbamate, respectively. Consequently, ETC inhibitors that result in mitochondrial dysfunction and affect production of reactive oxygen species can increase Miconazole's fungicidal activity against C. albicans biofilm cells.
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artemisinins new Miconazole potentiators resulting in increased activity against candida albicans biofilms
Antimicrobial Agents and Chemotherapy, 2015Co-Authors: Kaat De Cremer, Bruno P A Cammue, Katrijn De Brucker, Ellen Lanckacker, Tanne L Cools, Marijke Bax, Paul Cos, Karin ThevissenAbstract:Mucosal biofilm-related fungal infections are very common, and the incidence of recurrent oral and vulvovaginal candidiasis is significant. As resistance to azoles (the preferred treatment) is occurring, we aimed at identifying compounds that increase the activity of Miconazole against Candida albicans biofilms. We screened 1,600 compounds of a drug-repositioning library in combination with a subinhibitory concentration of Miconazole. Synergy between the best identified potentiators and Miconazole was characterized by checkerboard analyses and fractional inhibitory concentration indices. Hexachlorophene, pyrvinium pamoate, and artesunate act synergistically with Miconazole in affecting C. albicans biofilms. Synergy was most pronounced for artesunate and structural homologues thereof. No synergistic effect could be observed between artesunate and fluconazole, caspofungin, or amphotericin B. Our data reveal enhancement of the antibiofilm activity of Miconazole by artesunate, pointing to potential combination therapy consisting of Miconazole and artesunate to treat C. albicans biofilm-related infections.
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superoxide dismutases are involved in candida albicans biofilm persistence against Miconazole
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Anna Bink, Davy Vandenbosch, Hans Nelis, Tom Coenye, Bruno P A Cammue, Karin ThevissenAbstract:We investigated the cellular mechanisms responsible for the occurrence of Miconazole-tolerant persisters in Candida albicans biofilms. Miconazole induced about 30% killing of sessile C. albicans cells at 75 μM. The fraction of Miconazole-tolerant persisters, i.e., cells that can survive high doses of Miconazole (0.6 to 2.4 mM), in these biofilms was 1 to 2%. Since Miconazole induces reactive oxygen species (ROS) in sessile C. albicans cells, we focused on a role for superoxide dismutases (Sods) in persistence and found the expression of Sod-encoding genes in sessile C. albicans cells induced by Miconazole compared to the expression levels in untreated sessile C. albicans cells. Moreover, addition of the superoxide dismutase inhibitor N,N′-diethyldithiocarbamate (DDC) to C. albicans biofilms resulted in an 18-fold reduction of the Miconazole-tolerant persister fraction and in increased endogenous ROS levels in these cells. Treatment of biofilms of C. albicans clinical isolates with DDC resulted in an 18-fold to more than 200-fold reduction of their Miconazole-tolerant persister fraction. To further confirm the important role for Sods in C. albicans biofilm persistence, we used a Δsod4 Δsod5 mutant lacking Sods 4 and 5. Biofilms of the Δsod4 Δsod5 mutant contained at least 3-fold less of the Miconazole-tolerant persisters and had increased ROS levels compared to biofilms of the isogenic wild type (WT). In conclusion, the occurrence of Miconazole-tolerant persisters in C. albicans biofilms is linked to the ROS-detoxifying activity of Sods. Moreover, Sod inhibitors can be used to potentiate the activity of Miconazole against C. albicans biofilms.
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Miconazole induces changes in actin cytoskeleton prior to reactive oxygen species induction in yeast
Journal of Biological Chemistry, 2007Co-Authors: Karin Thevissen, Bruno P A Cammue, Kathryn R Ayscough, Marcel Borgers, An M Aerts, Katrijn De Brucker, Els M K Meert, Jannie Ausma, Isabelle E J A FrancoisAbstract:The antifungal compound Miconazole inhibits ergosterol biosynthesis and induces reactive oxygen species (ROS) in susceptible yeast species. To further uncover the mechanism of Miconazole antifungal action and tolerance mechanisms, we screened the complete set of haploid Saccharomyces cerevisiae gene deletion mutants for mutants with an altered Miconazole sensitivity phenotype. We identified 29 S. cerevisiae genes, which when deleted conferred at least 4-fold hypersensitivity to Miconazole. Major functional groups encode proteins involved in tryptophan biosynthesis, membrane trafficking including endocytosis, regulation of actin cytoskeleton, and gene expression. With respect to the antifungal activity of Miconazole, we demonstrate an antagonism with tryptophan and a synergy with a yeast endocytosis inhibitor. Because actin dynamics and induction of ROS are linked in yeast, we further focused on Miconazole-mediated changes in actin cytoskeleton organization. In this respect, we demonstrate that Miconazole induces changes in the actin cytoskeleton, indicative of increased filament stability, prior to ROS induction. These data provide novel mechanistic insights in the mode of action of a ROS-inducing azole.
