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6PPD and its oxidation product, 6PPD-quinone have garnered widespread attention due to their adverse effects on aquatic ecosystems and human health, and are recognized as emerging pollutants. In this study, we investigated the interaction mechanism between 6PPD/6PPD-quinone and human serum albumin (HSA) through various experiments. Experimental findings reveal that the IC 50 values of 6PPD-quinone and 6PPD against HEK293T cells were 11.78 and 40.04 μM, respectively. Additionally, the cytotoxicity of these compounds was regulated by HSA, displaying an inverse correlation with their binding affinity to HSA. Furthermore, 6PPD/6PPD-quinone can spontaneously insert into site I on HSA, forming a binary complex that induces changes in the secondary structure of HSA. However, their effects on the esterase-like activity of HSA exhibit a dichotomy. While 6PPD activates the esterase-like activity of HSA, 6PPD-quinone inhibits it. Molecular docking analyses reveal that both 6PPD and 6PPD-quinone interact with many amino acid residues on HSA, including TRP214, ARG222, ARG218, ALA291, PHE211. The π electrons on the benzene rings of 6PPD/6PPD-quinone play pivotal roles in maintaining the stability of complexes. Moreover, the stronger binding affinity observed between 6PPD and HSA compared to 6PPD-quinone, may be attributed to the larger negative surface potential of 6PPD., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

The eastern coastal region of China is the area with the highest emission of PAHs in China. Therefore, understanding the sources and health risk of parent polycyclic aromatic hydrocarbons (PPAHs) and their derivatives in eastern coastal cities of China is the main basis for air pollution control. In this study, we measured the concentrations of 18 parent PAHs, 17 nitrated PAHs, 7 oxygenated PAHs, 8 chlorinated PAHs, and 13 brominated PAHs in PM 1.0 and PM 2.5 samples collected at an urban coastal city site and a coastal background site in 2019. We analyzed the temporal distribution, molecular composition, and sources and performed health risk assessments for both winter and summer samples. The average concentration of the PPAHs and their derivatives (all 63 compounds combined) in the PM 1.0 samples accounted for 75.57% of the PAHs concentration in PM 2.5 samples. The average concentration of PM 2.5 - and PM 1.0 - bound PPAHs in winter was 114.70 times higher than in summer, and their derivatives was 27.51 times. Both the combined concentrations of the 18 PPAHs and the combined concentrations of the 45 derivatives were higher in the coastal city compared to the background site during the winter (1.90 and 1.48 times, respectively), but they were comparable during the summer. The positive matrix factorization analysis indicated that the compounds mainly originated from coal/biomass combustion, industrial sources, vehicle emissions, and secondary formation. In addition, the concentration-weighted trajectories model revealed that the PAHs were mainly emitted locally in Shandong Province and surrounding areas, such as Hebei Province, Henan Province, and Bohai Sea. The compounds 1-NPYR, 2+9-BrPHE, 9,10-Cl2PHE, and 1-ClPYR dominantly contributed to the derivatives of TEQ during the winter due to their high concentrations or the high TEFs of these compounds., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Phthalate esters (PAEs) are a type of persistent organic pollutants and have received widespread concerns due to their adverse effects on human health. Dicyclohexyl phthalate (DCHP) and its metabolite monocyclohexyl phthalate (MCHP) were selected to explore the mechanism for interaction of PAEs with human serum albumin (HSA) through molecular docking and several spectroscopic techniques. The results showed that DCHP/MCHP can spontaneously occupy site I to form a binary complex with HSA, and DCHP exhibited higher binding affinity to HSA than MCHP. At 298 K, the binding constants (K b ) of DCHP and MCHP to HSA were 24.82 × 10 4 and 1.04 × 10 4  M -1 , respectively. Hydrogen bonds and van der Waals forces were the major driving forces in DCHP/MCHP-HSA complex. The presence of DCHP/MCHP induced the secondary structure changes in HSA, and the pi electrons of the benzene ring skeleton of DCHP/MCHP played a key role in this binding processes. Exposure of DCHP/MCHP to TM4 cells revealed that interactions between PAEs and serum albumin can affect their cytotoxicity; DCHP showed higher toxicity than MCHP. The binding