Lung injuries induced by ozone exposure in female mice: Potential roles of the gut and lung microbes.

Ozone (O3) is one of the most harmful pollutants affecting health. However, the potential effects of O3 exposure on microbes in the gut-lung axis related to lung injuries remain elusive. In this study, female mice were exposed to 0-, 0.5- and 1-ppm O3 for 28 days, followed by routine blood tests, lung function tests and histopathological examination of the colon, nasal cavity and lung. Mouse faeces and lungs were collected for 16s rRNA sequencing to assess the overall microbiological profile and screen for key differential enriched microbes (DEMs). The key DEMs in faecal samples were Butyricimonas, Rikenellaceae RC9 and Escherichia-Shigella, whereas those in lung samples were DNF00809, Fluviicola, Bryobacter, Family XII AD3011 group, Sharpea, MND1 and unclassified Phycisphaeraceae. After a search in microbe-disease databases, these key DEMs were found to be associated with lung diseases such as lung neoplasms, cystic fibrosis, pneumonia, chronic obstructive pulmonary disease, respiratory distress syndrome and bronchiectasis. Subsequently, we used transcriptomic data from Gene Expression Omnibus (GEO) with exposure conditions similar to those in this study to cross-reference with Comparative Toxicogenomic Database (CTD). Il-6 and Ccl2 were identified as the key causative genes and were validated. The findings of this study suggest that exposure to O3 leads to significant changes in the microbial composition of the gut and lungs. These changes are associated with increased levels of inflammatory factors in the lungs and impaired lung function, resulting in an increased risk of lung disease. Altogether, this study provides novel insights into the role of microbes present in the gut-lung axis in O3 exposure-induced lung injury.

Triazole fungicides exert neural differentiation alteration through H3K27me3 modifications: In vitro and in silico study.

Considering that humans are unavoidably exposed to triazole fungicides through the esophagus, respiratory tract, and skin contact, revealing the developmental toxicity of triazole fungicides is vital for health risk assessment. This study aimed to screen and discriminate neural developmental disorder chemicals in commonly used triazole fungicides, and explore the underlying harmful impacts on neurogenesis associated with histone modification abnormality in mouse embryonic stem cells (mESCs). The triploblastic and neural differentiation models were constructed based on mESCs to expose six typical triazole fungicides (myclobutanil, tebuconazole, hexaconazole, propiconazole, difenoconazole, and flusilazole). The result demonstrated that although no cytotoxicity was observed, different triazole fungicides exhibited varying degrees of alterations in neural differentiation, including increased ectodermal differentiation, promoted neurogenesis, increased intracellular calcium ion levels, and disturbance of neurotransmitters. Molecular docking, cluster analysis, and multiple linear regressions demonstrated that the binding affinities between triazole fungicides and the Kdm6b-ligand binding domain were the dominant determinants of the neurodevelopmental response. This partially resulted in the reduced enrichment of H3K27me3 at the promoter region of the serotonin receptor 2 C gene, finally leading to disturbed neural differentiation. The data suggested potential adverse outcomes of triazole fungicides on embryonic neurogenesis even under sublethal doses through interfering histone modification, providing substantial evidence on the safety control of fungicides.

New insights into triazole fungicide-caused hematopoietic abnormality in zebrafish based on GRα screening developmental toxicity.

Triazole fungicides (TFs) are known to be common environmental contaminants that can be toxic to aquatic animals, but their developmental toxicity is not fully understood. To address this gap, we first used a glucocorticoid receptor α (GRα)-mediated dual luciferase reporter gene system to explore the possible development toxicity of ten TFs and found that flusilazole (FLU) exhibited stronger agonistic activity against GRα. Subsequent transcriptome sequencing showed that FLU exposure affected GRα activation and hematopoiesis associated with a variety of biological processes, including responses to corticosteroid release, embryonic hematopoiesis, erythroid differentiation, and the development of hematopoietic or lymphoid organs. Furthermore, based on in situ hybridization and staining techniques, we clarified that FLU decreased the expression of the primitive hematopoietic marker genes gata1 and pu.1. and caused the defects in the posterior blood island (PBI), thereby impacting intermediate hematopoietic processes. Also, FLU significantly reduced the expression of the crucial hematopoietic gene cmyb and disrupted the production of erythrocytes and bone marrow cells during definitive hematopoiesis. Consistently, we found that FLU induced lesions in the kidney, a hematopoietic organ, including the infiltration of inflammatory cells, tubular collapse, reduced tubular filtration area, and interstitial hydronephrosis. We also found that FLU increased aberrant red blood cells in the peripheral blood of zebrafish. These findings provide new insights into the developmental toxicity and ecotoxicological risk of TFs.

