Exploring the interference mechanisms of surface and aqueous complexes with groundwater arsenate and arsenite adsorption.

Ca2+, Mg2+, and HCO3- are extremely common coexisting ions with arsenic (As) in geogenic As-polluted groundwaters. Although extensive research has improved our knowledge of groundwater As removal techniques and mechanisms, there is still a lack of a definite explanation of the distinct influences of Ca2+ and Mg2+ on As immobilization. Furthermore, the question of whether the occurrence of metal-As aqueous complexes has positive or detrimental effects on As adsorption is still open, which hinders our ability to predict the effectiveness of groundwater As removal. The goal of our present work was to investigate the molecular-level interference mechanisms of Ca2+, Mg2+, and HCO3- on arsenic adsorption with batch/column filtration experiments and spectroscopic techniques. The results showed that the co-presence of Ca2+ and As significantly increased As(V) and As(III) adsorption by 22.1 and 12.2% in batch studies and by 20.1 and 16.7% in column adsorptive filtrations, which could be explained by forming a ternary Ca-As-TiO2 complex. Without the surface complex, Mg2+ only had a slightly positive effect on As removal. Co-existence of Ca2+ and HCO3- prevented the generation this surface complex, which significantly decreased the elimination of As(III). Inversely, the As(V) ternary complex and adsorption were not interfered by HCO3-. Moreover, an aqueous Ca-As(V) complex was detected without surface, which facilitated generation of the surface complex and As(V) adsorption. The results of this work clarified the distinct effects of Ca2+ and Mg2+ and As(V) and As(III) adsorption, which was critical in predicting the As adsorption efficiency in column filtration processes.

Chronic lead exposure exacerbates hepatic glucolipid metabolism disorder and gut microbiota dysbiosis in high-fat-diet mice.

Lead (Pb) and obesity are co-occurring risk factors for metabolic disorders. However, there is still a lack of study on the combined effects of both stressors on metabolism. C57BL/6J mice were exposed to 200 mg/L Pb or/and HFD for 24 weeks and were used to investigate the effects and underlying mechanisms of chronic Pb exposure on obese mice. The results showed that Pb significantly increased body weight, visceral obesity, fasting blood glucose levels, and insulin resistance, and aggravated liver damage, hepatic lipid accumulation and steatosis in HFD-fed mice. Further analysis showed that Pb significantly inhibited insulin signaling pathway PI3K/AKT and fatty acid ß-oxidation, and accelerated fatty acid synthesis. Moreover, Pb exacerbated HFD-induced disruption of gut microbiota homeostasis, manifested by increased proportions of pathogenic genera such as Desulfovibrio, Alistipes and Helicobacter, and decreased proportions of beneficial microbes Akkermansia and Barnesiella, which were negatively associated with obesity. These results indicated that Pb exposure exacerbated the disruption of liver glucolipid metabolism in HFD mice possibly by disrupting gut microbiota.