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Geunhwa Jung - One of the best experts on this subject based on the ideXlab platform.
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overexpression of shcyp51b and shatrd in sclerotinia homoeocarpa isolates exhibiting practical field resistance to a demethylation inhibitor fungicide
Applied and Environmental Microbiology, 2012Co-Authors: Jon Hulvey, James T Popko, Hyunkyu Sang, Andrew Berg, Geunhwa JungAbstract:We investigated genetic factors that govern the reduced Propiconazole sensitivity of Sclerotinia homoeocarpa field isolates collected during a 2-year field efficacy study on dollar spot disease of turf in five New England sites. These isolates displayed a >50-fold range of in vitro sensitivity to a sterol demethylation inhibitor (DMI) fungicide, Propiconazole, making them ideal for investigations of genetic mechanisms of reduced DMI sensitivity. The CYP51 gene homolog in S. homoeocarpa (ShCYP51B), encoding the enzyme target of DMIs, is likely a minor genetic factor for reduced Propiconazole sensitivity, since there were no differences in constitutive relative expression (RE) values and only 2-fold-higher induced RE values for insensitive than for sensitive isolate groups. Next, we mined RNA-Seq transcriptome data for additional genetic factors and found evidence for the overexpression of a homolog of Botrytis cinerea atrD (BcatrD), ShatrD, a known efflux transporter of DMI fungicides. The ShatrD gene showed much higher constitutive and induced RE values for insensitive isolates. Several polymorphisms were found upstream of ShatrD but were not definitively linked to overexpression. The screening of constitutive RE values of ShCYP51B and ShatrD in isolates from two golf courses that exhibited practical field resistance to Propiconazole uncovered evidence for significant population-specific overexpression of both genes. However, linear regression demonstrated that the RE of ShatrD displays a more significant relationship with Propiconazole sensitivity than that of ShCYP51B. In summary, our results suggest that efflux is a major determinant of the reduced DMI sensitivity of S. homoeocarpa genotypes in New England, which may have implications for the emergence of practical field resistance in this important turfgrass pathogen.
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the association between in vitro Propiconazole sensitivity and field efficacy of five new england sclerotinia homoeocarpa populations
Plant Disease, 2012Co-Authors: James T Popko, Katie Campbellnelson, Geunhwa JungAbstract:Dollar spot (Sclerotinia homoeocarpa) is a major turfgrass disease requiring fungicide application to maintain acceptable conditions for golf. A 2-year field experiment was conducted to determine the association between field efficacy of Propiconazole and in vitro fungicide sensitivity of isolates from five S. homoeocarpa populations. Four golf courses with prior Propiconazole exposure (Hartford Golf Club, Hickory Ridge Country Club, Shuttle Meadow Country Club, and Wintonbury Hills Golf Club), and a baseline site with no prior Propiconazole exposure (Joseph Troll Turf Research Facility) were chosen as field sites. Experimental plots at each site received the following treatments at 21-day intervals: untreated, Propiconazole (0.44, 0.88, 1.32, and 1.76 kg a.i. ha-1), and chlorothalonil (8.18 kg a.i. ha-1). S. homoeocarpa isolates were sampled at three time points during 2009 and 2010: initial (directly before fungicide treatment), 7 days after treatment (DAT), and 21 days after the last treatment. Isolates sampled from dollar spot infection centers at 7 DAT (2009 and 2010) were considered to exhibit "practical field resistance". In parallel, S. homoeocarpa isolates from each site were assayed for in vitro sensitivity to Propiconazole by determining relative mycelium growth percentages (RMG%) on potato dextrose agar amended with Propiconazole at a discriminatory concentration of 0.1 μg a.i. ml-1. S. homoeocarpa isolates from the four exposed populations displayed significantly higher RMG% values than the baseline population. In general, field efficacy at all Propiconazole rates tested was lower at the four locations with prior Propiconazole exposure when compared with the baseline population. Increased RMG% values on the Propiconazole discriminatory concentration 0.1 μg a.i. ml-1 were associated with decreased relative control values for all Propiconazole rates in 2009 and 2010. Results suggest RMG values above 50% at the Propiconazole discriminatory concentration of 0.1 μg a.i. ml-1 may be a suitable threshold for detection of S. homoeocarpa isolates that cause practical DMI field resistance.
