Rapid Monitoring of Mercury in Air from an Organic Chemical Factory in China Using a Portable Mercury Analyzer

A chemical factory, using a production technology of acetaldehyde with mercury catalysis, was located southeast of Qingzhen City in Guizhou Province, China. Previous research showed heavy mercury pollution through an extensive downstream area. A current investigation of the mercury distribution in ambient air, soils, and plants suggests that mobile mercury species in soils created elevated mercury concentrations in ambient air and vegetation. Mercury concentrations of up to 600 ng/m3 in air over the contaminated area provided evidence of the mercury transformation to volatile Hg(0). Mercury analysis of soil and plant samples demonstrated that the mercury concentrations in soil with vaporized and plant-absorbable forms were higher in the southern area, which was closer to the factory. Our results suggest that air monitoring using a portable mercury analyzer can be a convenient and useful method for the rapid detection and mapping of mercury pollution in advanced field surveys

Tonic B cell activation by Radioprotective105/MD-1 promotes disease progression in MRL/lpr mice

Toll-like receptors (TLRs) have a crucial role in sensing microbial products and triggering immune responses. Recent reports have indicated that TLR7 and TLR9 have an important role in activating autoreactive B cells. In addition to TLR7 and TLR9, mouse B cells express TLR2, TLR4 and structurally related Radioprotective105 (RP105). We have previously shown that RP105 works in concert with TLR2/4 in antibody response to TLR2/4 ligands. We here report that B cells are constitutively activated by TLR2/4 and RP105. Such B cell activation was revealed by the γ3 germ line transcript and serum IgG3 production, both of which were impaired by the lack of RP105 or TLR2/4. Serum IgG3 was not altered in germ-free or antibiotics-treated mice, suggesting that the microbial flora hardly contributes to the continuous activation of B cells. The lack of RP105-dependent B cell activation ameliorated disease progression in lupus-prone MRL/lpr mice. RP105−/− MRL/lpr mice showed less lymphoadenopathy/splenomegaly and longer survival than MRL/lpr mice. Whereas glomerulonephritis and auto-antibody production were not altered, improvement in blood urea nitrogen and lower incidence of renal arteritis indicated that renal function was ameliorated in the absence of RP105. Our results suggest that RP105-dependent tonic B cell activation has a pathogenic role in MRL/lpr mic

Sequestosome1/p62 protects mouse embryonic fibroblasts against low-dose methylercury-induced cytotoxicity and is involved in clearance of ubiquitinated proteins

Abstract Methylmercury (MeHg) is a widely distributed environmental pollutant that causes a series of cytotoxic effects. However, molecular mechanisms underlying MeHg toxicity are not fully understood. Here, we report that sequestosome1/p62 protects mouse embryonic fibroblasts (MEFs) against low-dose MeHg cytotoxicity via clearance of MeHg-induced ubiquitinated proteins. p62 mRNA and protein expression in MEFs were temporally induced by MeHg exposure p62-deficient MEFs exhibited higher sensitivity to MeHg exposure compared to their wild-type (WT) counterparts. An earlier and higher level of accumulation of ubiquitinated proteins was detected in p62-deficient cells compared with WT MEFs. Confocal microscopy revealed that p62 and ubiquitinated proteins co-localized in the perinuclear region of MEFs following MeHg treatment. Further analysis of MEFs revealed that ubiquitinated proteins co-localized with LC3-positive puncta upon co-treatment with MeHg and chloroquine, an autophagy inhibitor. In contrast, there was minimal co-localization in p62-deficient MEFs. The present study, for the first time, examined the expression and distribution of p62 and ubiquitinated proteins in cells exposed to low-dose MeHg. Our findings suggest that p62 is crucial for cytoprotection against MeHg-induced toxicity and is required for MeHg-induced ubiquitinated protein clearance

In vitro study of the effect of nanoparticle-rich diesel exhaust particles on IL-18 production in splenocytes

It has been shown that pulmonary exposure to diesel exhaust particles (DEP) disrupts the immune system, presenting as exacerbating effects on allergic manifestations (e.g., allergic asthma). However, since a model inhalation system has not been developed, the impact of nano-level DEP on health has not been satisfactorily investigated. Our institute (the National Institute for Environmental Studies) established an “environmental nanoparticle exposure system applied in animals” in 2005 and since then, we have explored the health effects of exposure to these types of agent. The present study was conducted to investigate the in vitro effects of nanoparticle-rich DEP (NRDEP) on primary splenocytes from atopy-prone hosts. NC/Nga mouse-derived splenic mononuclear cells were co-cultured with NRDEP (0-50 μg/ml); thereafter, the production/release of interleukin (IL)-18 in the culture supernatants was evaluated by means of ELISA. NRDEP increased IL-18 production/release by splenocytes in a dose-dependent manner with an overall trend (with significance vs. 10 μg/ml of NRDEP). In contrast, 50 μg/ml of NRDEP inhibited production/release. These results suggest that NRDEP can activate naïve splenic mononuclear cells from atopy-prone animals in terms of IL-18 induction