Latest Publications

@article{uhlik_bacterial_2014,

title = {Bacterial acquisition of hexachlorobenzene-derived carbon in contaminated soil.},

author = {Ondrej Uhlik and Michal Strejcek and Jan Vondracek and Lucie Musilova and Jakub Ridl and Petra Lovecka and Tomas Macek},

doi = {10.1016/j.chemosphere.2014.04.110},

issn = {1879-1298 0045-6535},

year  = {2014},

date = {2014-10-01},

journal = {Chemosphere},

volume = {113},

pages = {141–145},

abstract = {Pesticides are a class of xenobiotics intentionally released into the environment. Hexachlorobenzene (HCB) was used as a fungicide from 1945, leaving behind many contaminated sites. Very few studies have examined the biodegradation of HCB or the fate of HCB-derived carbon. Here we report that certain bacterial populations are capable of deriving carbon from HCB in contaminated soil under aerobic conditions. These populations are primarily Proteobacteria, including Methylobacterium and Pseudomonas, which predominated as detected by stable isotope probing (SIP) and 16S rRNA gene amplicon pyrosequencing. Due to the nature of SIP, which can be used as a functional method solely for assimilatory processes, it is not possible to elucidate whether these populations metabolized directly HCB or intermediates of its metabolism produced by different populations. The possibility exists that HCB is degraded via the formation of pentachlorophenol (PCP), which is further mineralized. With this in mind, we designed primers to amplify PCP 4-monooxygenase-coding sequences based on the available pcpB gene sequence from Methylobacterium radiotolerans JCM 2831. Based on 16S rRNA gene analysis, organisms closely related to this strain were detected in (13)C-labeled DNA. Using the designed primers, we were able to amplify pcpB genes in both total community DNA and (13)C-DNA. This indicates that HCB might be transformed into PCP before it gets assimilated. In summary, this study is the first report on which bacterial populations benefit from carbon originating in the pesticide HCB in a contaminated soil.},

note = {Place: England},

keywords = {*Soil Microbiology, 16S rRNA genes, 16S/genetics, Amplicon pyrosequencing, Biodegradation, Bioremediation, Carbon Isotopes/metabolism, Czech Republic, DNA, DNA Primers, Environmental, Hexachlorobenzene/chemistry/*metabolism, Isotope Labeling, Methylobacterium/*metabolism, Mixed Function Oxygenases/metabolism, Molecular Structure, Pentachlorophenol 4-monooxygenase, Pentachlorophenol/chemistry/metabolism, Pesticides, Pseudomonas/*metabolism, Real-Time Polymerase Chain Reaction, Ribosomal, RNA, Sequence Analysis, Soil Pollutants/*metabolism, Stable isotope probing},

pubstate = {published},

tppubtype = {article}

}

@article{prochazkova_aryl_2013,

title = {Aryl hydrocarbon receptor negatively regulates expression of the plakoglobin gene (jup).},

author = {Jiřina Procházková and Markéta Kabátková and Lenka Šmerdová and Jiří Pacherník and Dominika Sykorová and Jiří Kohoutek and Pavlína Šimečková and Eva Hrubá and Alois Kozubík and Miroslav Machala and Jan Vondráček},

doi = {10.1093/toxsci/kft110},

issn = {1096-0929},

year  = {2013},

date = {2013-08-01},

journal = {Toxicological sciences : an official journal of the Society of Toxicology},

volume = {134},

number = {2},

pages = {258–270},

abstract = {Plakoglobin is an important component of intercellular junctions, including both desmosomes and adherens junctions, which is known as a tumor suppressor. Although mutations in the plakoglobin gene (Jup) and/or changes in its protein levels have been observed in various disease states, including cancer progression or cardiovascular defects, the information about endogenous or exogenous stimuli orchestrating Jup expression is limited. Here we show that the aryl hydrocarbon receptor (AhR) may regulate Jup expression in a cell-specific manner. We observed a significant suppressive effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a model toxic exogenous activator of the AhR signaling, on Jup expression in a variety of experimental models derived from rodent tissues, including contact-inhibited rat liver progenitor cells (where TCDD induces cell proliferation), rat and mouse hepatoma cell models (where TCDD inhibits cell cycle progression), cardiac cells derived from the mouse embryonic stem cells, or cardiomyocytes isolated from neonatal rat hearts. The small interfering RNA (siRNA)-mediated knockdown of AhR confirmed its role in both basal and TCDD-deregulated Jup expression. The analysis of genomic DNA located textasciitilde2.5kb upstream of rat Jup gene revealed a presence of evolutionarily conserved AhR binding motifs, which were confirmed upon their cloning into luciferase reporter construct. The siRNA-mediated knockdown of Jup expression affected both proliferation and attachment of liver progenitor cells. The present data indicate that the AhR may contribute to negative regulation of Jup gene expression in rodent cellular models, which may affect cell adherence and proliferation.},

