Oxidative transformation of organic contaminants by manganese oxides was commonly investigated with pure MnO(2) suspension, which deviates from the fact that natural manganese oxides are seldom present as a pure form in the natural environment. In this study, we prepared manganese oxide-coated sand (MOCS) and evaluated its oxidative capacity using bisphenol A (BPA) as the model compound. BPA was transformed by MOCS and the reaction followed an exponential decay model. The reaction was pH dependent and followed the order of pH 4.5>pH 5.5>pH 6.5>pH 7.5>pH 8.6>pH 9.6, indicating that acidic conditions facilitated BPA transformation while basic conditions disfavored the reaction. Coexisting metal ions exhibited inhibitory effects and followed the order of Fe(3+) > Zn(2+) > Cu(2+) > Ca(2+) > Mg(2+) > Na(+). Transformation of BPA by MOCS was much slower than that by pure MnO(2) suspension. However, similar transformation products were identified in both studies, suggesting the same reaction pathways. This work suggests that the reactivity of MnO(2) in the environment might be overestimated if extrapolating the result from the pure MnO(2) suspension because natural MnO(2) is mainly present as coating on the surface of soils and sediments.

The gut microbiota of amphibians is affected by exogenous and endogenous factors. We performed a comprehensive analysis using high-throughput sequencing technology and functional predictions and observed general changes in the gut microbiota of frogs in different growth stages, seasons, and growth environments. There were no significant differences in microbial richness and diversity between juvenile and adult wild frogs, between the summer and autumn groups of captive frogs, or between wild and captive frogs. There were significant differences in the gut microbiota community structure of Rana dybowskii between the summer and autumn groups of captive frogs and between wild and captive R. dybowskii , whereas the differences between juvenile and adult wild frogs were not significant. The dominant gut bacterial phyla in frogs from both captive and wild environments included Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. Linear discriminant effect size (LEfSe) analysis showed that Bacteroidetes and Firmicutes were significantly enriched in captive and wild R. dybowskii , respectively linear discriminant analysis (LDA > 4). The core operational taxonomical units (OTUs) that were found in >90% of all frogs tested encompassed 15 core OTUs. The captive frogs exhibited 15 core OTUs in addition to the above overall core microbiota, whereas the wild frogs exhibited 19 core OTUs in addition to the above overall core microbiota. Predictions made using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) suggested that eleven KEGG pathways, such as infectious diseases, immune system diseases, metabolism, metabolism of other amino acids, metabolism of cofactors and vitamins, metabolism of terpenoids and polyketides, neurodegenerative diseases, and transport and catabolism, were enriched in captive frogs. The relative abundance of several red-leg-syndrome-related pathogens increased significantly in captive frogs compared with that in wild frogs. To our knowledge, this is the first study on the effects of individual seasons and captivity on the gut microbiota of frogs.

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Tetrabromobisphenol A (TBBPA) is one of the most widely used brominated flame retardants and is ubiquitously present in the environment. In this study, we investigated the debromination of TBBPA by nanoscale zerovalent iron (nZVI) in methanol/water (50/50) solutions. Zerovalent iron nanoparticles demonstrated an excellent capacity to debrominate TBBPA to tribromobisphenol A, dibromobisphenol A, bromobisphenol A, and bisphenol A. More than 86% of TBBPA was debrominated within 16 h in a pH 7.5 reaction solution initially containing 3.0 g/L of nZVI. Debromination of TBBPA was apparently accompanied by the release of bromine ions and the elevation of solution pH. The debromination kinetics could be well-described by a three-parameter pseudo-first-order decay model. A higher loading of nZVI and acidic conditions facilitated the debromination process, while coexisting Ca2+ and Na+ species inhibited the reaction. On the basis of identified reaction intermediates and products, TBBPA debromination pathways by nZVI were proposed. This study suggests that nZVI may be potentially employed to debrominate TBBPA in soil and sediment.

Bovine laminitis causes substantial economic losses and animal welfare problems in dairy farms worldwide. Previously published studies have reported that the inflammatory response plays a central role in the pathogenesis of the disease. To our knowledge, inflammation associated with bovine laminitis induced by high levels of exposure to oligofructose (OF) has not been reported and characterized. In fact, the disease manifestations in this model closely approximate those of clinical laminitis. The objective of this study was to characterize the inflammatory response in OF-induced bovine laminitis. A total of 12 Chinese Holstein dairy heifers were utilized in this study. The heifers were randomly divided into two groups, treatment (n = 6) and control (n = 6). The treatment group heifers were administered OF solutions via a stomach tube (dose: 17 g/kg of body weight). Upon development of a lameness score of 2 with consecutive positive reactions in the same claw, they would be humanely euthanized. Control heifers were administered deionized water (dose: 2 L/100 kg of body weight) and humanely euthanized at 72 h. Real-time quantitative PCR (qPCR) assays were performed to determine the messenger RNA (mRNA) concentrations of inflammatory mediators in the lamellae. Concentrations of interleukin (IL)-1β, IL-6, IL-8, C-X-C motif chemokine ligand-1 (CXCL-1), macrophage cationic peptide-2 (MCP-2), E-selectin, intercellular adhesion molecule-1 (ICAM-1), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase-1 (iNOS-1), and plasminogen activator inhibitor-1 (PAI-1) were significantly increased (P < 0.05) in the treatment group. No significant difference was found for tumor necrosis factor alpha (TNF-α), IL-10, CXCL-6, and MCP-1. These results demonstrated and characterized the laminar inflammatory response leading to the pathogenesis of bovine laminitis at the early stages.

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