Delivering quality-changed water often contributes to the biological instability of drinking water distribution systems (DWDS). However, the potential effects of quality-changed water on the biostability within DWDS are not well understood, especially after water switching to quality-improved water. The objective of this study was to investigate the effects of quality-improved water on DWDS, focusing on the stability of biofilm. The practical aged-pipe was assembled into pipe reactors to simulate the effect of switching to quality-improve water. The adenosine triphosphate (ATP) concentration of bulk water in the pipe reactors increased from ∼1.2 ng/L to almost above 5 ng/L when fed water switching to TP 2. Biomass quantified by measuring ATP concentration confirmed that the risk of biofilm release through aged cast-iron (CI) pipe surfaces after water source switching. The changes in water characteristics due to quality-improved water source could cause bacteria release in DWDS at the initial period (at the first 7 days). However, the DWDS can establish the new stable phase after 42 days. Over time, biomass in the bulk water of the distribution system decreased significantly (The ATP concentration in the bulk maintains around 3 ng/L) after 42 days, indicating the improvement of water quality. The biofilm was dominated by bacteria related to iron-cycling process, and at the genus level, Desulfovibrio had the highest relative abundance, however, it decreased significantly (from 48% to 9.3%) after water source switching. And there was a slightly increase in the fraction of iron-oxidizing bacteria (IOB) and siderophore-producing bacteria (SPB), but a relatively higher increase in nitrate-reducing bacteria (NRB), nitrobacteria (NOB), and iron-reducing bacteria (IRB) was observed. Taken together, these results and the corrosion morphology, indicate that pipe biofilm and corrosion were chemically and microbially stable after re-stability under water source switching. In addition, the bulk water environment showed a marked decrease in selected bacteria at genus level, including pathogenic species, indicating the improvement of quality in drinking water.

Dibutyl phthalate (DBP) is widely used as plasticizer and has been detected in the environment, posing a threat to animal health. However, the effects of DBP on agricultural microbiomes are not known. In this study, DBP levels in black soil were evaluated, and the impact of DBP contamination on the uptake and metabolism of sugars in microbes was assessed by glucose absorption tests, metaproteomics, metabolomics, enzyme activity assays and computational simulation analysis. The results indicated that DBP contamination accelerated glucose consumption and upregulated the expression of porins and periplasmic monosaccharide ATP-binding cassette (ABC) transporter solute-binding proteins (SBPs). DBP and its metabolic intermediates (carboxymuconate and butanol) may form a stable complex with sugar transporters and enhance the rigidity and stability of these proteins. Sugar metabolism resulting in the generation of ATP and reducing agent (NADPH), as well as the expression of some key enzymes (dehydrogenases) were also upregulated by DBP treatment. Moreover, a diverse bacterial community appears to utilize sugar, suggesting that there are widespread effects of DBP contamination on soil microbial ecosystems. The results of this study provide a theoretical basis for investigating the toxicological effects of DBP on microbes in black soil.

Triclocarban (TCC), a broad-spectrum lipophilic antibacterial agent, is the main ingredient of personal and health care products. Nonetheless, its ubiquitous presence in the environment has been established to negatively affect the reproduction in humans and animals. In this work, we studied the possible toxic effects of TCC on mouse oocytes maturation in vitro. Our findings revealed that TCC-treated immature mouse oocytes had a significantly reduced rate of polar body extrusion (PBE) compared to that of control. Further study demonstrated that the cell cycle progression and cytoskeletal dynamics were disrupted after TCC exposure, which resulted in the continuous activation of spindle assembly checkpoint (SAC). Moreover, TCC-treated oocytes had mitochondrial damage, reduced ATP content, and decreased mitochondrial membrane potential (MMP). Furthermore, TCC exposure induced oxidative stress and subsequently triggered early apoptosis in mouse oocytes. Besides, the levels of histone methylation were also affected, as indicated by increased H3K27me2 and H3K27me3 levels. In summary, our results revealed that TCC exposure disrupted mouse oocytes maturation through affecting cell cycle progression, cytoskeletal dynamics, oxidative stress, early apoptosis, mitochondria function, and histone modifications in vitro.

