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3-monochloro-1,2-propanediol (3-MCPD) is a food contaminant believed to be harmful to human health. Previous studies showed that 3-MCPD exerts toxic effects in multiple tissues, but whether 3-MCPD affects female reproductive function remained unknown. Here, using mouse gastric lavage models, we report that 3-MCPD exposure for four weeks affected body growth, decreased the ovary/body weight ratio, and increased atretic follicle numbers. Expression levels of follicular development-related factors decreased. Further studies found that ovaries from 3-MCPD exposed mice had activated the Transforming Growth Factor-β (TGF-β) signaling pathway and promoted ovarian fibrosis. Increased TNF-α, IL-1 and NF-κB expression also indicated the occurrence of ovarian inflammation. Exposure to 3-MCPD stimulated the caspase pathway and enhanced granulosa cell apoptosis. Consistent with disrupted ovarian homeostasis, 3-MCPD exposure interfered with mitochondrial function, generated more reactive oxygen species, increased ferrous ion and lipid peroxidation levels, and resulted in decreased oocyte development potential. Collectively, these findings indicated that 3-MCPD exposure induced ovarian inflammation and fibrosis, and caused disorders of mitochondrial function and ferrous ion homeostasis in oocytes, which consequently disturbed follicle maturation and reduced oocyte quality. [Display omitted] • 3-MCPD exposure impaires mouse follicular development. • 3-MCPD exposure induces ovary fibrosis, inflammation and apoptosis. • 3-MCPD exposure decrease oocyte quality through oxidative stress. [ABSTRACT FROM AUTHOR]

Chloroacetonitrile (CAN) is a halogenated acetonitrile often produced while disinfecting drinking water. Previous studies have shown that maternal exposure to CAN interferes with fetal development; however, the adverse effects on maternal oocytes remain unknown. In this study, in vitro exposure of mouse oocytes to CAN reduced maturation significantly. Transcriptomics analysis showed that CAN altered the expression of multiple oocyte genes, especially those associated with the protein folding process. CAN exposure induced reactive oxygen species production, accompanied by endoplasmic reticulum (ER) stress and increased glucose regulated protein 78, C/EBP homologous protein and activating transcription factor 6 expression. Moreover, our results indicated that spindle morphology was impaired after CAN exposure. CAN disrupted polo-like kinase 1, pericentrin and p-Aurora A distribution, which may be an origin inducer that disrupts spindle assemble. Furthermore, exposure to CAN in vivo impaired follicular development. Taken together, our findings indicate that CAN exposure induces ER stress and affects spindle assembly in mouse oocytes. [Display omitted] [ABSTRACT FROM AUTHOR]

Herein, using manganese dioxide octahedral molecular sieve (Mn-OMS) as the catalyst, we investigate how pollutant electron property affects the peroxymonosulfate (PMS) activation mechanism. More than 95% of electron-rich pollutants are degraded in the Mn-OMS/PMS system after 30 min reaction time, but oxidative decomposition of electron-poor pollutants takes at least 150 min. This difference in reaction rate is proved to be pollutant-dependent. We then combine multiple methods to cross-validate the PMS activation mechanism, including the quenching test, EPR characterization, solvent-exchange experiment, PMS decomposition rate test, and electrochemical analysis. Catalyst-mediated electron transfer is determined as the main activation mechanism for electron-rich pollutants degradation, while removal of electron-poor pollutants relies on singlet oxygen (1O 2) and/or radicals. Additionally, the PMS activation mechanism depends on whether H 2 O or pollutants or low-valence Mn ions preferentially transfer electrons to the adsorbed PMS. This work provides mechanistic insights into the effect of pollutants type on PMS activation. [Display omitted] • Pollutant type can induce the transformation of PMS activation mechanism. • Water molecules are indispensable reactants in singlet oxygen generation. • The sources of singlet oxygen are water molecules and peroxides. [ABSTRACT FROM AUTHOR]

[Display omitted] • The genotoxicity of TiO 2 NPs was confirmed at the single-cell level. • CINP, RPA3, and PRKACA served as biomarkers of TiO2 NPs exposure. • 5 nm and 14 nm TiO 2 NPs caused a response similar to antivirus defense. • Unique gene expression patterns were found within the same exposure of TiO2 NPs. Titanium dioxide nanoparticles (TiO 2 NPs) have attracted substantial attention in various applications, including environmental remediation and nanomedicine. A detailed understanding of the toxicity of TiO 2 NPs and the underlying mechanisms is fundamental to further development of their environmental and biomedical applications. Herein, we determined the changes in the transcriptional profile of human bone marrow stromal cells (BMSCs) after a set of different sized TiO 2 NPs exposure using single-cell RNA-seq (scRNA-seq). By taking advantage of sensitivity of scRNA-seq, we found that TiO 2 NPs exposure led to profound changes in gene expression and DNA damage signaling played a pivotal role in cellular responses to TiO 2 NPs exposure. Smaller TiO 2 NPs (5, 14 nm) led to a response similar to antivirus defense, and bigger TiO 2 NPs (54, 135, and 228 nm) induced proliferation and differentiation changes in transcriptional levels. Validation experiments on representative genes showed that some genes might be served as biomarkers of TiO 2 NPs exposure. Furthermore, in vitro and in vivo analyses showed remarkable over-production of reactive oxygen species (ROS) but did not affect osteogenic differentiation potential in BMSCs. The results unveiled landscape changes in transcriptomes in BMSCs induced by TiO 2 NPs, which provides new insights into toxicity assessments of nanomaterials. [ABSTRACT FROM AUTHOR]