note = {Place: United States},

keywords = {Animals, Aryl hydrocarbon receptor, Aryl Hydrocarbon/*physiology, Base Sequence, cardiomyocytes., Cell Adhesion, Cell Line, Cell Proliferation, Cloning, desmosomes, dioxin, DNA Primers, Down-Regulation, gamma Catenin/*genetics, Gene Expression Regulation/*physiology, Genetic, Inbred F344, liver progenitor cells, Molecular, plakoglobin, Polychlorinated Dibenzodioxins/pharmacology, Promoter Regions, Rats, Real-Time Polymerase Chain Reaction, Receptors},

pubstate = {published},

tppubtype = {article}

}

@article{vondracek_7h-dibenzocgcarbazole_2006,

title = {7H-Dibenzo[c,g]carbazole and 5,9-dimethyldibenzo[c,g]carbazole exert multiple toxic events contributing to tumor promotion in rat liver epithelial 'stem-like' cells.},

author = {Jan Vondrácek and Lenka Svihálková-Sindlerová and Katerina Pencíková and Pavel Krcmár and Zdenek Andrysík and Katerina Chramostová and Sona Marvanová and Zuzana Valovicová and Alois Kozubík and Alena Gábelová and Miroslav Machala},

doi = {10.1016/j.mrfmmm.2005.11.005},

issn = {0027-5107},

year  = {2006},

date = {2006-04-01},

journal = {Mutation research},

volume = {596},

number = {1-2},

pages = {43–56},

abstract = {Immature liver progenitor cells have been suggested to be an important target of hepatotoxins and hepatocarcinogens. The goal of the present study was to assess the impact of 7H-dibenzo[c,g]carbazole (DBC) and its tissue-specific carcinogenic N-methyl (N-MeDBC) and 5,9-dimethyl (DiMeDBC) derivatives on rat liver epithelial WB-F344 cells, in vitro model of liver progenitor cells. We investigated the cellular events associated with both tumor initiation and promotion, such as activation of aryl hydrocarbon receptor (AhR), changes in expression of enzymes involved in metabolic activation of DBC and its derivatives, effects on cell cycle, cell proliferation/apoptosis and inhibition of gap junctional intercellular communication (GJIC). N-MeDBC, a tissue-specific sarcomagen, was only a weak inhibitor of GJIC or inducer of AhR-mediated activity, and it did not affect either cell proliferation or apoptosis. DBC was efficient GJIC inhibitor, while DiMeDBC manifested the strongest AhR inducing activity. Accordingly, DiMeDBC was also the most potent inducer of cytochrome P450 1A1 (CYP1A1) and CYP1A2 expression among the three compounds tested. Both DBC and DiMeDBC induced expression of CYP1B1 and aldo-keto reductase 1C9 (AKR1C9). N-MeDBC failed to significantly upregulate CYP1A1/2 and it only moderately increased CYP1B1 or AKR1C9. Only the potent liver carcinogens, DBC and DiMeDBC, caused a significant increase of p53 phosphorylation at Ser15, an increased accumulation of cells in S-phase and apoptosis at micromolar concentrations. In addition, DiMeDBC was found to stimulate cell proliferation of contact-inhibited WB-F344 cells at 1 microM concentration, which is a mode of action that might further contribute to its hepatocarcinogenicity. The present data seem to suggest that the AhR activation, induction of enzymes involved in metabolic activation, inhibition of GJIC or stimulation of cell proliferation might all contribute to the hepatocarcinogenic effects of DBC and DiMeDBC.},

note = {Place: Netherlands},

keywords = {Animals, Aryl Hydrocarbon Hydroxylases/genetics, Base Sequence, Carbazoles/*toxicity, Carcinogens/*toxicity, Cell Death/drug effects, Cytochrome P-450 CYP1A1/genetics, Cytochrome P-450 CYP1A2/genetics, Cytochrome P-450 CYP1B1, DNA Primers, Epithelial Cells/drug effects/*pathology, Inbred F344, Liver/*cytology/drug effects, Methylation, Molecular Structure, Mutagens, Rats, Reverse Transcriptase Polymerase Chain Reaction},

pubstate = {published},

tppubtype = {article}

}