Since ambient particulate matter (APM) is closely related to cardiovascular damage with mitochondria being its potential targets, this study was designed to explore the impact of APM on mitochondrial homeostasis, especially on mitochondrial dynamics and biogenesis in human vascular endothelial cells, using a kind of standard material, PM SRM1648a. As a result, internalized particles lead to mitochondrial dysfunction in EA.hy926 human endothelial cells, including mitochondrial reactive oxygen species (mtROS) overproduction, mitochondrial membrane potential (MMP) reduction and adenosine triphosphate (ATP) inhibition, coupled with additional release of mitochondrial DNA (mtDNA) into the cytosol. Moreover, morphological and structural changes in mitochondria are observed in response to PM SRM1648a. In that aspect, according to the evidence of shorter fragmented mitochondria dispersed throughout the cytoplasm, along with aberrant upregulation of fission-related mRNAs/proteins, the mitochondria exhibit a fission phenotype shifting from intact reticular network to fragmentized punctate shapes. Mechanistically, PM SRM1648a facilitates phosphorylation of DRP1 at Ser616 in HUVECs, and triggers its dephosphorylation at Ser637 residue in both EA.hy926 and HUVECs, which are supportive events for mitochondrial fission during particle exposure. Additionally, suppression of a master energy modulator, PGC-1α, reveals that PM SRM1648a has the ability to impair mitochondrial biogenesis. Collectively, it could be well concluded that PM SRM1648a interferes with the equilibrium of mitochondrial dynamics and biogenesis, which is likely to play a pivotal role in mitochondrial dysfunction driven by particles, eventually contributing to endothelial cell damage. Of note, it is more reasonable to conduct risk assessment from both cellular level and subcellular structures, among which mitochondria-targeted toxicity supplements more comprehensive understanding of APM inducible vascular toxicity.

Arsenic (As) is a metalloid element that is ubiquitous in the marine environment and its contamination has received worldwide attention due to its potential toxicity. Arsenic can induce multiple adverse effects, such as lipid metabolism disorder, immune system dysfunction, oxidative stress and carcinogenesis, in animals. Inorganic arsenic includes two chemical forms, arsenite (As (III)) and arsenate (As (V)), in natural environment. As (V) is the dominant form in natural waters. In the present study, metabolomic and proteomic alterations were investigated in juvenile rockfish Sebastes schlegelii exposed to environmentally relevant concentrations of As (V) for 14 d. The analysis of iTRAQ-based proteomics combined with untargeted NMR-based metabolomics indicated apparent toxicological effects induced by As (V) in juvenile rockfish. In details, the metabolites, including lactate, alanine, ATP, inosine and phosphocholine were significantly altered in As-treated groups. Proteomic responses suggested that As (V) could not only affected energy and primary metabolisms and signal transduction, but also influenced cytoskeleton structure in juvenile rockfish. This work suggested that the combined proteomic and metabolomic approach could shed light on the toxicological effects of pollutants in rockfish S. schlegelii.

Blueberry anthocyanin (BA) have strong health benefits as an active natural antioxidant and perfluorooctanoic acid (PFOA) can result in oxidative stress in animals. In our study, the protective effects of BA against stress induced by PFOA was investigated in the planarian Dugesia japonica using oxidative stress biomarkers, ATP contents, ATPase activity, DNA methylation and mRNA expression. PFOA exposure could resulted in malondialdehyde production. At the same time, treatment with BA decreased the production of malondialdehyde in BA-exposed and co-treatment planarians. PFOA caused activities increase in glutathione peroxidase (GPx), glutathione S-transferase (GST) and activities decrease in glutathione reductase (GR). PFOA exposure decreased the GSH and ATP contents. Additionally, it increased the GSSG contents and ATPase activity. BA administration increased the activities of GPx, GST and GR in BA and co-treatment planarians. Meanwhile BA maintained the contents of ATP, ATPase activity, GSH and GSSG by alleviating PFOA toxicity. Moreover, PFOA and BA increased the contents of 5-methylcytosine and decreased 5-hydroxymethylcytosine in all group. In addition, PFOA and BA treated planarians significantly altered the expression of genes associated with above biochemical parameters. The results showed that the mRNA expression of gpx, Djgst, gr, Djnak and dnmt1 were significantly elevated in all groups. Alterations in the mRNA expression levels indicated a stress response to PFOA exposure and anthocyanin protection. These alterations regulated biomarkers of oxidative stress, energy metabolism and DNA methylation levels in planarians. These results indicate that BA attenuated PFOA-induced oxidative stress, energy metabolism, DNA methylation and gene expression disorders.