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geographic distribution of fungicide insensitive sclerotinia homoeocarpa isolates from golf courses in the northeastern united states
Plant Disease, 2010Co-Authors: Alexander I Putman, Geunhwa Jung, John E KaminskiAbstract:Chemical management of dollar spot in turf may lead to the development of Sclerotinia homoeocarpa populations with reduced fungicide sensitivity. The objective of this study was to determine the scope of S. homoeocarpa insensitivity to fungicides commonly used to control dollar spot on golf courses in the northeastern United States. A total of 965 and 387 isolates of S. homoeocarpa from intensively or individually sampled sites, respectively, were evaluated for in vitro sensitivity to iprodione, Propiconazole, and thiophanate-methyl. Mean baseline sensitivities to iprodione and Propiconazole were 0.2763 and 0.0016 μg a.i. ml-1, respectively, and all baseline isolates were sensitive to thiophanate-methyl at 1,000 μg a.i. ml-1. When compared with the baseline population, 14 and 18 of 20 total populations were less sensitive to iprodione and Propiconazole, respectively. Individually sampled isolates obtained from fairways, putting greens, or tees were less sensitive to iprodione and Propiconazole when compared with the baseline. For thiophanate-methyl, five populations were sensitive, six were resistant, and the remaining nine populations contained various proportions (2 to 92%) of resistant isolates. Individually sampled isolates obtained from fairways and putting greens were evaluated for associations in sensitivity among the three fungicides. A weak but positive correlation in sensitivity to iprodione and Propiconazole was observed for isolates resistant to thiophanate-methyl but correlations for sensitive isolates were not significant. Furthermore, isolates with highly reduced sensitivity to iprodione clustered in a narrow range of Propiconazole sensitivity. These data suggest the possible existence of resistance mechanisms common to diverse fungicide classes. Overall, results indicate that insensitivity of S. homoeocarpa to iprodione, Propiconazole, and thiophanate-methyl exists in varying degrees on golf courses in the northeastern United States.
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geographic distribution of fungicide insensitive sclerotinia homoeocarpa isolates from golf courses in the northeastern united states
Plant Disease, 2010Co-Authors: Alexander I Putman, Geunhwa Jung, John E KaminskiAbstract:ABSTRACT Chemical management of dollar spot in turf may lead to the development of Sclerotinia homoeocarpa populations with reduced fungicide sensitivity. The objective of this study was to determine the scope of S. homoeocarpa insensitivity to fungicides commonly used to control dollar spot on golf courses in the northeastern United States. A total of 965 and 387 isolates of S. homoeocarpa from intensively or individually sampled sites, respectively, were evaluated for in vitro sensitivity to iprodione, Propiconazole, and thiophanate-methyl. Mean baseline sensitivities to iprodione and Propiconazole were 0.2763 and 0.0016 μg a.i. ml–1, respectively, and all baseline isolates were sensitive to thiophanate-methyl at 1,000 μg a.i. ml–1. When compared with the baseline population, 14 and 18 of 20 total populations were less sensitive to iprodione and Propiconazole, respectively. Individually sampled isolates obtained from fairways, putting greens, or tees were less sensitive to iprodione and Propiconazole wh...
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Thiophanate-methyl and Propiconazole sensitivity in Sclerotinia homoeocarpa populations from golf courses in Wisconsin and Massachusetts.