affinity of PAEs with HSA may be a valuable parameter for rapid assessment of their toxicity to organisms., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Microcystins-LR (MCLR) is a potent reproductive system toxin. We have previously shown that MCLR induced endoplasmic reticulum (ER) stress and apoptosis in testis. ER is the main calcium storage site in cells, and its calcium homeostasis plays an important role in the regulation of apoptosis. Hence, in the present study, we have investigated the role of calcium (Ca 2+ ) in inducing apoptosis and how it affect the mitochondria and endoplasmic reticulum in TM4 cells. Our study found that MCLR induced an increase in Ca 2+ concentration in TM4 cells. Compared to the controls, MCLR induced phosphorylation of calmodulin-dependent protein kinase II (CaMKII) which was involved in MAPKs activation, resulting in the induction of mitochondrial apoptosis pathways. Ca 2+ chelator Bapta-AM partially reversed MCLR-induced apoptosis, confirming the possible involvement of calcium homeostasis disruption after MCLR exposure. Meanwhile, MCLR activated unfolded protein response and activated the ER apoptotic pathway by activating caspase-12. In addition, exposure to MCLR causes mitochondrial defects and increased apoptosis by up-regulating caspase 3 and cytosol cytochrome c expression. Collectively, these results demonstrated that MCLR disturbed calcium homeostasis, which caused ER-mitochondria dysfunction, ultimately promoted cell apoptosis in Sertoli cells., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Obesity is considered as a chronic disease which seriously affecting people's health and daily life. Kiwifruit (Actinidia chinensis Planch) seed oil (KSO), as a by-product of kiwifruit processing, is rich in fatty acids. Conventional wisdom holds that KSO has many health benefits, but there is no scientific basis. Here, the relieving effects of KSO on obesity and its potential mechanism were investigated in high-fat diet (HFD)-induced C57BL/6 mice. Mice were divided into four groups: ND (normal diet); HFD; L-KSO and H-KSO (HFD supplemented with 1.0 and 3.0 mL/kg·bw of KSO per day, respectively). Results showed that continuous supplementation KSO for 12 weeks significantly decreased bodyweight, inguinal fat tissue weight, blood glucose, and HOMA-IR index and ameliorated serum lipids accumulation (TC, TG, HDL-C, and LDL-C). Relative mRNA expression of inflammatory cytokines (TNF-α, IL-6, IL-1β, COX-2, and iNOS) was down-regulated and expression of thermogenesis-related genes (PPAR-γ, UCP1, PGC1-α, and PRDM16) was up-regulated in the inguinal fat tissue of KSO treated mice. Principal component analysis showed that the microbial community compositions of four groups were different. KSO supplementation dramatically decreased the Firmicutes-to-Bacteroidetes ratio. Together, our findings demonstrated that long-term supplementation KSO ameliorates obesity by reducing inflammation, adipose thermogenesis and gut microbiota dysbiosis., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The presence of high concentrations of residual antibiotics and antibiotic resistance genes (ARGs) in soil may pose potential health and environmental risks. This study investigated the prevalence of plasmid-mediated quinolone resistance (PMQR) genes, copper resistance genes (CRGs), and the bacterial communities in a soil-ryegrass pot system co-polluted with copper and ciprofloxacin (CIP; 0, 20, or 80 mg kg -1 dry soil). Compared with the samples on day 0, the total relative abundances of the PMQR genes and mobile genetic elements (MGEs) were reduced significantly by 80-89% in the ryegrass and soil by the cutting stage (after 75 days). The abundances of PMQR genes and MGEs were reduced by 63-81% in soil treated with 20 mg kg -1 CIP compared with the other treatments, but the abundances of CRGs increased by 18-42%. The presence of 80 mg kg -1 CIP affected the microbial community structure in the soil by increasing the abundances of Acidobacteria and Thaumarchaeota, but decreasing those of Firmicutes. Redundancy analysis indicated that the pH and microbial composition were the main factors that affected the variations in PMQR genes, MGEs, and CRGs, where they could explain 42.2% and 33.3% of the variation, respectively. Furthermore, intI2 may play an important role in the transfer of ARGs. We found that 80 mg kg -1 CIP could increase the abundances of ARGs and CRGs in a soil-ryegrass pot system., (Copyright © 2018 Elsevier Ltd. All rights reserved.)