Enantioselective biomarkers of maize toxicity induced by hexabromocyclododecane based on submicroscopic structure, gene expression and molecular docking.

Hexabromocyclododecane (HBCD), as a monitored chemical of the Chemical Weapons Convention, the Stockholm Convention and the Action Plan for New Pollutants Treatment in China, raises significant concerns on its impact of human health and food security. This study investigated enantiomer-specific biomarkers of HBCD in maize (Zea mays L.). Upon exposure to HBCD enantiomers, the maize root tip cell wall exhibited thinning, uneven cell gaps, and increased deposition on the cell outer wall. Elevated malondialdehyde (MDA) indicated lipid peroxidation, with higher mitochondrial membrane potential (MMP) inhibition in (+)-enantiomer treatments (47.2%-57.9%) than (-)-enantiomers (14.4%-37.4%). The cell death rate significantly increased by 37.7%-108.8% in roots and 16.4%-62.4% in shoots, accompanied by the upregulation of superoxide dismutase isoforms genes. Molecular docking presenting interactions between HBCD and target proteins, suggested that HBCD has an affinity for antioxidant enzyme receptors with higher binding energy for (+)-enantiomers, further confirming their stronger toxic effects. All indicators revealed that oxidative damage to maize seedlings was more severe after treatment with (+)-enantiomers compared to (-)-enantiomers. This study elucidates the biomarkers of phytotoxicity evolution induced by HBCD enantiomers, providing valuable insights for the formulation of more effective policies to safeguard environmental safety and human health in the future.

Microwave-Assisted One Pot Cascade Conversion of Furfural to γ-Valerolactone over Sc(OTf)3.

γ-Valerolactone (GVL) is considered as a star biochemical which can be used as a green solvent, fuel additive and versatile organic intermediate. In this study, metal triflate (M(OTf)n ) was utilized as the catalyst for one-pot transformation of furfural (FF) to GVL in alcohol media under microwave irradiation. Alcohol plays multiple functions including solvent, hydrogen donor and alcoholysis reagent in this cascade reaction process. And process efficiency of GVL production from FF upgrading is strongly related to the effective charge density of selected catalyst and the reduction potential of selected alcohol. Complex (OTf)n -M-O(H)R, presenting both Brønsted acid and Lewis acid, is the real catalytic active species in this cascade reaction process. Among various catalysts, Sc(OTf)3 exhibited the best catalytic activity for GVL production. Various reaction parameters including the Sc(OTf)3 amount, reaction temperature and time were optimized by the response surface methodology with the central composite design (RSM-CCD). Up to 81.2 % GVL yield and 100 % FF conversion were achieved at 143.9 °C after 8.1 h in the presence of 0.16 mmol catalyst. This catalyst exhibits high reusability and can be regenerated by oxidative degradation of humins. In addition, a plausible cascade reaction network was proposed based on the distribution of product.

Recent advances in catalytic synthesis of 2,5-furandimethanol from 5-hydroxymethylfurfural and carbohydrates.

5-Hydroxymethylfurfural (HMF) is a versatile platform chemical derived from the dehydration of renewable carbohydrates (typically glucose/fructose-based monosaccharides, oligosaccharides, and polysaccharides). Some useful compounds, such as 2,5-furandimethanol (FDM), 2,5-dimethylfuran (DMF) and 2,5-dimethyltetrahydrofuran (DMTHF), have been synthesized by reduction of HMF. Among these, FDM is a promising diol and can be further converted towards fine chemicals, liquid fuels and polymer materials. In this review, some typical catalytic systems for the synthesis of FDM from both HMF and carbohydrates were summarized. The discussion focused on controlling the reaction networks for the reduction of HMF. The reaction mechanisms and the stability of the catalysts were introduced briefly. Last but not least, the prospects of effective production of FDM were discussed as well.

[Retracted] Methylation­induced downregulation and tumor-suppressive role of microRNA­98 in glioma through targeting Sal­like protein 4.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the cell Transwell assay data in the article (featured in Figs. 4D and 6D) were strikingly similar to data appearing in different form in other articles by different authors at different research institutions, which were already under consideration for publication or had already been published elsewhere at the time of the present article's submission. Owing to the fact that the contentious data in the above article had already appeared in different form in other articles prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 41: 2651-2659, 2018; DOI: 10.3892/ijmm.2018.3464].

Methylation-induced downregulation and tumor-suppressive role of microRNA-98 in glioma through targeting Sal-like protein 4.

MicroRNAs (miRs) have been found to play key roles in various human cancers, but the detailed regulatory mechanism of miR-98 in glioma remains largely unknown. The findings of the present study demonstrated that miR-98 was frequently downregulated in glioma tissues and cell lines (U87, U251, U373 and SHG44), and the decreased miR-98 levels were associated with DNA methylation. Treatment with 5-Aza-20-deoxycytidine, a DNA methyltransferase inhibitor, significantly increased the expression of miR-98 in glioma cells. Moreover, both miR-98 downregulation and methylation were significantly associated with a more aggressive tumor phenotype in glioma, as well as shorter survival time of glioma patients. Restoration of miR-98 expression caused a marked decrease in the migration and invasion of U87 cells, but did not affect cell proliferation. Sal-like protein 4 (SALL4) was further identified as a novel target gene of miR-98, and its protein expression was negatively regulated by miR-98 in U87 cells. Restoration of SALL4 expression reversed the suppressive effects of miR-98 on the migration and invasion of U87 cells. Furthermore, SALL4 was significantly upregulated in glioma tissues and cell lines, and an inverse correlation between miR-98 and SALL4 expression in glioma tissues was identified. In addition, the increased expression of SALL4 was significantly associated with glioma progression. Taken together, these data demonstrated that downregulation of miR-98, induced by methylation, promotes glioma cell migration and invasion via targeting SALL4. Therefore, miR-98 may become a potential therapeutic candidate for glioma.