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 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 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 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/H₂O₂ 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/H₂O₂) 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, H₂O₂ oxidation, and a UV/H₂O₂ 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, H₂O₂ or UV/H₂O₂ 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/cm²) and H₂O₂ preoxidation alone (2–20 mg/L) did not significantly change total HAcAm formation during subsequent chlorination. However, H₂O₂ preoxidation alone resulted in diiodoacetamide formation in two iodide-containing waters and increased bromine utilization. Alternatively, UV/H₂O₂ preoxidation using UV (585 mJ/cm²) and H₂O₂ (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 (N₂O) 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 N₂O 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 N₂O 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 N₂O. 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 N₂O emissions, which is likely to exacerbate water eutrophication and global warming