Plant Disease, 2009Co-Authors: Paul L. Koch, Craig R. Grau, Geunhwa JungAbstract:Management of dollar spot, caused by the fungus Sclerotinia homoeocarpa, is dependent upon repeated fungicide applications in intensively managed turfgrass such as golf course putting greens and fairways. Repeated fungicide applications could potentially select for fungicide-resistant isolates and result in a reduction of disease control. The objectives of this study were to determine the degree of S. homoeocarpa in vitro sensitivity to the fungicides thiophanate-methyl and Propiconazole using isolates collected from golf course putting greens, fairways, and roughs; and to determine the relationships of golf course age and fungicide history to the frequency of fungicide-insensitive isolates within the population. More than 1,400 S. homoeocarpa isolates were collected from putting greens, fairways, and roughs at six Wisconsin golf courses and one Massachusetts golf course and subjected to in vitro fungicide sensitivity assays with single discriminatory concentrations of thiophanate-methyl and Propiconazole. Five of seven pathogen populations from rough areas were not significantly different from one another in Propiconazole sensitivity. These populations were collectively the most sensitive to both fungicides and therefore, served as baseline populations for comparison with fungicide-exposed populations from putting greens and fairways. Greater Propiconazole insensitivity was observed in populations collected from fairways and putting greens that received more frequent applications of the fungicide than those isolated from the roughs. In nearly all the golf courses, the frequency of thiophanate-methyl insensitivity was higher among isolates of S. homoeocarpa collected from fairways than from roughs regardless of the age of the golf course or history of benzimidazole use. Thus, while the development of resistance to Propiconazole can be predicted in part by the relative frequency of demethylation inhibitor fungicide applications, the occurrence of populations resistant to thiophanate-methyl appears to be unrelated to recent use of the benzimidazole class of fungicides.
Stephen Nesnow - One of the best experts on this subject based on the ideXlab platform.
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Propiconazole increases reactive oxygen species levels in mouse hepatic cells in culture and in mouse liver by a cytochrome p450 enzyme mediated process
Chemico-Biological Interactions, 2011Co-Authors: Stephen Nesnow, Pei-jen Chen, Rachel D Grindstaff, Guy R Lambert, William T Padgett, Maribel Bruno, Charles E Wood, Lynea MurphyAbstract:Propiconazole induces hepatocellular carcinomas and hepatocellular adenomas in mice and promotes liver tumors in rats. Transcriptional, proteomic, metabolomic and biochemical studies of hepatic tissues from mice treated with Propiconazole under the conditions of the chronic bioassay indicated that Propiconazole induced oxidative stress. Here we sought to identify the source of the reactive oxygen species (ROS) induced by Propiconazole using both AML12 immortalized mouse hepatocytes in culture and liver tissues from mice. We also sought to further characterize the nature and effects of ROS formation induced by Propiconazole treatment in mouse liver. ROS was induced in AML12 cells by Propiconazole as measured by fluorescence detection and its formation was ameliorated by N-acetylcysteine. Propiconazole induced glutathione-S-transferase (GSTα) protein levels and increased the levels of thiobarbituric acid reactive substances (TBARS) in AML12 cells. The TBARS levels were decreased by diphenylene iodonium chloride (DPIC), a cytochrome P450 (CYP) reductase inhibitor revealing the role of CYPs in ROS generation. It has been previously reported that Cyp2b and Cyp3a proteins were induced in mouse liver by Propiconazole and that Cyp2b and Cyp3a proteins undergo uncoupling of their CYP catalytic cycle releasing ROS. Therefore, salicylic acid hydroxylation was used as probe for ROS formation using microsomes from mice treated with Propiconazole. These studies showed that levels of 2,3-dihydroxybenzoic acid (an ROS derived metabolite) were decreased by ketoconazole, melatonin and DPIC. In vivo, Propiconazole increased hepatic malondialdehyde levels and GSTα protein levels and had no effect on hepatic catalase or superoxide dismutase activities. Based on these observations we conclude that Propiconazole induces ROS in mouse liver by increasing CYP protein levels leading to increased ROS levels. Our data also suggest that Propiconazole induces the hydroxyl radical as a major ROS form.
