74 research outputs found
Glucose-sulfate conjugates as a new phase II metabolite formed by aquatic crustaceans
ArticleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 360(2): 490-495 (2007)journal articl
Estimation of sources and inflow of dioxins and polycyclic aromatic hydrocarbons from the sediment core of Lake Suwa, Japan
ArticleEnviromental Pollution. 138(3): 529-537 (2005)journal articl
Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation
Air pollutant exposure has been linked to a rise in wheezing illnesses. Clinical data highlight that exposure to mainstream tobacco smoke (MS) and environmental tobacco smoke (ETS) as well as exposure to diesel exhaust particles (DEP) could promote allergic sensitization or aggravate symptoms of asthma, suggesting a role for these inhaled pollutants in the pathogenesis of asthma. Mouse models are a valuable tool to study the potential effects of these pollutants in the pathogenesis of asthma, with the opportunity to investigate their impact during processes leading to sensitization, acute inflammation and chronic disease. Mice allow us to perform mechanistic studies and to evaluate the importance of specific cell types in asthma pathogenesis. In this review, the major clinical effects of tobacco smoke and diesel exhaust exposure regarding to asthma development and progression are described. Clinical data are compared with findings from murine models of asthma and inhalable pollutant exposure. Moreover, the potential mechanisms by which both pollutants could aggravate asthma are discussed
Effects of nano particles on antigen-related airway inflammation in mice
BACKGROUND: Particulate matter (PM) can exacerbate allergic airway diseases. Although health effects of PM with a diameter of less than 100 nm have been focused, few studies have elucidated the correlation between the sizes of particles and aggravation of allergic diseases. We investigated the effects of nano particles with a diameter of 14 nm or 56 nm on antigen-related airway inflammation. METHODS: ICR mice were divided into six experimental groups. Vehicle, two sizes of carbon nano particles, ovalbumin (OVA), and OVA + nano particles were administered intratracheally. Cellular profile of bronchoalveolar lavage (BAL) fluid, lung histology, expression of cytokines, chemokines, and 8-hydroxy-2'-deoxyguanosine (8-OHdG), and immunoglobulin production were studied. RESULTS: Nano particles with a diameter of 14 nm or 56 nm aggravated antigen-related airway inflammation characterized by infiltration of eosinophils, neutrophils, and mononuclear cells, and by an increase in the number of goblet cells in the bronchial epithelium. Nano particles with antigen increased protein levels of interleukin (IL)-5, IL-6, and IL-13, eotaxin, macrophage chemoattractant protein (MCP)-1, and regulated on activation and normal T cells expressed and secreted (RANTES) in the lung as compared with antigen alone. The formation of 8-OHdG, a proper marker of oxidative stress, was moderately induced by nano particles or antigen alone, and was markedly enhanced by antigen plus nano particles as compared with nano particles or antigen alone. The aggravation was more prominent with 14 nm of nano particles than with 56 nm of particles in overall trend. Particles with a diameter of 14 nm exhibited adjuvant activity for total IgE and antigen-specific IgG(1 )and IgE. CONCLUSION: Nano particles can aggravate antigen-related airway inflammation and immunoglobulin production, which is more prominent with smaller particles. The enhancement may be mediated, at least partly, by the increased local expression of IL-5 and eotaxin, and also by the modulated expression of IL-13, RANTES, MCP-1, and IL-6
Envenomations by Bothrops and Crotalus Snakes Induce the Release of Mitochondrial Alarmins
Skeletal muscle necrosis is a common manifestation of viperid snakebite envenomations. Venoms from snakes of the genus Bothrops, such as that of B. asper, induce muscle tissue damage at the site of venom injection, provoking severe local pathology which often results in permanent sequelae. In contrast, the venom of the South American rattlesnake Crotalus durissus terrificus, induces a clinical picture of systemic myotoxicity, i.e., rhabdomyolysis, together with neurotoxicity. It is known that molecules released from damaged muscle might act as ‘danger’ signals. These are known as ‘alarmins’, and contribute to the inflammatory reaction by activating the innate immune system. Here we show that the venoms of B. asper and C. d. terrificus release the mitochondrial markers mtDNA (from the matrix) and cytochrome c (Cyt c) from the intermembrane space, from ex vivo mouse tibialis anterior muscles. Cyt c was released to a similar extent by the two venoms whereas B. asper venom induced the release of higher amounts of mtDNA, thus reflecting hitherto some differences in their pathological action on muscle mitochondria. At variance, injection of these venoms in mice resulted in a different time-course of mtDNA release, with B. asper venom inducing an early onset increment in plasma levels and C. d. terrificus venom provoking a delayed release. We suggest that the release of mitochondrial ‘alarmins’ might contribute to the local and systemic inflammatory events characteristic of snakebite envenomations
Ambient air pollution and thrombosis