Potential toxicity of landfill leachate to zebrafish and mung beans.

Landfill leachate has become a major public health concern due to its adverse health effects. However, its toxicological effects have not been thoroughly determined because of its complex composition. To address this issue, two model organisms were used in this study, including mung beans and zebrafish. Bean seedlings were exposed to different concentrations of landfill leachate (1%, 5%, 10%, 15%, and 20%, v/v, leachate/deionized water) for 7 days. Low concentrations (1%) of landfill leachate increased the growth of mung beans, whereas high concentrations (15% and 20%) of landfill leachate inhibited the growth and development of seedlings. Furthermore, landfill leachate reduced chlorophyll levels but increased malondialdehyde levels, leading to an increased rate of root-tip micronuclei. Zebrafish embryos were exposed to different concentrations of landfill leachate (0.5%, 1.0%, 1.2%, and 1.5%, v/v, leachate/E3 medium) for 120 h. The results showed that landfill leachate significantly decreased lower levels of hatching rate and heart rate but increased the mortality and malformation rates of embryos. Moreover, 1.0% landfill leachate reduced the frequency of spontaneous movement and the light stimulation reaction of embryos. Embryos exposed to leachate showed less exploratory behavior and fewer mirror attacks in the black and white areas. Our results suggest that exposure to landfill leachate could cause developmental toxicity and genotoxicity in plants and fish. The findings can improve our understanding of the environmental toxicity of landfill leachate and provide additional evidence for its risk assessment and management.

Transcriptome sequencing analysis reveals a potential role of lncRNA NONMMUT058932.2 and NONMMUT029203.2 in abnormal myelin development of male offspring following prenatal PM2.5 exposure.

Numerous epidemiological studies have shown that PM2.5 exposure in early life can influence brain development and increase the risk of neurodevelopmental disorders in boys, but the underlying molecular mechanisms remain unclear. In the current study, pregnant C57BL/6 J mice were oropharyngeally administered with PM2.5 suspension (3mg/kg/2 days) until the birth of offspring. Based on mRNA expression profiles, two-way analysis of variance (two-way ANOVA) and weighted gene co-expression network analysis (WGCNA) were conducted to explore the most impacted neurodevelopmental processes in male offspring and the most significantly associated gene modules. Gene Ontology (GO) enrichment and Encyclopedia of Genes and Genomes (KEGG) pathway analyses suggested that prenatal PM2.5 exposure significantly altered several biological processes (such as substrate adhesion-dependent cell spreading, myelination, and ensheathment of neurons) and KEGG pathways (such as tight junction and axon guidance). We further found that PM2.5 exposure significantly changed the expression of myelination-related genes in male offspring during postnatal development and impaired myelin ultrastructure on PNDs 14 and 21, as demonstrated by the decreased thickness of myelin sheaths in the optic nerves, and mild loss of myelin in the corpus callosum. Importantly, lncRNA NONMMUT058932.2 and NONMMUT029203.2 played key roles in abnormal myelination by regulating the expression of several myelination-related genes (Fa2h, Mal, Sh3tc2, Trf and Tppp) through the binding to transcription factor Ctcf. Our work provides genomic evidence for prenatal PM2.5 exposure-induced neurodevelopmental disorders in male offspring.

Prenatal PM2.5 exposure impairs spatial learning and memory in male mice offspring: from transcriptional regulation to neuronal morphogenesis.

