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Agricultural pesticides serve as effective controls of unwanted weeds and pests. However, these same chemicals can exert toxic effects in non-target organisms. To determine chemical modes of action, the toxicity ratio (TR) and critical body residues (CBRs) of 57 pesticides were calculated for Daphnia magna. Results showed that the CBR values of inert compounds were close to a constant while the CBR values of pesticides varied over a wider range. Although herbicides are categorized as specifically-acting compounds to plants, herbicides did not exhibit excess toxicity to Daphnia magna and were categorized as inert compounds with an average logTR = 0.41, which was less than a threshold of one. Conversely, fungicides and insecticides exhibited strong potential for toxic effects to Daphnia magna with an average logTR &gt;2. [https://www.selleckchem.com/products/ca-074-methyl-ester.html https://www.selleckchem.com/products/ca-074-methyl-ester.html] Many of these chemicals act via disruption of the nervous, respiratory, or reproductive system, with high ligand-receptor binding activity which leads to higher toxicity for Daphnia magna. Molecular docking using acetylcholinesterase revealed that fungicides and insecticides bind more easily with the biological macromolecule when compared with inert compounds. Quantitative structure-activity relationship (QSAR) analysis revealed that the toxicity of fungicides was mainly dependent upon the heat of formation and polar surface area, while the toxicity of insecticides was more related to hydrogen-bond properties. This comprehensive analysis reveals that there are specific differences in toxic mechanisms between fungicides and insecticides. These results are useful for determining relative risk associated with pesticide exposure to aquatic crustaceans, such as Daphnia magna.<br /><br /> Exposure to ambient fine particulate matter (PM<br /><br /> ) is associated with various adverse health outcomes. Although several mechanisms have been proposed including oxidative stress and inflammatory responses, the exact mechanism is still unknown. Few studies have investigated the mechanism linking PM<br /><br /> and blood pressure (BP). In this study, we measured urinary metabolites and BP -related renin-angiotensin-aldosterone system (RAAS) to investigate the associations between ambient PM<br /><br /> exposure and BP in healthy C57BL/6 mice.<br /><br /> The C57BL/6 mice were exposed to ambient concentrated PM<br /><br /> or filtered air (FA) for 16 weeks. Systolic BP and diastolic BP were measured by noninvasive BP system. The urine metabolites were quantified using the untargeted metabolomics approach. The expression of RAAS-related proteins angiotensin-converting enzyme (ACE)2, angiotensin (Ang) II, Ang (1-7) and aldosterone (ALD) were measured using Western blot and ELISA kits.<br /><br /> The metabolomics analysis demonstrated that PM<br /><br /> exposure induced significant changes of some metabolites in urine, including stress hormones, amino acids, fatty acids, and lipids. Furthermore, there was an elevation of BP, increase of serous Ang II and ALD, along with the decrease of ACE2 and Ang (1-7) in kidney in the PM<br /><br /> -exposed mice compared with FA-exposed mice.<br /><br /> The results demonstrated that PM<br /><br /> exposure-induced BP elevation might be associated with RAAS activation. Meanwhile, PM<br /><br /> exposure-induced changes of stress hormone and lipid metabolism might mediate the activation of RAAS. The results suggested that the systemic stress hormone and lipid metabolism was associated with the development of hypertension.<br /><br />The results demonstrated that PM2.5 exposure-induced BP elevation might be associated with RAAS activation. Meanwhile, PM2.5 exposure-induced changes of stress hormone and lipid metabolism might mediate the activation of RAAS. The results suggested that the systemic stress hormone and lipid metabolism was associated with the development of hypertension.Although the production and use of PCB153 have been banned globally, PCB153 pollution remains because of its persistence and long half-life in the environment. There is ongoing evidence that exposure to PCB153 may influence gut microbiota health and increase the risk of host health. It is needed to illuminate whether there are associations between gut microbiota dysregulation and PCB153-induced host diseases. Importantly, it is urgently needed to find specific strains as biomarkers to monitor PCB153 pollution and associated disorders. The work aims to investigate the change of gut microbiota composition, structure and diversity and various host physiological indexes, to ravel the chain causality of PCB153, gut microbiota health and host health, and to find potential gut microbiota markers for PCB153 pollution. Here, adult female mice were administrated with PCB153. Obtained results indicated that PCB153 led to gut microbiota health deterioration. PCB153 exposure also induced obesity, hepatic lipid accumulation, abdominal adipose tissue depots and dyslipidemia in mice. Furthermore, specific gut microbiota significantly correlated with the host health indexes. This work provides support for the relationship between gut microbiota aberrance derived from PCB153 and risk of host health, and offers some indications of possible indicative functions of gut microbiota on PCB153 pollution.Diamide insecticides, such as chlorantraniliprole, cyantraniliprole, and tetrachlorantraniliprole, are a new class of insecticides that selectively target insects by affecting calcium homeostasis. While this class of insecticides are effective on a wide range of insect pests, the toxicities of diamide insecticides vary among species and life stages. In this study, we addressed the mechanism underlying the different responses of Plutella xylostella and