Carla Martins Lopes - One of the best experts on this subject based on the ideXlab platform.
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Miconazole loaded nanostructured lipid carriers nlc for local delivery to the oral mucosa improving antifungal activity
Colloids and Surfaces B: Biointerfaces, 2013Co-Authors: Alves Mendes, Ana Catarina Silva, Jose A M Catita, Fatima Cerqueira, Carla Gabriel, Carla Martins LopesAbstract:Miconazole is a widely used antifungal agent with poor aqueous solubility, which requires the development of drug delivery systems able to improve its therapeutic activity. For this purpose, a Miconazole-loaded nanostructured lipid carriers (NLC) dispersion was prepared and characterized. Further, the dispersion was used to prepare a NLC-based hydrogel formulation proposed as an alternative system to improve the local delivery of Miconazole to the oral mucosa. NLC dispersion showed particles in the nanometer range (≈ 200 nm) with low polidispersity index ( 87%). A controlled Miconazole release was observed from NLC and NLC-based hydrogel formulations, in contrast to a commercial oral gel formulation, which demonstrated a faster release. Additionally, it was observed that the encapsulation of Miconazole in the NLC improved its antifungal activity against Candida albicans. Therefore, it was demonstrated that the encapsulation of Miconazole in NLC allows for obtaining the same therapeutic effect of a commercial oral gel formulation, using a 17-fold lower dose of Miconazole.
Davy Vandenbosch - One of the best experts on this subject based on the ideXlab platform.
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genomewide screening for genes involved in biofilm formation and Miconazole susceptibility in saccharomyces cerevisiae
Fems Yeast Research, 2013Co-Authors: Davy Vandenbosch, Hans Nelis, Evelien De Canck, Inne Dhondt, Petra Rigole, Tom CoenyeAbstract:Infections related to fungal biofilms are difficult to treat due to the reduced susceptibility of sessile cells to most antifungal agents. Previous research has shown that 1-10% of sessile Candida cells survive treatment with high doses of Miconazole (a fungicidal imidazole). The aim of this study was to identify genes involved in fungal biofilm formation and to unravel the mechanisms of resistance of these biofilms to Miconazole. To this end, a screening of a Saccharomyces cerevisiae deletion mutant bank was carried out. Our results revealed that genes involved in peroxisomal transport and the biogenesis of the respiratory chain complex IV play an essential role in biofilm formation. On the other hand, genes involved in transcription and peroxisomal and mitochondrial organization seem to highly influence the susceptibility to Miconazole of yeast biofilms. Additionally, our data confirm previous findings on genes involved in biofilm formation and in general stress responses. Our data suggest the involvement of peroxisomes in biofilm formation and Miconazole resistance in fungal biofilms.