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protein carbonyl formation in response to Propiconazole induced oxidative stress
Journal of Proteome Research, 2009Co-Authors: Maribel E Bruno, Tanya Moore, Stephen NesnowAbstract:Propiconazole, a widely used fungicide, is hepatotoxic and hepatotumorigenic in mice. Previous genomic analysis of liver tissues from Propiconazole-treated mice identified genes and pathways involved in oxidative stress, suggesting that oxidative stress may play a role in Propiconazole-induced toxicity. To understand the contribution of oxidative stress on toxicity at the protein level, we developed an integrated approach for the systematic measurement of protein oxidation in the livers from Propiconazole-treated mice. Liver protein carbonylation increased significantly after treatment with Propiconazole, demonstrating Propiconazole-associated induction of oxidative stress. Utilizing two-dimensional gel electrophoresis (2-DE), immunoblotting, and mass spectrometry, we identified 17 carbonylated proteins that were altered with varying intensities by Propiconazole treatment. The potential effects of protein carbonylation on protein functions and cellular activities in the liver of Propiconazole-treated mice were further investigated. A significant negative correlation between protein carbonylation and cytochrome c reductase activity was found. We conclude that glycolysis, mitochondrial respiratory chain, ATP production, amino acid metabolism, CO2 hydration, cellular antioxidant defense and detoxification system, and tetrahydrobiopterin pathways are affected by oxygen radicals in the livers of Propiconazole-treated mice. This study suggests a mode of Propiconazole-induced toxicity in mouse liver which primarily involves oxidative damage to cellular proteins.
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cytotoxic effects of Propiconazole and its metabolites in mouse and human hepatoma cells and primary mouse hepatocytes
Toxicology in Vitro, 2008Co-Authors: Pei-jen Chen, Tanya Moore, Stephen NesnowAbstract:Propiconazole is a triazole-containing fungicide that is used agriculturally on grasses, fruits, grains, seeds, hardwoods, and conifers. Propiconazole is a mouse liver hepatotoxicant and a hepatocarcinogen that has adverse reproductive and developmental toxicities in experimental animals. The goal of this study was to investigate the cytotoxic responses of Propiconazole and its metabolites to determine if metabolism of this agent differentially affected its cytotoxic activities in hepatic tumor cell lines and in primary hepatocytes. To this end the cytotoxic effects of Propiconazole and five of its metabolites were examined in three hepatic cell types: The mouse hepatoma Hepa1c1c7 cell line, the human hepatoma HepG2 cell line, and primary cultures of mouse hepatocytes. We initially compared the responses of Propiconazole exposure in both Hepa1c1c7 and HepG2 cell lines over a concentration range of 0-200 microM using two assay systems: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the neutral red assay. Concentration-related cytotoxic responses were evident in both cell lines using both endpoints with the MTT assay providing enhanced sensitivity. The relative cytotoxic effects of Propiconazole and five Propiconazole metabolites were further assessed by the MTT assay using Hepa1c1c7 and HepG2 tumor cell lines. The cell cultures were exposed to various concentrations of Propiconazole and five of its metabolites over a range of 0-400 microM. Propiconazole was cytotoxic in both cell lines in a dose-dependent manner. All five metabolites were less cytotoxic in both cell lines compared to the parent compound. The most cytotoxic metabolites in Hepa1c1c7 and HepG2 cells among the five were 3-(2-((1H-1,2,4-triazol-1-yl)methyl)-2-(2,4-dichlorophenyl)-1,3-dioxolan-4-yl)propan-1-ol and 1-(2-((1H-1,2,4-triazol-1-yl)methyl)-2-(2,4-dichlorophenyl)-1,3-dioxolan-4-yl)propan-2-ol. Propiconazole was cytotoxic in primary mouse hepatocytes; however none of the five Propiconazole metabolites exerted cytotoxic activities. There was a linear relationship between the cLogP and the cytotoxic effects of Propiconazole and its five metabolites in Hepa1c1c7 cells. We conclude that these Propiconazole metabolites would not contribute to the Propiconazole-induced cytotoxicity process in primary mouse hepatocytes. Furthermore, since in tumor cell lines the metabolites were less cytotoxic than the parent Propiconazole, our results suggest that in the tumorigenesis process as tumor cells are formed they would be more susceptible to the cytotoxic effects of Propiconazole compared to the metabolites.