BACKGROUND: As one of the environmental risk factors for human health, atmospheric fine particulate matter (PM2.5) contributes to cognitive deterioration in addition to respiratory and cardiovascular injuries. Recently, increasing evidence implicates that PM2.5 inhalation can affect neurological functions in offspring, but the sex-specific outcomes and the underlying biological processes are largely unknown. OBJECTIVES: To observe the influence of prenatal PM2.5 exposure on cognitive performance in offspring, to elucidate the neuronal morphological alterations and possible transcriptional regulation based on mRNA-sequencing (mRNA-Seq) data after birth, and to determine the key components of PM2.5 contributing to the adverse effects. METHODS: Pregnant C57BL/6J mice were exposed to sterile saline or PM2.5 suspension. Morris water maze test was used to assess the cognitive function in weanling offspring. Microscopic observation was applied to detect neuronal morphogenesis in vivo and in vitro. The cortex tissues from male offspring were collected on postnatal days (PNDs) 1, 7, and 21 for mRNA-Seq analysis. The organic and inorganic components of PM2.5 were separated to assess their contributions using primary cultured neurons. RESULTS: Prenatal PM2.5 exposure impaired spatial learning and memory in weanling male mice, but not female mice. The sex-specific outcomes were associated with mRNA expression profiles of the cortex during postnatal critical windows, and the annotations in Gene Ontology (GO) of differentially expressed genes (DEGs) revealed that the exposure persistently disrupted the expression of genes involved in neuronal features in male offspring. Consistently, axonal growth impairment and dendritic complexity reduction were observed. Importantly, Homeobox A5 (Hoxa5), a critical transcription factor regulating all of the neuronal morphogenesis-associated hub genes on PNDs 1, 7, and 21, significantly decreased in the cortex of male offspring following PM2.5 exposure. In addition, both inorganic and organic components were harmful to axonal and dendritic growth, with organic components exhibiting stronger inhibition than inorganic ones. CONCLUSION: Prenatal PM2.5 exposure affected spatial learning and memory in male mice by disrupting Hoxa5-mediated neuronal morphogenesis, and the organic components, including polycyclic aromatic hydrocarbons (PAHs), posed more adverse effects than the inorganic components.

Association between maternal exposure to air pollution and gestational diabetes mellitus in Taiyuan, North China.

BACKGROUND: The effect of air pollution on human health has been a major concern, especially the association between air pollution and gestational diabetes mellitus (GDM). METHODS: In this study, we conducted a retrospective cohort study in Taiyuan, a typical energy production base in China. This study included 28,977 pairs of mothers and infants between January 2018 and December 2020. To screen for GDM, oral glucose tolerance test (OGTT) was performed in pregnant women at 24-28 weeks of gestation. Logistic regression was used to assess the trimester-specific association between 5 common air pollutants (PM10, PM2.5, NO2, SO2, and O3) and GDM, and the weekly-based association was also assessed using distributed lag non-linear models (DLNMs). Odds ratios (ORs) with 95 % confidence intervals (CIs) were calculated for the association between GDM and each air pollutant. RESULTS: The overall incidence of GDM was 3.29 %. PM2.5 was positively associated with GDM over the second trimester (OR [95 % CI], 1.105 [1.021, 1.196]). O3 was positively associated with GDM in the preconception period (OR [95 % CI], 1.125 [1.024, 1.236]), the first trimester (OR [95 % CI], 1.088 [1.019, 1.161]) and the 1st + 2nd trimester (OR [95 % CI], 1.643 [1.387, 1.945]). For the weekly-based association, PM2.5 was positively associated with GDM at 19-24 weeks of gestation, with the strongest association at week 24 (OR [95 % CI], 1.044 [1.021, 1.067]). PM10 was positively associated with GDM at 18-24 weeks of gestation, with the strongest association at week 24 (OR [95 % CI], 1.016 [1.003, 1.030]). O3 was positively associated with GDM during the 3rd week before conception to the 8th gestational week, with the strongest association at week 3 of gestation (OR [95 % CI], 1.054 [1.032, 1.077]). CONCLUSION: The findings are important for the development of effective air quality policies and the optimization of preventive strategies for preconception and prenatal care.

Tebuconazole mediates cognitive impairment via the microbe-gut-brain axis (MGBA) in mice.