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superoxide dismutases are involved in candida albicans biofilm persistence against Miconazole
Antimicrobial Agents and Chemotherapy, 2011Co-Authors: Anna Bink, Davy Vandenbosch, Hans Nelis, Tom Coenye, Bruno P A Cammue, Karin ThevissenAbstract:We investigated the cellular mechanisms responsible for the occurrence of Miconazole-tolerant persisters in Candida albicans biofilms. Miconazole induced about 30% killing of sessile C. albicans cells at 75 μM. The fraction of Miconazole-tolerant persisters, i.e., cells that can survive high doses of Miconazole (0.6 to 2.4 mM), in these biofilms was 1 to 2%. Since Miconazole induces reactive oxygen species (ROS) in sessile C. albicans cells, we focused on a role for superoxide dismutases (Sods) in persistence and found the expression of Sod-encoding genes in sessile C. albicans cells induced by Miconazole compared to the expression levels in untreated sessile C. albicans cells. Moreover, addition of the superoxide dismutase inhibitor N,N′-diethyldithiocarbamate (DDC) to C. albicans biofilms resulted in an 18-fold reduction of the Miconazole-tolerant persister fraction and in increased endogenous ROS levels in these cells. Treatment of biofilms of C. albicans clinical isolates with DDC resulted in an 18-fold to more than 200-fold reduction of their Miconazole-tolerant persister fraction. To further confirm the important role for Sods in C. albicans biofilm persistence, we used a Δsod4 Δsod5 mutant lacking Sods 4 and 5. Biofilms of the Δsod4 Δsod5 mutant contained at least 3-fold less of the Miconazole-tolerant persisters and had increased ROS levels compared to biofilms of the isogenic wild type (WT). In conclusion, the occurrence of Miconazole-tolerant persisters in C. albicans biofilms is linked to the ROS-detoxifying activity of Sods. Moreover, Sod inhibitors can be used to potentiate the activity of Miconazole against C. albicans biofilms.
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fungicidal activity of Miconazole against candida spp biofilms
Journal of Antimicrobial Chemotherapy, 2010Co-Authors: Davy Vandenbosch, Hans Nelis, Kevin Braeckmans, Tom CoenyeAbstract:OBJECTIVES: Although azole antifungals are considered to be fungistatic, Miconazole has fungicidal activity against planktonic Candida albicans cells, presumably associated with the induction of reactive oxygen species (ROS) production. Only few data are available concerning the effect of Miconazole against sessile C. albicans cells. In the present study, the fungicidal activity of Miconazole against in vitro-grown mature Candida biofilms, and its relationship with the induction of ROS and ROS-dependent apoptosis were examined. METHODS: The effect of Miconazole on mature biofilms formed by 10 C. albicans strains and 5 strains from other Candida species was evaluated by plate counting and measuring the level of ROS induction. MIC tests were performed in the absence and presence of ascorbic acid, a quencher of ROS. The apoptotic population in C. albicans cells was determined using annexin-Cy3. RESULTS: Miconazole showed a significant fungicidal effect against all mature Candida biofilms tested and caused elevated ROS levels, both in planktonic and sessile cells. Addition of ascorbic acid drastically reduced these levels. While ROS quenching decreased the susceptibility to Miconazole of planktonic cells of most Candida strains, no reduced fungicidal activity of Miconazole against biofilms was observed. Miconazole did not cause a significant increase in apoptosis. CONCLUSIONS: ROS levels increased in all Candida biofilms upon addition of Miconazole. However, ROS induction was not the only factor that underlies its fungicidal activity, as quenching of ROS did not lead to an enhanced survival of biofilm cells. ROS-induced apoptosis was not observed in C. albicans cells after Miconazole treatment.
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fungicidal activity of Miconazole against candida spp biofilms
Journal of Antimicrobial Chemotherapy, 2010Co-Authors: Davy Vandenbosch, Hans Nelis, Kevin Braeckmans, Tom CoenyeAbstract:OBJECTIVES: Although azole antifungals are considered to be fungistatic, Miconazole has fungicidal activity against planktonic Candida albicans cells, presumably associated with the induction of reactive oxygen species (ROS) production. Only few data are available concerning the effect of Miconazole against sessile C. albicans cells. In the present study, the fungicidal activity of Miconazole against in vitro-grown mature Candida biofilms, and its relationship with the induction of ROS and ROS-dependent apoptosis were examined. METHODS: The effect of Miconazole on mature biofilms formed by 10 C. albicans strains and 5 strains from other Candida species was evaluated by plate counting and measuring the level of ROS induction. MIC tests were performed in the absence and presence of ascorbic acid, a quencher of ROS. The apoptotic population in C. albicans cells was determined using annexin-Cy3. RESULTS: Miconazole showed a significant fungicidal effect against all mature Candida biofilms tested and caused elevated ROS levels, both in planktonic and sessile cells. Addition of ascorbic acid drastically reduced these levels. While ROS quenching decreased the susceptibility to Miconazole of planktonic cells of most Candida strains, no reduced fungicidal activity of Miconazole against biofilms was observed. Miconazole did not cause a significant increase in apoptosis. CONCLUSIONS: ROS levels increased in all Candida biofilms upon addition of Miconazole. However, ROS induction was not the only factor that underlies its fungicidal activity, as quenching of ROS did not lead to an enhanced survival of biofilm cells. ROS-induced apoptosis was not observed in C. albicans cells after Miconazole treatment.