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transcriptional profiles in liver from rats treated with tumorigenic and non tumorigenic triazole conazole fungicides Propiconazole triadimefon and myclobutanil
Toxicologic Pathology, 2006Co-Authors: Susan D Hester, Stephen Nesnow, Douglas C Wolf, Sheaufung ThaiAbstract:Conazoles are a class of fungicides used as pharmaceutical and agricultural agents. In chronic bioassays in rats, triadimefon was hepatotoxic and induced follicular cell adenomas in the thyroid gland, whereas, Propiconazole and myclobutanil were hepatotoxic but had no effect on the thyroid gland. These conazoles administered in the feed to male Wistar/Han rats were found to induce hepatomegaly, induce high levels of pentoxyresorufin-O-dealkylase, increase cell proliferation in the liver, increase serum cholesterol, decrease serum T3 and T4, and increase hepatic uridine diphosphoglucuronosyl transferase activity. The goal of the present study was to define pathways that explain the biologic outcomes. Male Wistar/Han rats (3 per group), were exposed to the 3 conazoles in the feed for 4, 30, or 90 days of treatment at tumorigenic and nontumorigenic doses. Hepatic gene expression was determined using high-density Affymetrix GeneChips (Rat 230_2). Differential gene expression was assessed at the probe level using Robust Multichip Average analysis. Principal component analysis by treatment and time showed within group sample similarity and that the treatment groups were distinct from each other. The number of altered genes varied by treatment, dose, and time. The greatest number of altered genes was induced by triadimefon and Propiconazole after 90 days of treatment, while myclobutanil had minimal effects at that time point. Pathway level analyses revealed that after 90 days of treatment the most significant numbers of altered pathways were related to cell signaling, growth, and metabolism. Pathway level analysis for triadimefon and Propiconazole resulted in 71 altered pathways common to both chemicals. These pathways controlled cholesterol metabolism, activation of nuclear receptors, and N-ras and K-ras signaling. There were 37 pathways uniquely changed by Propiconazole, and triadimefon uniquely altered 34 pathways. Pathway level analysis of altered gene expression resulted in a more complete description of the associated toxicological effects that can distinguish triadimefon from Propiconazole and myclobutanil.
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Propiconazole induced cytochrome p450 gene expression and enzymatic activities in rat and mouse liver
Toxicology Letters, 2005Co-Authors: Guobin Sun, Guy R Lambert, Sheaufung Thai, Douglas B Tully, Amber K Goetz, Douglas C Wolf, David J Dix, Stephen NesnowAbstract:Propiconazole is a N-substituted triazole used as a fungicide on fruits, grains, seeds, hardwoods, and conifers. In the present study, Propiconazole was examined for its effects on the expression of hepatic cytochrome P450 genes and on the activities of P450 enzymes in male Sprague-Dawley rats and male CD-1 mice. Rats and mice were administered Propiconazole by gavage daily for 14 days at doses of 10, 75, and 150 mg/kg body weight/day. Quantitative real time RT-PCR assays of rat hepatic RNA samples from animals treated at the 150 mg/kg body weight/day dose revealed significant mRNA overexpression of the following genes compared to control: CYP1A2 (1.62-fold), CYP2B1 (10.8-fold), CYP3A1/CYP3A23 (2.78-fold), and CYP3A2 (1.84-fold). In mouse liver, Propiconazole produced mRNA overexpression of Cyp2b10 (2.39-fold) and Cyp3a11 (5.19-fold). mRNA expression of CYP1A1 was not detected in liver tissues from treated or controls animals from either species. Propiconazole significantly induced both pentoxyresorufin O-dealkylation (PROD) and methoxyresorufin O-dealkylation (MROD) activities in both rat and mouse liver at the 150 mg/kg body weight/day and 75 mg/kg body weight/day doses. In summary, these results indicated that Propiconazole induced CYP1A2 in rat liver and CYP2B and CYP3A families of isoforms in rat and mouse liver.
John E Kaminski - One of the best experts on this subject based on the ideXlab platform.
