The overnight stagnation of tap water in plumbing systems can lead to water quality deterioration. Meanwhile, the indoor heating can improve the indoor temperature in cold areas during winter, which may affect the quality of tap water during stagnation. However, indoor heating drives bacterial ecological links with tap water stagnation during winter are not well understood. The results indicated that the water temperature increased significantly after stagnation during indoor heating periods. Moreover, the average intact cell number and total adenosine triphosphate (ATP) concentration increased 1.53-fold and 1.35-fold after stagnation, respectively (P < 0.01). In addition, the increase in the ATP per cell number indicated that the combined effects of stagnation and indoor heating could enhance the bacterial activity. Biolog data showed that the bacterial community metabolic capacity was significantly higher in stagnant water than that of fresh water. Co-occurrence networks suggested that the bacterial metabolic profile changed after stagnation during the heating periods. DNA analysis indicated that the composition of the bacterial community changed dramatically after stagnation. The abundances of potential pathogens such as Mycobacterium sp. and Pseudomonas sp. also increased after stagnation. These results will give novel insights on comprehensive understanding the combined effects of indoor heating and overnight stagnation on the water bacterial community ecology of plumbing systems, and provide a scientific basis for tap water quality management after overnight stagnation during the indoor heating periods.

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.

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.

Glyphosate-based herbicides, the most extensively used herbicides in the world, are available in an enormous number of commercial formulations with varying additives and adjuvants. Here, we study the effects of one such formulation, Credit41, in two genetically diverse yeast strains. A quantitative trait loci (QTL) analysis between a sensitive laboratory strain and a resistant strain linked mitochondrial function to Credit41 resistance. Two genes encoding mitochondrial proteins identified through the QTL analysis were HFA1, a gene that encodes a mitochondrial acetyl CoA carboxylase, and AAC3, which encodes a mitochondrial inner membrane ATP/ADP translocator. Further analysis of previously studied whole-genome sequencing data showed that, although each strain uses varying routes to attain glyphosate resistance, most strains have duplications of mitochondrial genes. One of the most well-studied functions of the mitochondria is the assembly of Fe–S clusters. In the current study, the expression of iron transporters in the transcriptome increased in cells resistant to Credit41. The levels of iron within the cell also increased in cells exposed to Credit41 but not pure glyphosate. Hence, the additives in glyphosate-based herbicides have a significant contribution to the negative effects of these commercial formulations on biological systems.

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.

Natural environments are receiving an increasing number of contaminants. Therefore, the evaluation and identification of early responses to pollution in these complex habitats is an urgent and challenging task. Doñana National Park (DNP, SW Spain) has been widely used as a model area for environmental studies because, despite its strictly protected core, it is surrounded by numerous threat sources from agricultural, mining and industrial activities. Since many pollutants often induce oxidative stress, redox proteomics was used to detect redox-based variations within the proteome of Mus spretus mice captured in DNP and the surrounding areas. Functional analysis showed that most differentially oxidized proteins are involved in the maintenance of homeostasis, by eliciting mechanisms to respond to toxic substances and oxidative stress, such as antioxidant and biotransformation processes, immune and inflammatory responses, and blood coagulation. Furthermore, changes in the overall protein abundance were also analysed by label-free quantitative proteomics. The upregulation of phase I and II biotransformation enzymes in mice from Lucio del Palacio may be an alert for organic pollution in the area located at the heart of DNP. Metabolic processes involved in protein turnover (proteolysis, amino acid catabolism, new protein biosynthesis and folding) were activated in response to oxidative damage to these biomolecules. Consequently, aerobic respiratory metabolism increased to address the greater ATP demands. Alterations of cholesterol metabolism that could cause hepatic steatosis were also detected. The proteomic detection of globally altered metabolic and physiological processes offers a complete view of the main biological changes caused by environmental pollution in complex habitats.

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.