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membrane rafts are involved in intracellular Miconazole accumulation in yeast cells
Journal of Biological Chemistry, 2009Co-Authors: Isabelle E J A Francois, Anna Bink, Jo Vandercappellen, Kathryn R Ayscough, Alexandre Toulmay, Roger Schneiter, Elke Van Gyseghem, Guy Van Den Mooter, Marcel Borgers, Davy VandenboschAbstract:Azoles inhibit ergosterol biosynthesis, resulting in ergosterol depletion and accumulation of toxic 14α-methylated sterols in membranes of susceptible yeast. We demonstrated previously that Miconazole induces actin cytoskeleton stabilization in Saccharomyces cerevisiae prior to induction of reactive oxygen species, pointing to an ancillary mode of action. Using a genome-wide agar-based screening, we demonstrate in this study that S. cerevisiae mutants affected in sphingolipid and ergosterol biosynthesis, namely ipt1, sur1, skn1, and erg3 deletion mutants, are Miconazole-resistant, suggesting an involvement of membrane rafts in its mode of action. This is supported by the antagonizing effect of membrane raft-disturbing compounds on Miconazole antifungal activity as well as on Miconazole-induced actin cytoskeleton stabilization and reactive oxygen species accumulation. These antagonizing effects point to a primary role for membrane rafts in Miconazole antifungal activity. We further show that this primary role of membrane rafts in Miconazole action consists of mediating intracellular accumulation of Miconazole in yeast cells.
Feng Chen - One of the best experts on this subject based on the ideXlab platform.
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typical azole biocides in biosolid amended soils and plants following biosolid applications
Journal of Agricultural and Food Chemistry, 2013Co-Authors: Zhifeng Chen, Guangguo Ying, Feng ChenAbstract:Biosolid application on agricultural land may contaminate soils with various household chemicals and personal care products. This study investigated the occurrence and dissipation of typical azole biocides climbazole, clotrimazole, and Miconazole in biosolid-amended soils as well as the uptake of these biocides by plants. The field trial includes two treatment groups: old groups with biosolid application at rates of 5, 10, 20, and 40 t/ha every year within 5 years, and new groups with only one biosolid application. The results showed that climbazole, clotrimazole, and Miconazole were detected in biosolid-amended soils, but not detected in control soils. These biocides were not found in the crop plants collected from the trial plots. The dissipation half-lives for climbazole, clotrimazole, and Miconazole under the field conditions were 175–179, 244, and 130–248 days, respectively. High biosolid application rates and repeated biosolid applications could lead to higher persistence of the biocides in the agri...
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occurrence and dissipation of three azole biocides climbazole clotrimazole and Miconazole in biosolid amended soils
Science of The Total Environment, 2013Co-Authors: Zhifeng Chen, Guangguo Ying, Feng ChenAbstract:This study investigated the occurrence and dissipation of three azole biocides climbazole, clotrimazole and Miconazole in biosolid-amended soils of the three sites (Zhejiang, Hunan and Shandong) in China following three treatments (CK: control without biosolid application; T1: one biosolid application; T2: biosolid application every year). The results showed that climbazole, clotrimazole and Miconazole were present in the biosolid and biosolid-amended soils, but absent in the control soils. In the soils treated with biosolids, the concentrations of climbazole, clotrimazole and Miconazole were mostly lower in the Zhejiang soils than in the Shandong or Hunan soils, suggesting that these three biocides are more readily dissipated under the flooding condition. During the one year monitoring, the concentrations of climbazole, clotrimazole and Miconazole in the biosolid-applied soils showed only slight variations. The dissipation half-lives for Miconazole calculated under the field conditions of Shandong site were 440 days for T1 and the half-lives for clotrimazole were 365 days for T2. The results suggested the persistence of these three biocides in the soil environments.