Only limited information is available on the effects of dissolved organic phosphorus (DOP) on arsenate (As(V)) bioaccumulation and biotransformation in organisms. In this study, we examined the influence of three different DOP forms (β-sodium glycerophosphate (βP), adenosine 5′-triphosphate (ATP), and D-Glucose-6-phosphate disodium (GP) salts) and inorganic phosphate (IP) on As(V) toxicity, accumulation, and biotransformation in Microcystis aeruginosa. Results showed that M. aeruginosa utilized the three DOP forms to sustain its growth. At a subcellular level, the higher phosphorus (P) distribution in metal-sensitive fractions (MSF) observed in the IP treatments could explain the comparatively lower toxic stress of algae compared to the DOP treatments. Meanwhile, the higher MSF distribution of arsenic (As) in M. aeruginosa in the presence of DOP could explain the higher toxicity with lower 96-h half maximal effective concentration (EC50) values. Although we observed As(V) and P discrimination in M. aeruginosa under IP treatments with high intracellular P/As, we did not find this discrimination under the DOP treatments. As accumulation in algal cells was therefore greatly enhanced by DOP, especially βP, given its lower transformation rate to phosphate compared to ATP and GP in media. Additionally, As(V) reduction and, subsequently, As(III) methylation were greatly facilitated in M. aeruginosa by the presence of DOP, particularly GP, which was confirmed by the higher relative expression of its two functional genes (arsC and arsM). Our findings indicate that As(V) accumulation and its subsequent biotransformation were enhanced by organic P forms, which provides new insight into how DOP modulates As metabolism in algae.

The immunotoxicity of synthetic pyrethroid (SPs) has garnered much attention, and our previous research demonstrated that β-CYP causes immunotoxicity and oxidative stress in macrophages. Nevertheless, the underlying mechanism remains largely unknown. In this study, the murine macrophage RAW 264.7 cells and murine peritoneal macrophages (PMs) were exposed to β-CYP. The results showed that β-CYP elevated intracellular ROS levels in both RAW 264.7 cells and PMs. Exposure to β-CYP also caused mitochondrial dysfunction with reduced mitochondrial membrane potential (MMP), intracellular ATP level and mitochondrial DNA (mtDNA) content in the two cell types. In addition, exposure of RAW 264.7 cells to β-CYP for 12 h and 24 h enhanced autophagy, with elevated Beclin1, Rab7, Lamp1 and LC3-II expression levels, while 48 h of exposure attenuated autophagy. In contrast, exposure of PMs to β-CYP for 12 h promoted autophagy, whereas exposure for 24 h and 48 h impaired autophagy. Cotreatment with an antioxidant, N-acetyl-L-cysteine (NAC), partially blocked the reduced MMP, intracellular ATP level and autophagy disturbance. Moreover, cotreatment with an autophagy agonist, rapamycin (RAPA), partially blocked mitochondrial dysfunction and oxidative stress in the two cell types, whereas cotreatment with an autophagy inhibitor, 3-methyladenine (3-MA), augmented the abovementioned toxic effects. Furthermore, mitochondrial ROS levels in both RAW 264.7 cells and PMs were elevated by exposure to β-CYP, and molecular docking showed that β-CYP docked with mouse respiratory chain complex I by binding to the ND2, ND4, and ND5 subunits of the protein complex. Taken together, the data obtained in the present study demonstrate that oxidative stress partially mediates mitochondrial dysfunction and autophagy disturbance upon exposure to β-CYP in macrophages, and autophagy plays a protective role against the toxic effects.

