Unraveling the mechanisms behind sodium persulphate-induced changes in petroleum-contaminated aquifers' biogeochemical parameters and microbial communities.

Sodium persulphate (PS) is a highly effective oxidising agent widely used in groundwater remediation and wastewater treatment. Although numerous studies have examined the impact of PS with respect to the removal efficiency of organic pollutants, the residual effects of PS exposure on the biogeochemical parameters and microbial ecosystems of contaminated aquifers are not well understood. This study investigates the effects of exposure to different concentrations of PS on the biogeochemical parameters of petroleum-contaminated aquifers using microcosm batch experiments. The results demonstrate that PS exposure increases the oxidation-reduction potential (ORP) and electrical conductivity (EC), while decreasing total organic carbon (TOC), dehydrogenase (DE), and polyphenol oxidase (PO) in the aquifer. Three-dimensional excitation-emission matrix (3D-EEM) analysis indicates PS is effective at reducing fulvic acid-like and humic acid-like substances and promoting microbial metabolic activity. In addition, PS exposure reduces the abundance of bacterial community species and the diversity index of evolutionary distance, with a more pronounced effect at high PS concentrations (31.25 mmol/L). Long-term (90 d) PS exposure results in an increase in the abundance of microorganisms with environmental resistance, organic matter degradation, and the ability to promote functional genes related to biological processes such as basal metabolism, transmission of genetic information, and cell motility of microorganisms. Structural equation modeling (SEM) further confirms that ORP and TOC are important drivers of change in the abundance of dominant phyla and functional genes. These results suggest exposure to different concentrations of PS has both direct and indirect effects on the dominant phyla and functional genes by influencing the geochemical parameters and enzymatic activity of the aquifer. This study provides a valuable reference for the application of PS in ecological engineering.

Mukonal Inhibits Cell Proliferation, Alters Mitochondrial Membrane Potential and Induces Apoptosis and Autophagy in Human CNE1 Nasopharyngeal Carcinoma Cells.

BACKGROUND Nasopharyngeal carcinoma results in high patient morbidity and mortality, due to early metastasis, and toxicity due to chemotherapy. Mukonal is plant-derived carbazole alkaloid that has been used in traditional Chinese medicine to treat several types of cancer. This study aimed to investigate the effects of mukonal on cell proliferation, apoptosis, autophagy, and the mitochondrial membrane potential of nasopharyngeal carcinoma cells in vitro. MATERIAL AND METHODS CNE1 human nasopharyngeal carcinoma cells and NP69 normal nasopharyngeal epithelial cells were cultured with and without treatment with increasing doses of mukonal. Cell viability was determined by the MTT assay. Fluorescence microscopy was used to detect reactive oxygen species (ROS), mitochondrial membrane potential, and the release of cytochrome C. Flow cytometry was used to examine changes in the cell cycle, electron microscopy examined cell autophagy, and Western blot was performed to measure levels of proteins associated with autophagy and apoptosis. RESULTS Mukonal had an antiproliferative effect on CNE1 cells, with an IC50 of 9 µM and there were effects of toxicity on normal NP69 cells. Mukonal triggered ROS-mediated changes in mitochondrial membrane potential which was also accompanied by the discharge of cytochrome C in the CNE1 cells. Mukonal activated autophagy and apoptosis in CNE1 cells, which was also associated with upregulation of the autophagy-related proteins, LC3 II and beclin-1, as well as apoptosis-associated proteins, Bax, cleaved caspase-3 and -9. Mukonal treatment also resulted in CNE1 cells cycle arrest at G2/M. CONCLUSIONS Mukonal inhibited the growth of human CNE1 nasopharyngeal carcinoma cells in vitro.

Association of Parental Environmental Exposures and Supplementation Intake with Risk of Nonsyndromic Orofacial Clefts: A Case-Control Study in Heilongjiang Province, China.

The aim of present study was to check the possible association of potential parental environmental exposures and maternal supplementation intake with the risk of nonsyndromic orofacial clefting (NSOC). A retrospective study comprised 499 cases and 480 controls was conducted in Heilongjiang Province. Chi-square analysis and unconditional multiple logistic regression were used in the study. The results showed that maternal history of fever and the common cold without fever (ORCL/P = 3.11 and 5.56, 95%CI: 1.67-5.82 and 2.96-10.47, ORCPO = 3.31 and 8.23, 95%CI: 1.58-6.94 and 4.08-16.95), paternal smoking and alcohol consumption (ORCL/P = 2.15 and 5.04, 95%CI: 1.37-3.38 and 3.00-8.46, ORCPO = 1.82 and 4.40, 95%CI: 1.06-3.13 and 2.50-7.74), maternal exposure to organic solvents, heavy metals, or pesticides (ORCL/P = 6.07, 5.67 and 5.97, 95%CI: 1.49-24.76, 1.34-24.09 and 2.10-16.98, ORCPO = 10.65, 7.28 and 3.48, 95%CI: 2.54-44.67, 1.41-37.63 and 1.06-11.46) and multivitamin use during the preconception period (ORCL/P = 0.06, 95%CI: 0.02-0.23, ORCPO = 0.06, 95%CI: 0.01-0.30) were associated with cleft lip or without cleft palate (CL/P) and cleft palate only (CPO). Maternal history of skin disease and negative life events (ORCL/P = 12.07 and 1.67, 95%CI: 1.81-80.05 and 1.95-2.67) were associated with CL/P. Some potential parental hazardous exposures during the periconception period and maternal use of multivitamins during the preconception period were associated with risk of NSOC.