16 research outputs found
The miRNA-BP term network of BDE47-induced biological effects.
<p>(A) downregulated miRNAs. (B) upregulated miRNAs. Green: downregulated; red: upregulated. The color depths of circular nodes indicated the enrichment values of BP terms by functional enrichment analysis. The widths of edges indicated the gene numbers in BP terms regulated by source miRNAs.</p
The fold changes and predicted target gene amounts of differentially expressed miRNAs under BDE47 treatments.
<p>The locations of bubble centers indicated fold changes of the miRNAs, and the sizes of bubbles indicated predicted target gene amounts. Blue: high concentration exposure; yellow: low concentration exposure.</p
The quantitative miRNA expressions using sequencing and RT-PCR.
<p>The asterisk indicated only for dre-miR-142b-5p in low concentration BDE47 treatment, the result of statistical significance by RT-PCR determination was inconsistent with miRNA sequencing.</p
The most significantly altered enriched terms based on GO definitions and KEGG pathway definitions.
<p>(A) KEGG pathway terms. (B) GO BP terms. (C) GO CC terms. (D) GO MF terms. Yellow columns: significant in high concentration group; green columns: significant in high concentration group.</p
The quality information of sequencing.
<p>(A) The gene structure distributions. (B) The proportions of various type of RNAs. (C) Mapping status of vehicle control group. (D) Mapping status of 5 μg/L BDE47 group. (E) Mapping status of 500 μg/L BDE47 group.</p
The comparison of numbers of predicted and negatively-correlated target genes in the group of high concentration of BDE47.
<p>The comparison of numbers of predicted and negatively-correlated target genes in the group of high concentration of BDE47.</p
Contribution of the Antibiotic Chloramphenicol and Its Analogues as Precursors of Dichloroacetamide and Other Disinfection Byproducts in Drinking Water
Dichloroacetamide (DCAcAm), a disinfection
byproduct, has been
detected in drinking water. Previous research showed that amino acids
may be DCAcAm precursors. However, other precursors may be present.
This study explored the contribution of the antibiotic chloramphenicol
(CAP) and two of its analogues (thiamphenicol, TAP; florfenicol, FF)
(referred to collectively as CAPs), which occur in wastewater-impacted
source waters, to the formation of DCAcAm. Their formation yields
were compared to free and combined amino acids, and they were investigated
in filtered waters from drinking-water-treatment plants, heavily wastewater-impacted
natural waters, and secondary effluents from wastewater treatment
plants. CAPs had greater DCAcAm formation potential than two representative
amino acid precursors. However, in drinking waters with ng/L levels
of CAPs, they will not contribute as much to DCAcAm formation as the
μg/L levels of amino acids. Also, the effect of advanced oxidation
processes (AOPs) on DCAcAm formation from CAPs in real water samples
during subsequent chlorination was evaluated. Preoxidation of CAPs
with AOPs reduced the formation of DCAcAm during postchlorination.
The results of this study suggest that CAPs should be considered as
possible precursors of DCAcAm, especially in heavily wastewater-impacted
waters
Impact of UV/H<sub>2</sub>O<sub>2</sub> Pre-Oxidation on the Formation of Haloacetamides and Other Nitrogenous Disinfection Byproducts during Chlorination
Haloacetamides
(HAcAms), an emerging class of nitrogen-based disinfection
byproducts (N-DBPs) of health concern in drinking water, have been
found in drinking waters at μg/L levels. However, there is a
limited understanding about the formation, speciation, and control
of halogenated HAcAms. Higher ultraviolet (UV) doses and UV advanced
oxidation (UV/H<sub>2</sub>O<sub>2</sub>) processes (AOPs) are under
consideration for the treatment of trace organic pollutants. The objective
of this study was to examine the potential of pretreatment with UV
irradiation, H<sub>2</sub>O<sub>2</sub> oxidation, and a UV/H<sub>2</sub>O<sub>2</sub> AOP for minimizing the formation of HAcAms,
as well as other emerging N-DBPs, during postchlorination. We investigated
changes in HAcAm formation and speciation attributed to UV, H<sub>2</sub>O<sub>2</sub> or UV/H<sub>2</sub>O<sub>2</sub> followed by
the application of free chlorine to quench any excess hydrogen peroxide
and to provide residual disinfection. The results showed that low-pressure
UV irradiation alone (19.5–585 mJ/cm<sup>2</sup>) and H<sub>2</sub>O<sub>2</sub> preoxidation alone (2–20 mg/L) did not
significantly change total HAcAm formation during subsequent chlorination.