Pieris rapae to diamide insecticides. The susceptibility to insecticides of P. xylostella and P. rapae larvae was assessed 2 and 4 days after exposure to chlorantraniliprole, cyantraniliprole, and tetrachlorantraniliprole. P. xylostella larvae treated with distilled water (Group A), chlorantraniliprole (Group B), cyantraniliprole (Group C), and tetrachlorantraniliprole (Group D) and P. rapae larvae treated with distilled water (Group E), chlorantraniliprole (Group F), cyantraniliprole (Group G) and tetrachlorantraniliprole (Group H) were subjected to metabolomics analysis. The differential metabolites in the B vs. F, C vs. G, and D vs. H groups were analyzed, followed by pathway enrichment analysis. Chlorantraniliprole, cyantraniliprole, and tetrachlorantraniliprole all showed high toxicities for P. xylostella and P. rapae larvae. P. rapae larvae were more sensitive to the diamide insecticides than P. xylostella larvae. There were 65 overlapped differential metabolites between P. xylostella and P. rapae larvae treated with these three diamide insecticides. Pathway analysis showed that the differential metabolites were closely related with fatty acid biosynthesis and metabolism-related pathways. The differential regulation of fatty acid biosynthesis and metabolism may contribute to the different response to diamide insecticides in P. xylostella and P. rapae.Bone mineral density (BMD) changes were reported to be associated with excessive fluoride exposure and abnormal expression of RUNX2. However, whether the alteration of methylation status, a most commonly used marker for the alteration of gene expression in epidemiological investigation, of RUNX2 is associated with low-to-moderate fluoride exposure and BMD changes has not been reported. Our study aims to explore the role of RUNX2 promoter methylation in BMD changes induced by low-to-moderate fluoride exposure. A total of 1124 adults (413 men and 711 women) were recruited from Kaifeng City in 2017. We measured BMD using ultrasound bone densitometer. Concentrations of urinary fluoride (UF) were measured using ion-selective electrode, and the participants were grouped into control group (CG) and excessive fluoride group (EFG) according to the concentration of UF. We extracted DNA from fasting peripheral blood samples and then detected the promoter methylation levels of RUNX2 using quantitative methylation-specific PCR. Relationships between UF concentration, RUNX2 promoter methylation and BMD changes were analyzed using generalized linear model and logistic regression. Results showed in EFG (UF concentration &gt; 1.6 mg/L), BMD was negatively correlated with UF concentration (β -0.14; 95%CI -0.26, -0.01) and RUNX2 promoter methylation (β -0.13; 95%CI -0.22, -0.03) in women. The methylation rate of RUNX2 promoter increased by 2.16% for each 1 mg/L increment in UF concentration of women in EFG (95%CI 0.37, 3.96). No any significant associations between UF concentration, RUNX2 promoter methylation, and BMD were observed in the individuals in CG. Mediation analysis showed that RUNX2 promoter methylation mediated 18.2% (95% CI 4.2%, 53.2%) of the association between UF concentration and BMD of women in EFG. In conclusion, excessive fluoride exposure (&gt;1.6 mg/L) is associated with changes of BMD in women, and this association is mediated by RUNX2 promoter methylation.The chitin synthesis inhibitor teflubenzuron (TFB) is a feed antiparasitic agents used to impede molting of the salmon lice, an ecto-parasite that severely affects the salmon industry. Low absorption of oral administered TFB may cause elevated concentrations in the feces discharged from the salmon into the benthic environment. The polychaete Capitella sp. are often dominant in such habitats and consume organic waste deposited on the sediment. In the present study, Capitella sp. were exposed to doses of TFB in salmon feed of 1, 2 and 4 g TFB kg-1 (0 g TFB kg-1 in control group) over an experimental period of 32 days. Cumulative mortality was 12%-15% in both treatment groups with 1 and 2 g TFB kg-1 and reached 27% in the group with 4 g TFB kg-1. Only the highest dose (4 g TFB kg-1) negatively affected feed intake, growth and respiration of the polychaetes while food conversion efficiency was not affected. At the end of the experiment, the concentrations of TFB in the Capitella sp. were high, in the range of 9.24-10.32 μg g-1 for the three treatment groups. It was suggested that a maximum level of absorption rate was reached, also for the lowest dose. High concentrations of TFB in the Capitella sp. might pose a risk to crustaceans that forage for polychaetes in the vicinity of fish farms. We conclude that the effects of TFB on Capitella sp. may therefore primarily be to the predators rather than the Capitella sp.To evaluate the aquatic hazards of the insect juvenile hormone analogue fenoxycarb, a single application (0, 48.8, 156.3, 500, 1600, and 5120 μg/L) of it was done in indoor freshwater systems dominated by Daphnia carinata (daphnid) and Dolerocypris sinensis (ostracoda). The responses of zooplankton (counted by abundance and the activity and immuno-reactive content of free N-Acetyl-β-D-glucosaminidase (NAGase)), phytoplankton (counted by chlorophyll and phycocyanin), planktonic bacteria and fungi, and some water quality parameters were investigated in a period of 35 d. Results of the study showed that the ostracoda was more sensitive than daphnid, with time-weighted average (TWA)-based no observed effect concentrations (NOECs) to be 8.45 and 12.66 μg/L in systems without humic acid addition (HA-) and to be 6.37 and 9.54 μg/L in systems with humic acid addition (HA+). The duration of treatment-related effects in the ostracoda population was longer than the daphnid population (21 vs. 14 days). Besides, the data analysis indicated that the toxicity of fenoxycarb was significantly enhanced in the HA+ systems.