New insights into the degradation mechanism and risk assessment of HFPO-DA by advanced oxidation processes based on activated persulfate in aqueous solutions.

Hexafluoropropylene oxide dimer acid (HFPO-DA) is widely used as a substitute for perfluorooctanoic acid (PFOA). HFPO-DA exhibits high water solubility and low adsorption potential, conferring significant fluidity in aquatic environments. Given that the toxicity of HFPO-DA is similar to PFOA, it is necessary to control its content in aquatic environments. Electrochemical and thermally-activated persulfates have been successfully used to degrade HFPO-DA, but UV-activated persulfates cannot degrade the compound. Given that research on degradation mechanisms is still incomplete and lacks kinetic research, the mechanism and kinetic calculations of oxidative degradation were studied in detail using DFT calculations. And the toxicity of HFPO-DA degradation intermediates and products was evaluated to reveal the feasibility of using advanced oxidation process (AOP) technology based on persulfate to degrade HFPO-DA in wastewater. The results showed that the committed step of HFPO-DA degradation was initiated by the electron transfer reaction of SO4•- radicals. This reaction is not spontaneous at room temperature and requires sufficient electrical or thermal energy to be absorbed from the external environment. The perfluoroalcohol produced during this reaction can subsequently undergo four possible reactions: H atom abstraction from alcohol groups by an OH radical; H atom abstraction by SO4•-; direct HF removal; and HF removal with water as the catalyst. The final degradation products of HFPO-DA mainly include CO2, CF3CF2COOH, CF3COOH, FCOOH and HF, which has been identified through previous experimental analysis. Ecotoxicity assessment indicates that degradation does not produce highly toxic intermediates, and that the final products are non-toxic, supporting the feasibility of persulfate-based AOP technologies.

Persulfate-Based Advanced Oxidation Process for Chlorpyrifos Degradation: Mechanism, Kinetics, and Toxicity Assessment.

Persulfate-based advanced oxidation process has been proven to be a promising method for the toxic pesticide chlorpyrifos (CPY) degradation in wastewater treatment. However, due to the limitation for the short-lived intermediates detection, a comprehensive understanding for the degradation pathway remains unclear. To address this issue, density functional theory was used to analyze the degradation mechanism of CPY at the M06-2X/6-311++G(3df,3pd)//M06-2X/6-31+G(d,p) level, and computational toxicology methods were employed to explore the toxicity of CPY and its degradation products. Results show that hydroxyl radicals (·OH) and sulfate radicals (SO4•-) initiate the degradation reactions by adding to the P=S bond and abstracting the H atom on the ethyl group, rather than undergoing α-elimination of the pyridine ring in the persulfate oxidation process. Moreover, the addition products were attracted and degraded by breaking the P-O bond, while the abstraction products were degraded through dealkylation reactions. The transformation products, including 3,5,6-trichloro-2-pyridynol, O,O-diethyl phosphorothioate, chlorpyrifos oxon, and acetaldehyde, obtained through theoretical calculations have been detected in previous experimental studies. The reaction rate constants of CPY with ·OH and SO4•- were 6.32 × 108 and 9.14 × 108 M-1·s-1 at room temperature, respectively, which was consistent with the experimental values of 4.42 × 109 and 4.5 × 109 M-1 s-1. Toxicity evaluation results indicated that the acute and chronic toxicity to aquatic organisms gradually decreased during the degradation process. However, some products still possess toxic or highly toxic levels, which may pose risks to human health. These research findings contribute to understanding the transformation behavior and risk assessment of CPY in practical wastewater treatment.

The PTBP1­NCOA4 axis promotes ferroptosis in liver cancer cells.

Polypyrimidine tract­binding protein 1 (PTBP1) plays an important role in tumor immunity, cell proliferation, apoptosis, and autophagy by regulating RNA metabolism. However, the specific function and mechanism of PTBP1 in ferroptosis remain unclear. In the present study, it was investigated whether PTBP1 regulates ferroptosis and the exact mechanism. The iron, malondialdehyde (MDA), and GSH levels were detected in sorafenib (SF)­treated liver cancer cells. si­PTBP1 introduction into SF­treated liver cancer cells resulted in a significant reduction in the levels of MDA and iron. Additionally, a significant recovery of GSH levels was observed after silencing PTBP1. StarBase v2.0 database was used to predict potential transcripts that can physically interact with PTBP1 and nuclear receptor coactivator 4 (NCOA4) mRNA was identified as the most enriched binding partner in the PTBP1­RNA complex. A dual­luciferase assay then demonstrated that PTBP1 directly interacted with NCOA4. PTBP1 silencing did not affect NCOA4 stability following treatment with cycloheximide. A pull­down assay revealed that the PTBP1­binding region was in the 5'­UTR of the NCOA4 mRNA sequence. These results suggest that PTBP1 mediates ferroptosis in liver cancer cells by regulating NCOA4 translation. In vivo experiments reconfirmed the role of the PTBP1­NCOA4 axis in a xenograft transplantation model. It was observed that the mean tumor weight increased after PTBP1 knockout. In conclusion, silencing of PTBP1 decreased the sensitivity of liver cancer cells to ferroptosis after SF treatment and regulated ferritinophagy by mediating NCOA4 translation.

Abundant bacteria and fungi attached to airborne particulates in vegetable plastic greenhouses.

The proliferation of modern vegetable plastic greenhouses (VPGS) supplies more and more vegetables for food all over the world. The airborne bacteria and fungi induce more exposure opportunities for workers toiling in confined plastic greenhouses. Culture-independent approaches by qPCR and high-throughput sequencing technology were used to study the airborne particulates microbiota in typic VPGS in Shandong, a large base of vegetables in China. The result revealed the mean airborne bacteria concentrations reached 1.67 × 103 cells/m3 (PM2.5) and 2.38 × 103 cells/m3 (PM10), and the mean airborne fungal concentrations achieved 1.49 × 102 cells/m3 (PM2.5) and 3.19 × 102 cells/m3 (PM10) in VPGS. The predominant bacteria in VPGS included Ralstonia, Alcanivorax, Pseudomonas, Bacillus, and Acinetobacter. Botrytis, Alternaria, Fusarium, Sporobolomyces, and Cladosporium were frequently detected fungal genera in VPGS. A higher Chao1 of bacteria in PM10 was significantly different from PM2.5 in VPGS. The potential pathogens in VPGS include Raltonia picketti, Acinetobacter lwoffii, Bacillus anthracis, Botrytis cinerea, and Cladosporium sphaerospermum. The network analysis indicated that airborne microbiota was associated with soil microbiota which was affected by anthropologic activities. The predicted gene functions revealed that bacterial function mainly involved metabolism, neurodegenerative diseases, and fungal trophic mode dominated by Pathotroph-Saprotroph in VPGS. These findings unveiled airborne microbiomes in VPGS so that a strategy for improving air quality can be applied to safeguard health and vegetation.