Perfluorooctanoic acid (PFOA) toxicity is of considerable concern due to its wide application, environmental persistence, and bioaccumulation. In the current study, we used a scaffold-free three-dimensional (3D) spheroid model of mouse liver cells (AML12) to explore the toxicity of PFOA and emerging alternatives (HFPO-DA and PFO4DA). Comparing the short-term (24 and 72 h treatment) toxicity of PFOA between conventional 2D monolayer cells and 3D spheroids, we found that spheroids had higher EC₅₀ values and lower ROS levels after treatment, indicating their greater resistance to PFOA. Cell viability (i.e., adenosine triphosphate (ATP) content and lactate dehydrogenase (LDH) leakage) and liver-specific function (i.e., albumin secretion) were stable in spheroids through 28 day of culture. However, under 100 and 200 μM-PFOA treatment for 28 day, ROS levels, LDH leakage, and caspase3/7 activity all increased significantly. As a sensitive parameter, ROS showed a significant increase at 21 day, even in the 50 μM-PFOA group. Consistent with the elevation of ROS and caspase3/7, the expressions of oxidative stress- and apoptosis-related genes, including Gsta2, Nqo1, Ho-1, caspase3, p53, and p21, were induced in dose- and time-dependent manners after PFOA exposure. The peroxisome proliferator-activated receptor alpha (PPARα) pathway was also activated after treatment, with significant induction of its target genes, Fabp4 and Scd1. Similar to PFOA, both HFPO-DA and PFO4DA activated the PPARα pathway, induced ROS levels, and initiated cell damage, though at a relatively lower extent than that of PFOA. Our results imply that the 3D spheroid model is a valuable tool in chronic toxicological studies.

Di-(2-ethylhexyl) phthalate (DEHP) is a prevalent environmental contaminant that severely impacts the health of human and animals. Taxifolin (TAX), a plant flavonoid isolated from yew, exerts protective effects on cardiac diseases. Nevertheless, whether DEHP could induce cardiomyocyte hypertrophy and its mechanism remains unclear. This study aimed to highlight the specific molecular mechanisms of DEHP-induced cardiomyocyte hypertrophy and the protective potential of TAX against it. Chicken primary cardiomyocytes were treated with DEHP (500 μM) and/or TAX (0.5 μM) for 24 h. The levels of glucose and adenosine triphosphate (ATP) were detected, and cardiac hypertrophy-related genes were validated by real-time quantitative PCR (qRT-PCR) and Western blot (WB) in vitro. The results showed that DEHP-induced cardiac hypertrophy was ameliorated by TAX, as indicated by the increased cardiomyocyte area and expression of atrial natriuretic peptide (ANP), natriuretic peptides A-like (BNP) and β-myosin heavy cardiac muscle (β-MHC). Furthermore, DEHP induced cardiac hypertrophy via the interleukin 6 (IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway in vitro. In addition, DEHP disrupted mitochondrial function and glycometabolism by activating the insulin-like growth factor 1 (IGF1)/phosphatidylinositol 3-kinase (PI3K) pathway and the peroxisome proliferator activated receptors (PPARs)/PPARG coactivator 1 alpha (PGC-1α) pathway to induce cardiac hypertrophy in vitro. Intriguingly, those DEHP-induced changes were obviously alleviated by TAX treatment. Taken together, cardiac hypertrophy was induced by DEHP via activating the IL-6/JAK/STAT3 signaling pathway, triggering glycometabolism disorder and mitochondrial dysfunction in vitro, can be ameliorated by TAX. Our findings may provide a feasible molecular mechanism for the treatment of cardiomyocyte hypertrophy induced by DEHP.

The top-selling strobilurin, azoxystrobin (AZ), is a broad-spectrum fungicide that protects against many kinds of pathogenic fungi by preventing their ATP production. The extensive use of AZ can have negative consequences on non-target species and its effects and toxic mechanisms on algae are still poorly understood. In this work, Chlorella pyrenoidosa that had been grown in BG-11 medium was exposed to AZ (0.5–10 mg L⁻¹) for 10 d. The physiological and molecular responses of the algae to AZ treatment, including photosynthetic efficiency, lipid peroxidation level, antioxidant enzyme activities, as well as transcriptome-based analysis of gene expression, were examined to investigate the potential toxic mechanism. Results shows that the photosynthetic pigment (per cell) increased slightly after AZ treatments, indicating that the photosystem of C. pyrenoidosa may have been strengthened. Glutathione and ascorbate contents were increased, and antioxidant enzyme activities were induced to relieve oxidative damage (e.g., from lipid peroxidation) in algae after AZ treatment. Transcriptome-based analysis of gene expression combined with physiological verification suggested that the 5 mg L⁻¹ AZ treatment did not inhibit ATP generation in C. pyrenoidosa, but did significantly alter amino acid metabolism, especially in aspartate- and glutamine-related reactions. Moreover, perturbation of ascorbate synthesis, fat acid metabolism, and RNA translation was also observed, suggesting that AZ inhibits algal cell growth through multiple pathways. The identification of AZ-responsive genes in the eukaryotic alga C. pyrenoidosa provides new insight into AZ stress responses in a non-target organism.