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geographic distribution of fungicide insensitive sclerotinia homoeocarpa isolates from golf courses in the northeastern united states
Plant Disease, 2010Co-Authors: Alexander I Putman, Geunhwa Jung, John E KaminskiAbstract:Chemical management of dollar spot in turf may lead to the development of Sclerotinia homoeocarpa populations with reduced fungicide sensitivity. The objective of this study was to determine the scope of S. homoeocarpa insensitivity to fungicides commonly used to control dollar spot on golf courses in the northeastern United States. A total of 965 and 387 isolates of S. homoeocarpa from intensively or individually sampled sites, respectively, were evaluated for in vitro sensitivity to iprodione, Propiconazole, and thiophanate-methyl. Mean baseline sensitivities to iprodione and Propiconazole were 0.2763 and 0.0016 μg a.i. ml-1, respectively, and all baseline isolates were sensitive to thiophanate-methyl at 1,000 μg a.i. ml-1. When compared with the baseline population, 14 and 18 of 20 total populations were less sensitive to iprodione and Propiconazole, respectively. Individually sampled isolates obtained from fairways, putting greens, or tees were less sensitive to iprodione and Propiconazole when compared with the baseline. For thiophanate-methyl, five populations were sensitive, six were resistant, and the remaining nine populations contained various proportions (2 to 92%) of resistant isolates. Individually sampled isolates obtained from fairways and putting greens were evaluated for associations in sensitivity among the three fungicides. A weak but positive correlation in sensitivity to iprodione and Propiconazole was observed for isolates resistant to thiophanate-methyl but correlations for sensitive isolates were not significant. Furthermore, isolates with highly reduced sensitivity to iprodione clustered in a narrow range of Propiconazole sensitivity. These data suggest the possible existence of resistance mechanisms common to diverse fungicide classes. Overall, results indicate that insensitivity of S. homoeocarpa to iprodione, Propiconazole, and thiophanate-methyl exists in varying degrees on golf courses in the northeastern United States.
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geographic distribution of fungicide insensitive sclerotinia homoeocarpa isolates from golf courses in the northeastern united states
Plant Disease, 2010Co-Authors: Alexander I Putman, Geunhwa Jung, John E KaminskiAbstract:ABSTRACT Chemical management of dollar spot in turf may lead to the development of Sclerotinia homoeocarpa populations with reduced fungicide sensitivity. The objective of this study was to determine the scope of S. homoeocarpa insensitivity to fungicides commonly used to control dollar spot on golf courses in the northeastern United States. A total of 965 and 387 isolates of S. homoeocarpa from intensively or individually sampled sites, respectively, were evaluated for in vitro sensitivity to iprodione, Propiconazole, and thiophanate-methyl. Mean baseline sensitivities to iprodione and Propiconazole were 0.2763 and 0.0016 μg a.i. ml–1, respectively, and all baseline isolates were sensitive to thiophanate-methyl at 1,000 μg a.i. ml–1. When compared with the baseline population, 14 and 18 of 20 total populations were less sensitive to iprodione and Propiconazole, respectively. Individually sampled isolates obtained from fairways, putting greens, or tees were less sensitive to iprodione and Propiconazole wh...
Chengju Wang - One of the best experts on this subject based on the ideXlab platform.
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life cycle exposure to Propiconazole reduces fecundity by disrupting the steroidogenic pathway and altering dna methylation in zebrafish danio rerio
Environment International, 2020Co-Authors: Miaomiao Teng, Xiangguang Chen, Chen Wang, Min Song, Jie Zhang, Chengju WangAbstract:Propiconazole is fungicide widely used in agriculture, which may enter aquatic ecosystems and affect organisms. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant levels of Propiconazole throughout the life cycle, from embryo to sexually mature adults, and the effects on growth, reproduction, and offspring viability were investigated. To investigate the mechanisms of Propiconazole action, the sex steroid hormones and the expression of genes related to the hypothalamus-pituitary-gonad-liver (HPGL) axis and DNA methylation were examined. Growth decreased in the parental zebrafish (F0) after exposure to Propiconazole for 120 days. In males, increases in the levels of 17β-estradiol and vitellogenin were observed. The alterations in sex steroid hormones were regulated by the expression of genes involved with the HPGL axis. The decreases in fecundity and fertilization of the F0 was induced by the global DNA methylation, and then may result in the abnormal development of the F1. Therefore, Propiconazole disrupted the steroidogenic pathway and caused changes in global DNA methylation that induced reproductive toxicity.