Because of its analgesic properties, acetaminophen (AAP) is widely used to relieve headache. AAP is generally considered safe for humans, but its effects on aquatic organisms are not well known. Here, we have hypothesis that effects of AAP on aquatic organisms would be environmental temperature dependent, because their physiological function depend on the temperature. To test this hypothesis, we used medaka (Oryzias latipes) as a model, because they can live at a wide range of temperatures (0–40 °C). We exposed medaka larvae to 0 (control), 50, or 150 mg/L of AAP at 15, 25 (optimal temperature), or 30 °C for 4 days. Egg yolk absorption was accelerated with raising temperature at any AAP dose. AAP exposure did not have biologically significant effects on survival ratio and body length of larvae at any tested temperature or dose, but heart rate decreased as the dose of AAP and environmental temperature increased. In addition, as the temperature increased, amount of ATP in individual larvae increased in control group, but decreased in AAP exposed group. Subsequently, exposure to 150 mg/L of AAP at 30 °C decreased the number of red blood cells in the gills; we used 150 mg/L of AAP in subsequent hematological and histological analyses. Hematological analysis showed that rising temperature increased the proportion of morphologically abnormal red blood cells in AAP-exposed larvae, suggesting that AAP induced anemia-like signs in larvae. Histological observation of the kidney, which is a hematopoietic organ in fish, revealed no abnormalities. However, in the liver, which is responsible for drug metabolism, the proportion of vacuoles increased with increasing temperature. Although the exposure concentration we tested was higher than environmentally relevant concentrations, our data indicated that rising temperature enhances the toxicity of AAP to medaka larvae, suggesting an ecological risk of AAP due to global warming.

In order to clarify whether the mitochondrial dysfunction is closely related to the cell homeostasis maintenance after particulate matter (PM₂.₅) exposure, oxidative, inflammatory, apoptotic and mitochondrial endpoints were carefully studied in human bronchial epithelial BEAS-2B, normal human bronchial epithelial (NHBE) and chronic obstructive pulmonary disease (COPD)-diseased human bronchial epithelial (DHBE) cells acutely or repeatedly exposed to air pollution-derived PM₂.₅. Some modifications of the mitochondrial morphology were observed within all these cell models repeatedly exposed to the highest dose of PM₂.₅. Dose- and exposure-dependent oxidative damages were reported in BEAS-2B, NHBE and particularly COPD-DHBE cells acutely or repeatedly exposed to PM₂.₅. Nuclear factor erythroid 2-p45 related factor 2 (NRF2) gene expression and binding activity, together with the mRNA levels of some NRF2 target genes, were directly related to the number of exposures for the lowest PM₂.₅ dose (i.e., 2 μg/cm²), but, surprisingly, inversely related to the number of exposures for the highest dose (i.e., 10 μg/cm²). There were dose- and exposure-dependent increases of both nuclear factor kappa-B (NF-κB) binding activity and NF-κB target cytokine secretion in BEAS-2B, NHBE and particularly COPD-DHBE cells exposed to PM₂.₅. Mitochondrial ROS production, membrane potential depolarization, oxidative phosphorylation, and ATP production were significantly altered in all the cell models repeatedly exposed to the highest dose of PM₂.₅. Collectively, our results indicate a cytosolic ROS overproduction, inducing oxidative damage and activating oxygen sensitive NRF2 and NF-ₖB signaling pathways for all the cell models acutely or repeatedly exposed to PM₂.₅. However, one of the important highlight of our findings is that the prolonged and repeated exposure in BEAS-2B, NHBE and in particular sensible COPD-DHBE cells further caused an oxidative boost able to partially inactivate the NRF2 signaling pathway and to critically impair mitochondrial redox homeostasis, thereby producing a persistent mitochondrial dysfunction and a lowering cell energy supply.