Selective oxidation of organic pollutants based on reactive oxygen species and the molecular structure: Degradation behavior and mechanism analysis.

The selective and rapid elimination of refractory organic pollutants from surface water is significant. However, the relationship of between reactive oxygen species (ROSs) and diversified pollutants molecular structures still needs to be further clarified. Here, we utilize polydopamine (PDA)-assisted coating strategy to prepare hollow 2D carbon nanosheet (ZPL-HCNS) and 2D Co3O4 nanosheet (ZPL-Co3O4) by thermolysis of PDA coated ZIF-L (ZIF-L@PDA) precursor under different gas atmosphere, which realizes the controlled generation of radicals and non-radicals. Organic pollutants including bisphenols, sulfonamides, quinolones, tetracyclines, and azo dyes are applied to assess the catalytic performance. Results show that dyes containing azo structure are more likely to be degraded by radical process, which is due to that the energy (ΔE) requirements to break the azo bond is higher than energy released from singlet oxygen to oxygen molecule and lower than that of sulfate radical to sulfate. Frontier molecular orbital theory HOMO-LUMO and Fukui function expounded the possible selectivity mechanism. In addition, the degradation pathway and biotoxicity test are carried out. This work provides a reference to illustrate the selective degradation for ROSs and molecular structure of pollutants.

Interaction mechanism between chlorinated polyfluoroalkyl ether potassium sulfonate (F-53B) and chromium on different types of soil surfaces.

The coexistence of per- and polyfluoroalkyl substances (PFASs) and heavy metals have been found in soils. However, the interaction between the combined pollutants in soils remains unclear. In this study, the adsorption processes of single and combined Cr(VI) and chlorinated polyfluoroalkyl ether potassium sulfonate (F-53 B) in red, yellow and black soils were simulated. When compared with the single F-53 B and Cr(VI), the adsorption amount of the combined F-53 B and Cr(VI) on soils changed with the types of soils. The interactions between F-53 B and Cr(VI) in soils affected their adsorption behavior. The adsorption of the combined F-53 B and Cr(VI) best fit second-order kinetics and the Freundlich equation. Moreover, aluminum and iron oxides are highly correlated with adsorption of F-53 B and Cr(VI). Both F-53 B and Cr(VI) can form complexes with aluminum and iron oxides through electrostatic interactions, but PFOS could be bridged with iron oxides to form an inner sphere complex and with aluminum oxides to form an outer sphere complex. The coexistence of F-53 B and Cr(VI) could change the fluorescent group of dissolved organic matter (DOM) in soils due to the complexation between F-53 B and DOM. In addition, F-53 B increased the acid-soluble portion of Cr and decreased its residual form, which promoted the environmental risk of Cr in soils.

Regulation of the formation and structure of biofilms by quorum sensing signal molecules packaged in outer membrane vesicles.

Quorum sensing signal molecules can be used to regulate the formation of biofilm, but it has not been reported that outer membrane vesicles (OMVs) can package and mediate signal molecules to regulate biofilm. We isolated and purified OMVs packaged with Pseudomonas quinolone signal (PQS) released by Pseudomonas aeruginosa and studied the effects of OMV-mediated PQS on the formation and structure of biofilms. OMV-mediated PQS promoted the growth of biofilm, and the cells in the biofilm were stretched, deformed and "bridged" with the surrounding cells. Raman spectrometry showed that the structure and components of the extracellular polymeric substances of P. aeruginosa changed; moreover extracellular proteins rather than polysaccharides played the dominant role in the formation of P. aeruginosa biofilms when regulated by OMV-mediated PQS. In the combination biofilm formed by P. aeruginosa and Staphylococcus aureus, the mediation of OMVs enhanced the inhibitory effect of PQS to the growth of S. aureus, resulting a decrease in EPS produced by the two bacteria. OMV-mediated PQS led to changes in the biodiversity, richness and structure of the microbial community in biofilms formed by active sludge. This work reveals the mechanism of OMVs mediated signal molecules regulating biofilm, which lays a new theoretical and practical foundation for guiding the operation of low-level of biofouling MBRs.

Fetal malnutrition is associated with impairment of endogenous melatonin synthesis in pineal via hypermethylation of promoters of protein kinase C alpha and cAMP response element-binding.