[Display omitted] • Defective MoS 2 enhanced PCA removal of Fe3+/PS system compared with pristine MoS 2. • S defects in MoS 2 facilitated the cycle of Fe3+/Fe2+ to enhance PCA degradation. • S defects in MoS 2 increased the electron density around Mo. • S defects in MoS 2 enhanced the adsorption of Fe3+. Advanced oxidation processes (AOPs) based on persulfate (PS) has attracted great attention because of its outstanding performance for decomposing chlorinated aromatic hydrocarbons in wastewater. While Fe-based materials can effectively activate PS and are environment-friendly, the low stability of Fe2+ and little activation capability of Fe3+ limit the broad applications of Fe2+ (or Fe3+) activated PS system in practical applications. In this work, taking molybdenum disulfide (MoS 2) as the co-catalyst in Fe3+/PS system, we report a strongly enhanced persulfate activation efficiency of Fe3+/PS system by engineering S defects in MoS 2. The combination of experiments and density functional theory (DFT) calculation demonstrate that S defects in MoS 2 modify the surface charge distribution, leading to the formation of an electron deficient center near S defect and increasing the electron density near Mo site. As a result, more Fe3+ in Fe3+/PS system is reduced into Fe2+ by MoS 2 with S defects, resulting in more reactive oxygen species generated. Furthermore, S defects promote the adsorption of Fe3+ on the MoS 2 surface, which further enhance the activating performance for PS through promoting to form cycle of Fe3+/Fe2+. This work provides a new strategy for improving co-catalytic properties of MoS 2 and expands the application of Fe3+/PS system for contaminants remediation. [ABSTRACT FROM AUTHOR]

We report here the fabrication of BHPB loaded free-standing multilayered film via alternately depositing HA and PLL-BHPB complex and explore the underlying mechanism for its enhancing wound repair process. Of note, pre-assemble PLL with BHPB amplify PLL/HA film growth via accelerating the diffusion coefficient of PLL inside the film. [Display omitted] • LBL exponential growth is amplified by precursor assembly with charge-switchable BHPB. • BHPB neutralizes excess ROS and activates intracellular ROS scavenging mechanism. • BHPB incorporated PEM can stimulate Keap1/Nrf2/HO-1 axis to combat oxidative stress. The local oxidizing microenvironment and bacterial infection, as crucial internal and external factors that hinder the healing of diabetic wounds, are two main issues to be addressed in the design of novel wound dressing materials. As an attempt to provide optimal solution to the aforementioned problems, free-standing (FS) polyelectrolyte multilayer films (PEMs) loaded with bis[2-(4-hydroxyphenyl) benzimidazole] (BHPB) were constructed by layer-by-layer (LBL) self-assembly method. The exponential growth of LBL deposition as well as the film degradation were extensively studied, our results revealed that by pre-assembling polycation with the pH-sensitive BHPB molecule, the polycation diffusivity was largely accelerated thus greatly amplified LBL film growth, ensuring the facile detachment of the PEMs from the substrates to achieve FS films. The increase in BHPB content leaded to faster film growth and slower film degradation and more sustainable BHPB release. In terms of multifunctionality, which was ideal for the design of wound dressing material, the obtained FS films exhibited effective antimicrobial and antioxidant properties thanks to the addition of bioactive BHPB. Notably, unlike traditional antioxidant materials that only neutralize reactive oxygen species (ROS), the BHPB-loaded films stimulated the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) axis, which is a vital intercellular ROS scavenging system blocked by hyperglycemia. Moreover, the wound treated by BHPB-incorporated PEMs exhibited faster healing with increased collagen deposition, enhanced angiogenesis, and rapid re-epithelialization in rat diabetic cutaneous defect models. Overall, in the perspective of cost-effectiveness and simple fabrication, the composite BHPB incorporated FS films reported in the current study showed rather promising potential in the application of diabetic wound healing. [ABSTRACT FROM AUTHOR]