However, H<sub>2</sub>O<sub>2</sub> preoxidation alone resulted in
diiodoacetamide formation in two iodide-containing waters and increased
bromine utilization. Alternatively, UV/H<sub>2</sub>O<sub>2</sub> preoxidation
using UV (585 mJ/cm<sup>2</sup>) and H<sub>2</sub>O<sub>2</sub> (10
mg/L) doses typically employed for trace contaminant removal controlled
the formation of HAcAms and several other N-DBPs in drinking water
Model of Hormesis and Its Toxicity Mechanism Based on Quorum Sensing: A Case Study on the Toxicity of Sulfonamides to <i>Photobacterium phosphoreum</i>
During the past two decades, the phenomenon of hormesis
has gained
increasing recognition in environmental and toxicological communities.
However, the mechanistic understanding of hormesis, to date, is extremely
limited. Herein is proposed a novel parametric model with a mechanistic
basis and two model-based parameters for hormesis that was successfully
applied to the hormetic dose–response observed in the chronic
toxicity of sulfonamides on <i>Photobacterium phosphoreum</i>. On the basis of the methods of molecular docking and quantitative
structure–activity relationships (QSARs), we proposed a mechanistic
hypothesis for hormesis that introduces for the first time the concept
of quorum sensing in toxicological studies and explains the mechanism
at the level of the receptors. The mechanistic hypothesis stated that
(1) specific target binding like interaction with LuxR may contribute
to transcriptional activation leading to enhanced luciferase activity
at low dose exposure of sulfonamides, and (2) as the dose of sulfonamides
increases, more sulfonamides competitively bind to dihydropteroate
synthase, which inhibit the biosynthesis of folic acid and thus provoke
toxicity. This mechanistic hypothesis, which explains both the dose-dependent
and time-dependent features of hormesis, could give new insight into
the mechanistic study of hormesis
Zinc Oxide Nanoparticles Cause Inhibition of Microbial Denitrification by Affecting Transcriptional Regulation and Enzyme Activity
Over the past few decades, human
activities have accelerated the
rates and extents of water eutrophication and global warming through
increasing delivery of biologically available nitrogen such as nitrate
and large emissions of anthropogenic greenhouse gases. In particular,
nitrous oxide (N<sub>2</sub>O) is one of the most important greenhouse
gases, because it has a 300-fold higher global warming potential than
carbon dioxide. Microbial denitrification is a major pathway responsible
for nitrate removal, and also a dominant source of N<sub>2</sub>O
emissions from terrestrial or aquatic environments. However, whether
the release of zinc oxide nanoparticles (ZnO NPs) into the environment
affects microbial denitrification is largely unknown. Here we show
that the presence of ZnO NPs lead to great increases in nitrate delivery
(9.8-fold higher) and N<sub>2</sub>O emissions (350- and 174-fold
higher in the gas and liquid phases, respectively). Our data further
reveal that ZnO NPs significantly change the transcriptional regulations
of glycolysis and polyhydroxybutyrate synthesis, which causes the
decrease in reducing powers available for the reduction of nitrate
and N<sub>2</sub>O. Moreover, ZnO NPs substantially inhibit the gene
expressions and catalytic activities of key denitrifying enzymes.
These negative effects of ZnO NPs on microbial denitrification finally
cause lower nitrate removal and higher N<sub>2</sub>O emissions, which
is likely to exacerbate water eutrophication and global warming