Tebuconazole, one of the most widely used triazole fungicides, is reported to potentially pose a risk of inducing neurological disorders in human beings. Considering the increasing exposure, whether it could influence cognitive function remains to be elucidated. Herein, we used a mouse model to evaluate the potential cognitive risks and possible mechanisms from the continuous edible application of tebuconazole at low concentrations. Our study revealed that tebuconazole deteriorated spatial learning and memory and downregulated the expression of glutamate receptor subunits. Importantly, metagenomic analysis indicated that tebuconazole not only led to significant shifts in the composition and diversity of the gut microbiota but also changed intestinal homeostasis. Specifically, after exposure, tebuconazole circulated in the bloodstream and largely entered the gut-brain axis for disruption, including disturbing the Firmicutes/Bacteroidetes ratio, interrelated neurotransmitters and systemic immune factors. Moreover, pretreatment with probiotics improved immune factor expression and restored the deterioration of synaptic function and spatial learning and memory. The current study provides novel insights concerning perturbations of the gut microbiome and its functions as a potential new mechanism by which tebuconazole exposes cognitive function-related human health.

Environmental exposure to triazole fungicide causes left-right asymmetry defects and contributes to abnormal heart development in zebrafish embryos by activating PPARγ-coupled Wnt/ß-catenin signaling pathway.

Triazole fungicides have been widely used all over the world. However, their potential ecological safety and health risks remain unclear, especially their cardiac developmental toxicity. This study systematically investigated whether and how triazole fungicides could activate peroxisome proliferative activity receptor γ (PPARγ) to cause abnormal heart development. Among ten triazole fungicides, difenoconazole (DIF) exhibited the strongest agonistic activity and caused severe pericardial edema in zebrafish embryos, accompanied by a reduction in heart rate, blood flow and cardiac function. In vitro transcriptomic profile implicated that DIF inhibited the Wnt signaling pathway, and in vivo DIF exposure significantly increased the phosphorylation of ß-catenin (p = 0.0002) and altered the expression of related genes in zebrafish embryos. Importantly, exposure to DIF could activate PPARγ and inhibit the Wnt/ß-catenin signaling pathway, which changed the size of Kupffer's vesicle (KV) (p = 0.02), altered the expression of left-right (LR) asymmetry-related genes, caused cardiac LR asymmetry defect, and eventually led to abnormal heart development. These findings provide evidence for potential developmental toxicity of triazole fungicides and highlight the necessity of assessing their ecological safety and human health risks.

Prenatal PM2.5 exposure contributes to neuronal tau lesion in male offspring mice through mitochondrial dysfunction-mediated insulin resistance.

The epidemiological evidence has linked prenatal exposure to fine particulate matter (PM2.5) pollution with neurological diseases in offspring. However, the biological process and toxicological mechanisms remain unclear. Tau protein is a neuronal microtubule-associated protein expressed in fetal brain and plays a critical role in mediating neuronal development. Aberrant expression of tau is associated with adverse neurodevelopmental outcomes. To study whether prenatal exposure to PM2.5 pollution induce tau lesion in mice offspring and elucidate the underlying pathogenic mechanism, we exposed pregnant mice to PM2.5 (3 mg/kg b.w.) by oropharyngeal aspiration every other day. The results indicate that prenatal PM2.5 exposure induced hyperphosphorylation of tau in the cortex of postnatal male offspring, which was accompanied by insulin resistance through the IRS-1/PI3K/AKT signaling pathway. Importantly, we further found that prenatal PM2.5 exposure induced mitochondrial dysfunction by disrupting mitochondrial ultrastructure and decreasing the expression of rate-limiting enzymes (CS, IDH2 and FH) in the Krebs cycle and the subunits of mitochondrial complex IV and V (CO1, CO4, ATP6, and ATP8) during postnatal neurodevelopment. The findings suggest that prenatal PM2.5 exposure could induce tauopathy-like changes in male offspring, in which mitochondrial dysfunction-induced insulin resistance might play an important role.

Maternal NO2 exposure disturbs the long noncoding RNA expression profile in the lungs of offspring in time-series patterns.