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effect of Propiconazole on the lipid metabolism of zebrafish embryos danio rerio
Journal of Agricultural and Food Chemistry, 2019Co-Authors: Miaomiao Teng, Feng Zhao, Yimeng Zhou, Sen Yan, Sinuo Tian, Jin Yan, Zhiyuan Meng, Chengju WangAbstract:Propiconazole is a triazole fungicide that has been widely used in agriculture and has been detected in the aquatic environment. This study aimed to investigate the effects of Propiconazole exposure on lipid metabolism in the early life stages of zebrafish for 120 h postfertilization (hpf). Using the early life stages of zebrafish to address scientific questions is lower in cost, more efficient, and suitable to meeting current legislation than those in other traditional fish species. Exposure to Propiconazole significantly inhibited the development of zebrafish embryos and larvae. This exposure also caused reduced locomotor activities in zebrafish. Furthermore, total cholesterol levels, lipoprotein lipase, and fatty acid synthase activities were significantly decreased. The expression levels of genes involved in lipid metabolism were significantly up-regulated in response to Propiconazole exposure. GC-MS/MS analysis revealed that fatty acids were significantly decreased. Together, the findings indicate the potential environmental risks of Propiconazole exposure in the aquatic ecosystem.
Sharon L Midland - One of the best experts on this subject based on the ideXlab platform.
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sensitivity distributions of california populations of colletotrichum cereale to the dmi fungicides Propiconazole myclobutanil tebuconazole and triadimefon
Plant Disease, 2007Co-Authors: F P Wong, Sharon L MidlandAbstract:The baseline sensitivity of a California population of Colletotrichum cereale (turfgrass anthracnose) to the sterol demethylation inhibitor (DMI) fungicide Propiconazole was determined using an in vitro assay with known reproducibility. The 50% effective dose (ED50) values for Propiconazole for a nonexposed, baseline population ranged from 0.025 to 0.35 μg/ml with a mean of 0.14 μg/ml. Examination of two DMI-exposed populations indicated an approximate increase of 6.5× in mean ED50 values. In vivo testing of two isolates with ED50 values of Propiconazole at 0.15 and 0.90 μg/ml indicated reduced control for the less sensitive isolate by Propiconazole at rates ≤38 μg/ml. It was determined that single discriminatory dose testing in vitro with Propiconazole at 0.50 μg/ml could differentiate sensitive and resistant isolates. Using this dose, six additional populations were tested and DMI-exposed populations were found to be three to nine times less sensitive compared with the baseline population. Two populations were assayed for sensitivity to myclobutanil, tebuconazole, and triadimefon. Mean ED50 values for a nonexposed population were 0.72, 0.082, and 5.6 μg/ml, respectively; for a DMI-exposed population, mean ED50 values were 3.8, 0.35, and 18 μg/ml, respectively. This work provides information on the development of DMI resistance in populations of C. cereale in California and methodologies for future resistance monitoring for this pathogen.
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sensitivity distributions of california populations of colletotrichum cereale to the dmi fungicides Propiconazole myclobutanil tebuconazole and triadimefon
Plant Disease, 2007Co-Authors: F P Wong, Sharon L MidlandAbstract:ABSTRACT The baseline sensitivity of a California population of Colletotrichum cereale (turfgrass anthracnose) to the sterol demethylation inhibitor (DMI) fungicide Propiconazole was determined using an in vitro assay with known reproducibility. The 50% effective dose (ED50) values for Propiconazole for a nonexposed, baseline population ranged from 0.025 to 0.35 μg/ml with a mean of 0.14 μg/ml. Examination of two DMI-exposed populations indicated an approximate increase of 6.5× in mean ED50 values. In vivo testing of two isolates with ED50 values of Propiconazole at 0.15 and 0.90 μg/ml indicated reduced control for the less sensitive isolate by Propiconazole at rates ≤38 μg/ml. It was determined that single discriminatory dose testing in vitro with Propiconazole at 0.50 μg/ml could differentiate sensitive and resistant isolates. Using this dose, six additional populations were tested and DMI-exposed populations were found to be three to nine times less sensitive compared with the baseline population. Two ...
