2014
Uhlik, Ondrej; Strejcek, Michal; Vondracek, Jan; Musilova, Lucie; Ridl, Jakub; Lovecka, Petra; Macek, Tomas
Bacterial acquisition of hexachlorobenzene-derived carbon in contaminated soil. Journal Article
In: Chemosphere, vol. 113, pp. 141–145, 2014, ISSN: 1879-1298 0045-6535, (Place: England).
Abstract | Links | BibTeX | Tags: *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
@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}
}
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.
2007
Vondrácek, Jan; Svihálková-Sindlerová, Lenka; Pencíková, Katerina; Marvanová, Sona; Krcmár, Pavel; Ciganek, Miroslav; Neca, Jirí; Trosko, James E.; Upham, Brad; Kozubík, Alois; Machala, Miroslav
In: Environmental toxicology and chemistry, vol. 26, no. 11, pp. 2308–2316, 2007, ISSN: 0730-7268, (Place: United States).
Abstract | Links | BibTeX | Tags: Animals, Anthracenes/toxicity, Aryl Hydrocarbon/metabolism, Carcinogens/*toxicity, Cell Line, Cell Proliferation/*drug effects, Cytochrome P-450 CYP1A1/genetics/metabolism, Czech Republic, Dose-Response Relationship, Drug, Environmental Pollutants/*toxicity, Gap Junctions/*drug effects/metabolism, Gene Expression Regulation/*drug effects/physiology, Geologic Sediments/*chemistry, Liver/cytology/pathology, Methylation, Naphthalenes/toxicity, Phenanthrenes/toxicity, Rats, Receptors, Rivers/*chemistry, Tumor, Tumor Suppressor Protein p53/metabolism
@article{vondracek_concentrations_2007,
title = {Concentrations of methylated naphthalenes, anthracenes, and phenanthrenes occurring in Czech river sediments and their effects on toxic events associated with carcinogenesis in rat liver cell lines.},
author = {Jan Vondrácek and Lenka Svihálková-Sindlerová and Katerina Pencíková and Sona Marvanová and Pavel Krcmár and Miroslav Ciganek and Jirí Neca and James E. Trosko and Brad Upham and Alois Kozubík and Miroslav Machala},
doi = {10.1897/07-161R.1},
issn = {0730-7268},
year = {2007},
date = {2007-11-01},
journal = {Environmental toxicology and chemistry},
volume = {26},
number = {11},
pages = {2308–2316},
abstract = {Alkylated polycyclic aromatic hydrocarbons (PAHs) are important environmental pollutants. In the present study, we determined levels of monomethylated naphthalenes (MeNap), phenanthrenes (MePhe), and anthracenes (MeAnt) in Czech river sediments. The levels of MePhe generally were lower than the concentrations of phenanthrene. In contrast, both MeNap and MeAnt were found at levels higher than their respective parent compounds in the majority of sampling sites. We then investigated their aryl hydrocarbon receptor (AhR)-mediated activity, accumulation of phosphorylated p53 protein, induction of expression of cytochrome P450 1A1 (CYP1A1), inhibition of gap junctional intercellular communication (GJIC), and effects on cell proliferation in rat liver cell models to evaluate the relative importance of these toxicity mechanisms of low-molecular-weight methylated PAHs. Methylated phenanthrene and anthracene compounds were weak inducers of AhR-mediated activity as determined both in a reporter gene assay system and by detection of the endogenous gene (Cyp1a1) induction. 2-Methylphenanthrene was the most potent AhR ligand. Contribution of MeAnt and MePhe to overall AhR-inducing potencies should be taken into account in PAH-contaminated environments. Nevertheless, their effects on AhR were not sufficient to modulate cell proliferation in a normal rat liver progenitor cell model system. These PAHs only had a marginal effect on p53 phosphorylation at high doses of 1-, 3-, and 9-MePhe as well as 1 MeAnt. On the other hand, both 2- and 9-MeAnt as well as all the MePhe under study were efficient inhibitors of GJIC, suggesting that these compounds might act as tumor promoters. In summary, inhibition of GJIC and partial activation of AhR seem to be the most prominent toxic effects of the methylated PAHs in the present study.},
note = {Place: United States},
keywords = {Animals, Anthracenes/toxicity, Aryl Hydrocarbon/metabolism, Carcinogens/*toxicity, Cell Line, Cell Proliferation/*drug effects, Cytochrome P-450 CYP1A1/genetics/metabolism, Czech Republic, Dose-Response Relationship, Drug, Environmental Pollutants/*toxicity, Gap Junctions/*drug effects/metabolism, Gene Expression Regulation/*drug effects/physiology, Geologic Sediments/*chemistry, Liver/cytology/pathology, Methylation, Naphthalenes/toxicity, Phenanthrenes/toxicity, Rats, Receptors, Rivers/*chemistry, Tumor, Tumor Suppressor Protein p53/metabolism},
pubstate = {published},
tppubtype = {article}
}
Alkylated polycyclic aromatic hydrocarbons (PAHs) are important environmental pollutants. In the present study, we determined levels of monomethylated naphthalenes (MeNap), phenanthrenes (MePhe), and anthracenes (MeAnt) in Czech river sediments. The levels of MePhe generally were lower than the concentrations of phenanthrene. In contrast, both MeNap and MeAnt were found at levels higher than their respective parent compounds in the majority of sampling sites. We then investigated their aryl hydrocarbon receptor (AhR)-mediated activity, accumulation of phosphorylated p53 protein, induction of expression of cytochrome P450 1A1 (CYP1A1), inhibition of gap junctional intercellular communication (GJIC), and effects on cell proliferation in rat liver cell models to evaluate the relative importance of these toxicity mechanisms of low-molecular-weight methylated PAHs. Methylated phenanthrene and anthracene compounds were weak inducers of AhR-mediated activity as determined both in a reporter gene assay system and by detection of the endogenous gene (Cyp1a1) induction. 2-Methylphenanthrene was the most potent AhR ligand. Contribution of MeAnt and MePhe to overall AhR-inducing potencies should be taken into account in PAH-contaminated environments. Nevertheless, their effects on AhR were not sufficient to modulate cell proliferation in a normal rat liver progenitor cell model system. These PAHs only had a marginal effect on p53 phosphorylation at high doses of 1-, 3-, and 9-MePhe as well as 1 MeAnt. On the other hand, both 2- and 9-MeAnt as well as all the MePhe under study were efficient inhibitors of GJIC, suggesting that these compounds might act as tumor promoters. In summary, inhibition of GJIC and partial activation of AhR seem to be the most prominent toxic effects of the methylated PAHs in the present study.