Gestation is a sensitive window to nitrogen dioxide (NO2) exposure, which may disturb fetal lung development and lung function later in life. Animal and epidemiological studies indicated that long noncoding RNAs (lncRNAs) participate in abnormal lung development induced by environmental pollutant exposure. In the present study, pregnant C57BL/6J mice were exposed to 2.5 ppm NO2 (mimicking indoor occupational exposure) or clean air, and lncRNAs expression profiles in the lungs of offspring mice were determined by lncRNA-seq on embryonic day 13.5 (E13.5), E18.5, postnatal day 1 (P1), and P14. The lung histopathology examination of offspring was performed, followed by weighted gene coexpression network analysis (WGCNA), prediction of lncRNAs-target genes, and the biological processes enrichment analysis of lncRNAs. Our results indicated that maternal NO2 exposure induced hypoalveolarization on P14 and differentially expressed lncRNAs showed a time-series pattern. Following WGCNA and enrichment analysis, 2 modules participated in development-related pathways. Importantly, the expressions of related genes were altered, some of which were confirmed to be related to abnormal vascular development and even lung diseases. The research points out that the maternal NO2 exposure leads to abnormal lung development in offspring that might be related to altered lncRNAs expression profiles with time-series-pattern.

NO2 exposure contributes to cardiac hypertrophy in male mice through apoptosis signaling pathways.

Nitrogen dioxide (NO2) is one of the most common indoor and outdoor air pollutants. Inhalation of NO2 is associated with an increased risk of health problems, especially cardiovascular diseases. However, the underlying pathogenic mechanisms still remain unclear. In this study, we exposed C57BL/6J mice to NO2 (2.5 ppm, 5 h/d) for 28 days and found that NO2 inhalation induced cardiac dysfunction in male mice, but not in female mice, including left ventricular dilation and cardiac systolic dysfunction. Pathological staining showed that NO2 inhalation induced eccentric hypertrophy with enlarged individual cardiomyocytes, dilated left ventricle, and thinning of the left ventricular wall in male mice. The transcriptional analysis suggested that NO2 exposure could disrupt Ca2+ homeostasis, actin cytoskeletal reorganization, myocardial contractility, and vascular dilation in male mice. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that differentially expressed genes (DEGs) were closely associated with the apoptotic signaling pathways. These findings suggested that NO2 exposure caused cardiac eccentric hypertrophy and cardiac dysfunction through apoptotic signaling pathways, and contributed to cardiotoxicity.

Time series of transcriptome analysis in entire lung development stages provide insights into the origin of NO2 related lung diseases.

Lung growth is a critical window, when exposure to various pollutants can disturb the finely-tuned lung development and enhance risk of long-term structural and functional sequelae of lung. In this study, pregnant C57/6 mice were treated with NO2, and lungs of fetus/offspring were collected at different developmental windows and dynamic lung development was determined. The results showed that maternal NO2 exposure suppressed fetal weight, implying that fetal development can be disturbed. The time-series RNA-seq analysis of lungs showed that maternal NO2 exposure induced significant time-dependent changes in the expression profiles of genes associated with lung vein myocardium development in fetus/offspring. Most of these genes in NO2 exposure group were suppressed at middle gestation and at birth. Our results also indicated that the gene expressions of Nkx2.5 in NO2 exposure were suppressed to 0.27- and 0.44-fold of the corresponding Air group at E13.5 and PND1, and restored at later time points. This indicated that the transcription factor Nkx2.5 played an important role in abnormal lung development in fetus/offspring caused by maternal NO2 exposure. Importantly, gene expressions of lung vein myocardium development were related to transcription factors (TFs) and lung functions, and TFs showed similar trends with lung function. These results provide a comprehensive view of the adverse effects of maternal NO2 exposure on fetal lung development by uncovering molecular targets and related signaling pathways at the transcriptional level.

Bisphenol A Analogs Induce Cellular Dysfunction in Human Trophoblast Cells in a Thyroid Hormone Receptor-Dependent Manner: In Silico and In Vitro Analyses.

