Coupling isotopic signatures and partial extraction method to examine lead pollution in mangrove sediments.

Elevated lead (Pb) has been widely observed in mangrove sediments due to human activities, yet understanding the sources of Pb in these sediments and the factors influencing Pb accumulation is challenging. Here, we combined Pb isotopes with partial extraction methods to study Pb contamination levels in mangrove sediments from the eastern and western parts of the Maowei Sea, China. Our results showed that the Pb in the leachate and residual fraction was mainly from anthropogenic and natural sources, respectively. The use of 204Pb isotope analysis can reveal some overlooked differences between anthropogenic and natural sources. Calculation by Bayesian mixing model showed no significant difference in the total anthropogenic contribution between the two sites, but the relative contribution of each end member differed. The contribution of Pb/Zn ores was much higher in the eastern sites (30.9 ± 5.1%) than in the west (18.4 ± 5.5%), while that of agricultural activities was much lower in the east (5.2 ± 3.1%) than in the west (13.5 ± 4.6%). The elevated anthropogenic Pb accumulation in mangrove sediments was ascribed to organic matter. This study provides more data on Pb isotopic composition and new insights into Pb biogeochemistry in the mangrove environment.

The non-coevolution of DIC and alkalinity and the CO2 degassing in a karst river affected by acid mine drainage in Southwest China.

Dissolved inorganic carbon (DIC) in mine water generated during coal mining is a large and potential source of atmospheric CO2, however its geochemical behaviors under the influence of AMD in relation to CO2 degassing and carbonate buffering are not well known. In this study, water temperature, pH, DO, alkalinity, Ca2+ concentration, and the carbon isotope of DIC were measured monthly from November 2020 to November 2021 and carbonate chemistry and CO2 emission flux were calculated to reveal the processes of DIC evolution and CO2 degassing from the Chetian River draining a karst region, which is materially affected by the input of large quantities of AMD. The results showed that carbonate erosion, the mineralization of terrestrial organic matter, and domestic sewage input are all identified to contribute DIC to different degrees to the river. Throughout the year, the Chetian River undergoes high-intensity CO2 degassing, which is dominated by HCO3--neutralized degassing and proton-enhanced degassing in different reaches. The pCO2 in the river under the influence of AMD is as high as 237,482 µatm, while the F-CO2 approaches 316.9 g C m-2 d-1. Meanwhile, the carbonate system in the downstream karst river buffers an average of 85.2 % of DIC release at the river's outlet. The input of AMD significantly altered the carbon cycle of the surface watershed in the headwaters of tributaries, and greatly enhanced the release of CO2 from surface water to the atmosphere; meanwhile, the buffering of carbonates on acidity in the water of main streams causes pCO2 to rapidly reduce over a short distance. Obviously, the carbon emission effect generated by the interaction between AMD and carbonate mainly occurs in the tributary water system. Considering the huge amount of AMD worldwide, this large potential source of atmospheric CO2 requires a specific and precise quantitative analysis based on actual observations.

Polychlorinated biphenyl quinone induces hepatocytes iron overload through up-regulating hepcidin expression.

Polychlorinated biphenyls (PCBs) are infamous industry by-products or additives, and increasing evidences demonstrated that their exposure is associate with adverse effects on human health. Liver, as the dominate site for xenobiotic metabolism, is apt to be the primary target of PCBs insult. Although PCBs' hepatic toxic effects have been extensively studied, however, the biotransformation of PCBs in liver and the toxicities of associated PCB metabolites are neglected at some extent. Thus, we choose 2,3,5-trichloro-6-phenyl-[1,4]-benzoquinone (PCB29-pQ), a surrogate PCB29 metabolite, and evaluated its contribution on hepatotoxicity. In the current study, we discovered PCB29-pQ-induced lipid peroxidation and iron overload both in vivo and in vitro. Further mechanistic research confirmed iron overload is caused by reactive oxygen species (ROS)-driven hepcidin disorder in hepatic cells, and the increase of hepcidin is regulated by the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2).

Polychlorinated biphenyl quinone promotes macrophage polarization to CD163+ cells through Nrf2 signaling pathway.

Polychlorinated biphenyls (PCBs) are notorious environmental pollutants. For their hydrophobic and lipophilic capability, they are wildly spread to environment to threat human health thus attracts more attention. In this study, we observed increasing numbers of CD163 positive (CD163+) macrophages in aortic valve of ApoE-/- mice after 2,3,5-trichloro-6-phenyl-[1,4]-benzoquinone (PCB29-pQ) treatment, the metabolite of polychlorinated biphenyl. In addition, in vitro studies identified that PCB29-pQ exposure significantly provoked the shifting of RAW264.7 macrophages and bone marrow derived monocytes (BMDMs) to CD163+ macrophages. Upon PCB29-pQ administration, CD163 and CD206 levels were enhanced in RAW264.7 cells as well as in BMDMs. However, the concentration of iron and total cholesterol (TC) were reduced due to the boosting of ferroportin (Fpn) and ATP binding cassette transporter, subfamily A, member 1 (ABCA1) which are efflux transporters of iron and cholesterol individually. Further investigation on mechanism indicated that PCB29-pQ exposure induced reactive oxygen species (ROS), which may result in activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a protein responsible for macrophage polarization. After that, we blocked Nrf2 through Nrf2 shRNA and ROS scavenger NAC, which significantly reversed the shifting of macrophage to CD163+ sub-population. These results confirmed the importance of Nrf2 in inducing macrophage polarization. In short, our study uncovered that PCB29-pQ could promote macrophage/monocyte polarization to CD163+ macrophage which would be a potential incentive to accelerate atherosclerosis through Nrf2 signaling pathway.