Abstract Air pollution is a growing public health concern of global significance. Acute and chronic exposure is known to impair cardiovascular function, exacerbate disease and increase cardiovascular mortality. Several plausible biological mechanisms have been proposed for these associations, however, at present, the pathways are incomplete. A seminal review by the American Heart Association (2010) concluded that the thrombotic effects of particulate air pollution likely contributed to their effects on cardiovascular mortality and morbidity. The aim of the current review is to appraise the newly accumulated scientific evidence (2009–2016) on contribution of haemostasis and thrombosis towards cardiovascular disease induced by exposure to both particulate and gaseous pollutants. Seventy four publications were reviewed in-depth. The weight of evidence suggests that acute exposure to fine particulate matter (PM2.5) induces a shift in the haemostatic balance towards a pro-thrombotic/pro-coagulative state. Insufficient data was available to ascertain if a similar relationship exists for gaseous pollutants, and very few studies have addressed long-term exposure to ambient air pollution. Platelet activation, oxidative stress, interplay between interleukin-6 and tissue factor, all appear to be potentially important mechanisms in pollution-mediated thrombosis, together with an emerging role for circulating microvesicles and epigenetic changes. Overall, the recent literature supports, and arguably strengthens, the contention that air pollution contributes to cardiovascular morbidity by promoting haemostasis. The volume and diversity of the evidence highlights the complexity of the pathophysiologic mechanisms by which air pollution promotes thrombosis; multiple pathways are plausible and it is most likely they act in concert. Future research should address the role gaseous pollutants play in the cardiovascular effects of air pollution mixture and direct comparison of potentially susceptible groups to healthy individuals
Environmental Controls of Diffusive and Ebullitive Methane Emissions at a Subdaily Time Scale in the Littoral Zone of a Midlatitude Shallow Lake
Environmental controls on methane (CH4) emission from lakes are poorly understood at subdaily time scales due to a lack of continuous data, especially for ebullition. We used a novel technique to partition eddy covariance CH4 flux observed in the littoral zone of a midlatitude shallow lake in Japan and examined the environmental controls on diffusion and ebullitive CH4 flux separately at a subdaily time scale in different seasons. Using the high‐frequency data, we investigated how CH4 accumulation in the water and sediment layers alters the dynamics and environmental controls of fluxes. The contribution of ebullitive flux to total flux was 57% on average. Environmental controls of diffusive and ebullitive fluxes known in the literature were confirmed. We further found that the environmental controls were different in different seasons and suggested that additional consideration of CH4 accumulation could explain the variability. The transfer of accumulated dissolved CH4 from the bottom water layer to the surface in summer and the accumulation of dissolved CH4 under surface ice in winter were suggested to be important for explaining the variability of diffusive flux. In summer, a higher ebullitive flux tended to occur following triggers such as a decrease in hydrostatic pressure. In winter, the impact of triggers was not obvious, and a higher ebullitive flux tended to occur in the morning. We suggested that the low CH4 production rate in winter slowed the replenishment of bubbles in the sediment, negating the effect of triggers on ebullition.ArticleJournal of Geophysical Research-Biogeoscience 125(9) : e2020JG005753-(2020)journal articl
Organ distribution and bioaccumulation of microcystins in freshwater fish at different trophic levels from the eutrophic Lake Chaohu, China
This article reports the organ distribution and bioaccumulation of hepatotoxic microcystins (MCs) in freshwater fishes at different trophic levels from the large, shallow, eutrophic Lake Chaohu in September 2003, when there were heavy surface blooms of toxic cyanobacteria. Among all fish, intestines and blood had the highest average content of MC-RR + MC-LR (22.0 and 14.5 mu g g(-1) DW, respectively), followed by liver, bile, and kidney (7.77, 6.32, and 5.81 mu g g(-1) DW, respectively), whereas muscle had the least (1.81 mu g g(-1) DW). MC content in muscle was highest in carnivorous fish (Culter ilishaeformis, 2.22 mu g g(-1) DW) and omnivorous fish (Carassius auratus, 1.96 mu g g(-1) DW) and was lowest in phytoplanktivorous fish (Hypophthalmichthys molitrix, 1.65 mu g g(-1) DW) and herbivorous fish (Parabramis pekinensis 0.660 mu g g(-1) DW). However, the amount of MC in the gut of H. molitrix (137 mu g g(-1) DW) was more than 20 times that in the other fish (< 6.50 mu g g(-1) DW). The MCs showed a tendency to accumulate up the food chain, and piscivorous fish at the top of the food chain were at high risk of exposure to MCs in Lake Chaohu. Our study is the first to report MC concentrations in the bile and blood of wild fish. One hundred grams of fish muscle would contain 2.64-49.7 mu g of MC-LR equivalent, or about 1.3-25 times the recommended tolerable daily intake of MC-LR by humans, indicating that fish are already severely contaminated by MCs and that the local authorities should warn the public of the risk of poisoning by eating the contaminated fish. (c) 2005 Wiley Periodicals, Inc
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