Bisphenol A (BPA) and its analogs are frequently detected in human daily necessities and environmental media. Placental thyroid hormone plays an important role in fetal development. Herein, we followed the adverse outcome pathway (AOP) to explore the toxic mechanisms of BPA and its analogs toward placental thyroid hormone receptor (TR). First, the TOX21 database was used, and the interactions between BPA analogs and the ligand-binding domains (LBDs) of two subtypes of TR (TRα and TRß) were subjected to in silico screening using molecular docking (MD) and molecular dynamics simulation (MDS). Fluorescence spectra and circular dichroism (CD) showed that BPA and its analogs interfere with TRs as a molecular initiation event (MIE), including static fluorescence quenching and secondary structural content changes in TR-LBDs. Key events (KEs) of the AOP, including the toxicity induced in placental chorionic trophoblast cells (HTR-8/SVneo) by an inverted U-shaped dose effect and changes in ROS levels, were tested in vitro. BPA, BPB, and BPAF significantly changed the expression level of TRß, and only BPAF significantly downregulated the expression level of TRα. In conclusion, our study contributes to the health risk assessment of BPA and its analogs regarding placental adverse outcomes (AOs).

Gestational exposure to NO2 aggravates placental senescence.

Placental senescence is a normal physiological process of placenta, while premature placental senescence has been confirmed to be associated with some adverse pregnancy complications. Epidemiological studies indicate that NO2 exposure can aggravate placental senescence which is represented by fibrosis and abnormal telomere homeostasis, etc. In this study, pregnant C57BL/6 mice were exposed to NO2 (2.5 ppm, 5 h/day) daily in a dynamic exposure chamber throughout the gestation period, and were sacrificed at embryonic day 13.5 (E13.5), E15.5 and E18.5. Placenta were harvested and conducted for histopathological examination and telomere evaluation. Our results showed that gestational NO2 exposure significantly aggravated placental fibrosis and calcification, and up-regulated the related bio-markers (connective tissue growth factor (Ctgf) and transforming growth factor-ß1 (Tgf-ß1)) at E18.5. In addition, gestational exposure to NO2 also activated senescence related pathway (p53/p21) at E18.5. Furthermore, gestational NO2 exposure significantly shortened telomere length at E18.5, and the expression of telomere homeostasis regulation genes telomeric repeat binding factor 1 (Trf1), protection of telomeres 1a (Pot1a) and Pot1b were significantly increased while telomerase reverse transcriptase (Tert) was suppressed after NO2 exposure at E13.5 or E18.5, respectively. Importantly, DNA methylation status of the 22nd at E13.5 and 32nd at E18.5 site in sub-telomeric region of chromosome 1 was significantly altered. Based on the above results, our present study indicated that gestational NO2 exposure could lead to premature placental senescence during the late trimester of pregnancy via aggravation of fibrosis and telomere length shortening regulated by telomere regulatory enzyme and DNA methylation.

Insights into the removal of polystyrene nanoplastics using the contaminated corncob-derived mesoporous biochar from mining area.

Nanoplastic has become a prominent threat to the aquatic ecosystem, and the cost-effective technologies for controlling that are still insufficient. The aim of this study is to use contaminated corncobs collected in mining area to prepare functional mesoporous biochar (MBC) and to investigate its ability to remove polystyrene nanoplastics (PSNPs) from water. The adsorption of PSNPs by MBC could be better described by the Sips isotherm and followed the second-order kinetics, with the theoretical maximum adsorption capacity of MBC for PSNPs was 56.02 mg·g-1. Then the PSNPs adsorbed on MBC could be hydrothermally degraded and the biochar could be simultaneously regenerated. The ability was affected by various factors, including oxygen-containing functional groups, metallic components, superoxide radicals and holes. The degradation products were dominated as low-molecule-weight oligomers and the main possible pathways involved scission, hydrolysis and radical reaction. The findings highlight the great potential of biochar prepared using contaminated biowaste in mining area to remove the nanoplastic pollutants in the aqueous environment.

New insights into potential estrogen agonistic activity of triazole fungicides and coupled metabolic disturbance.