This study investigated whether and how fetal malnutrition would influence endogenous melatonin synthesis, and whether such effect of fetal malnutrition would transmit to the next generation. We enrolled 2466 participants and 1313 of their offspring. The urine 6-hydroxymelatonin sulfate and serum melatonin rhythm were measured. Methylation microarray detection and bioinformatics analysis were performed to identify hub methylated sites. Additionally, rat experiment was performed to elucidate mechanisms. The participants with fetal malnutrition had lower 6-hydroxymelatonin sulfate (16.59 ± 10.12 µg/24 hours vs 24.29 ± 11.99 µg/24 hours, P < .001) and arear under curve of melatonin rhythm (67.11 ± 8.16 pg/mL vs 77.11 ± 8.04 pg/mL, P < .001). We identified 961 differentially methylated sites, in which the hub methylated sites were locating on protein kinase C alpha (PRKCA) and cAMP response element-binding protein (CREB1) promoters, mediating the association of fetal malnutrition with impaired melatonin secretion. However, such effects were not observed in the offspring (all P > .05). Impaired histomorphology of pineal, decreased melatonin in serum, pineal, and pinealocyte were also found in the in vivo and in vitro experiments (P < .05 for the differences of the indicators). Hypermethylation of 10 CpG sites on the PRKCA promoter and 8 CpG sites on the CREB1 promoter were identified (all P < .05), which down-regulated PRKCA and CREB1 expressions, leading to decreased expression of AANAT, and then resulting in the impaired melatonin synthesis. Collectively, fetal malnutrition can impair melatonin synthesis through hypermethylation of PRKCA and CREB1 promoters, and such effects cannot be transmitted to the next generation.

Aging-related markers in rat urine revealed by dynamic metabolic profiling using machine learning.

The process of aging and metabolism is intimately intertwined; thus, developing biomarkers related to metabolism is critical for delaying aging. However, few studies have identified reliable markers that reflect aging trajectories based on machine learning. We generated metabolomic profiles from rat urine using ultra-performance liquid chromatography/mass spectrometry. This was dynamically collected at four stages of the rat's age (20, 50, 75, and 100 weeks) for both the training and test groups. Partial least squares-discriminant analysis score plots revealed a perfect separation trajectory in one direction with increasing age in the training and test groups. We further screened 25 aging-related biomarkers through the combination of four algorithms (VIP, time-series, LASSO, and SVM-RFE) in the training group. They were validated in the test group with an area under the curve of 1. Finally, six metabolites, known or novel aging-related markers, were identified, including epinephrine, glutarylcarnitine, L-kynurenine, taurine, 3-hydroxydodecanedioic acid, and N-acetylcitrulline. We also found that, except for N-acetylcitrulline (p < 0.05), the identified aging-related metabolites did not differ between tumor-free and tumor-bearing rats at 100 weeks (p > 0.05). Our findings reveal the metabolic trajectories of aging and provide novel biomarkers as potential therapeutic antiaging targets.

An isocaloric moderately high-fat diet extends lifespan in male rats and Drosophila.

The health effect of dietary fat has been one of the most vexing issues in the field of nutrition. Few animal studies have examined the impact of high-fat diets on lifespan by controlling energy intake. In this study, we found that compared to a normal diet, an isocaloric moderately high-fat diet (IHF) significantly prolonged lifespan by decreasing the profiles of free fatty acids (FFAs) in serum and multiple tissues via downregulating FFA anabolism and upregulating catabolism pathways in rats and flies. Proteomics analysis in rats identified PPRC1 as a key protein that was significantly upregulated by nearly 2-fold by IHF, and among the FFAs, only palmitic acid (PA) was robustly and negatively associated with the expression of PPRC1. Using PPRC1 transgenic RNAi/overexpression flies and in vitro experiments, we demonstrated that IHF significantly reduced PA, which could upregulate PPRC1 through PPARG, resulting in improvements in oxidative stress and inflammation and prolonging the lifespan.

Association of Prenatal Famine Exposure With Inflammatory Markers and Its Impact on Adulthood Liver Function Across Consecutive Generations.

Although there has been increasing recognition that famine exposure in the fetal stage damages liver function in adulthood, this deteriorated effect could be extended to the next generation remains vague. This study aimed to explore whether famine exposure was associated with liver function in the two consecutive generations, and its association with the mediation role of inflammatory markers. We analyzed the data of 2,681 participants from Suihua rural area, Heilongjiang Province, China. According to the date of birth, the participants were classified as fetal exposed and nonexposed. The F2 subjects were classified as having no parents exposed to famine, maternal famine exposure, paternal famine exposure, or parental famine exposure. In the mixed-effect models, prenatal exposure to famine was associated with the elevation of Δ aspartate aminotransferase (ΔAST) (ß: 0.22, 95% CI: 0.01, 0.43) and Δ alanine aminotransferase (ΔALT) (ß: 0.42, 95% CI: 0.19, 0.66) levels in F1 adults. The mediation analysis showed that the inflammatory markers including serum C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) might mediate the famine-liver function association. This longitudinal data were consistent with the hypothesis that the inflammatory markers explained part of the influence of prenatal famine exposure on liver function injury, and the natal mechanism was needed to be elucidated in the future study.