Triazole fungicides are highly effective pesticides widely used in plant protection, which has caused potential hazards to human health and ecological safety. To fully understand their potential hepatotoxicity, we first analyzed the transcriptome profiles in HepG2 cells treated with five triazole fungicides (hexiconazole (HEX), tebuconazole (TEB), propiconazole (PRO), cyproconazole (CYP), and difenoconazole (DIF)), and found that these pesticides remarkably affected estrogen signaling pathways, especially estrogen synthesis. Furthermore, we found that TEB, CYP, PRO and DIF had agonistic activity towards estrogen receptor alpha (ERα) and elucidated the binding mode of triazole ligands with ERα using the reporter gene assay and molecular docking. Four triazole fungicides regulated eight major genes involved in estrogen synthesis (StAR, CYP11A1, 3ßHSD2, CYP17, CYP19, CYP3A4, CYP1A2 and SCP2) and stimulated the secretion of 17ß-estradiol (E2). Finally, we assessed possible metabolic outcomes caused by abnormal estrogen synthesis, and found that triazole fungicides affected the metabolism of various macromolecules (such as lipid, amino acid, and carbohydrate) and signal transduction. These findings will provide new insights into endocrine-disrupting effects of triazole fungicides and highlight their potential ecological and health risks.

Perioperative parenteral fish oil supplementation improves postoperative coagulation function and outcomes in patients undergoing colectomy for ulcerative colitis.

OBJECTIVE: Ulcerative colitis (UC) is an independent risk factor for thromboembolism, especially during the perioperative period. This study aimed to determine the effects of perioperative parenteral nutrition (PN) supplemented with fish oil (FO) on coagulation function and postoperative outcomes in patients with UC. METHODS: This retrospective cohort included 92 consecutive patients who underwent colectomy for UC. Postoperative coagulation indices and outcomes, including thromboelastography (TEG) findings and comprehensive complication index (CCI), were compared. The relative change in serum D-dimer (ΔD-dimer) levels and maximal amplitude (ΔMA) on TEG were also determined. RESULTS: Patients receiving PN supplemented with FO (n = 48) had lower D-dimer (P = .036) levels on postoperative day (POD) 5 and a higher MA (P < 0.001) on POD 1 than those who did not receive it (n = 44). A lower ΔD-dimer level (P = .048) and ΔMA (P < 0.001) were also observed in patients receiving FO. The incidence of major postoperative complications (6.3 vs 22.7%; P = .017) and CCI (20.9 vs 23.4%; P = .044) were significantly lower in patients receiving FO. In multivariate analysis, FO (odds ratio, 0.231; 95% confidence interval, 0.055-0.971; P = .046) was a positive protector of major postoperative complications. CONCLUSION: Perioperative PN supplemented with FO improved coagulation function and reduced major postoperative complications in patients with UC requiring colectomy. These results may provide cues in formulating management strategies for preventing thromboembolisms and postoperative complications in patients with UC.

Photo-degradation behavior of seven benzoylurea pesticides with C3N4 nanofilm and its aquatic impacts on Scendesmus obliquus.

Present concerns on the residual benzoylurea pesticides (BUPs) are rapidly climbing as their market shares increase and now seven typical compounds were picked to study their photo-degradation behavior and ecological impacts. Carbon nitride (C3N4) nanofilm at a thickness of 50-80 nm was built on the glass slides and utilized to evaluate the photostability of pesticides under visible light. The results showed that the nano-C3N4 can promote the degradation efficiency of BUPs and it follows the first-order dynamic mechanism. They could be divided into three categories with the substituents and their degradations were discriminated in order of chlorofluoro-, chlorofluoroalkoxy- and chlorofluorophenoxy- substituted ones. Analyzing the intermediates by UHPLC-MS, it can be speculated that the similar pathways came to BUPs such as cleavage of urea-bridge, hydroxylation and dehalogenation. It is attractive that they all passed into a same molecule, 2-fluorobenzamide (m/z, 301.14). Moreover Scendesmus obliquus was applied to indicate the ecological impacts of originals and their photoproducts. Exposed to pesticides, the levels of chlorophyll a demonstrated much more inhibition than chlorophyll b. Lufenuron and chlorfuazuron among seven showed the higher toxicity for algal cells and finally the photodegradation products showed the lowest toxicity. The activities of antioxidant enzymes happened to a significant remedy after photodegradation. It can be concluded that the residual BUPs under visible-light irradiation may degrade through similar pathways and reduce the aquatic toxicity with the presence of C3N4 nanofilm.