937 resultados para Mercury toxicity
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Economic development, including resource extraction, can cause toxic exposures that interact with endemic infectious diseases. Mercury is an immunotoxic metal used in the amalgamation of gold, resulting in both occupational exposures and environmental pollution. A cross-sectional medical survey was conducted in 1997 on 135 garimpeiros in Para, Brazil, because of their risks of both mercury exposure and malaria transmission. Mean levels of blood and urine mercury were well above non-exposed background levels. Twenty-six subjects had malaria parasitemia: Health symptoms consistent with mercury exposure were reported, but neither symptoms nor signs correlated with mercury levels in blood or urine. We did not find a dose response relationship between mercury exposure and likelihood of prevalent malaria infection, but there was a possible reduction in acquisition of immunity that may be associated with conditions in gold mining, including mercury exposure.
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prova tipográfica / uncorrected proof
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Despite the considerable environmental importance of mercury (Hg), given its high toxicity and ability to contaminate large areas via atmospheric deposition, little is known about its activity in soils, especially tropical soils, in comparison with other heavy metals. This lack of information about Hg arises because analytical methods for determination of Hg are more laborious and expensive compared to methods for other heavy metals. The situation is even more precarious regarding speciation of Hg in soils since sequential extraction methods are also inefficient for this metal. The aim of this paper is to present a technique of thermal desorption associated with atomic absorption spectrometry, TDAAS, as an efficient tool for quantitative determination of Hg in soils. The method consists of the release of Hg by heating, followed by its quantification by atomic absorption spectrometry. It was developed by constructing calibration curves in different soil samples based on increasing volumes of standard Hg2+ solutions. Performance, accuracy, precision, and quantification and detection limit parameters were evaluated. No matrix interference was detected. Certified reference samples and comparison with a Direct Mercury Analyzer, DMA (another highly recognized technique), were used in validation of the method, which proved to be accurate and precise.
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There is a need for more efficient methods giving insight into the complex mechanisms of neurotoxicity. Testing strategies including in vitro methods have been proposed to comply with this requirement. With the present study we aimed to develop a novel in vitro approach which mimics in vivo complexity, detects neurotoxicity comprehensively, and provides mechanistic insight. For this purpose we combined rat primary re-aggregating brain cell cultures with a mass spectrometry (MS)-based metabolomics approach. For the proof of principle we treated developing re-aggregating brain cell cultures for 48h with the neurotoxicant methyl mercury chloride (0.1-100muM) and the brain stimulant caffeine (1-100muM) and acquired cellular metabolic profiles. To detect toxicant-induced metabolic alterations the profiles were analysed using commercial software which revealed patterns in the multi-parametric dataset by principal component analyses (PCA), and recognised the most significantly altered metabolites. PCA revealed concentration-dependent cluster formations for methyl mercury chloride (0.1-1muM), and treatment-dependent cluster formations for caffeine (1-100muM) at sub-cytotoxic concentrations. Four relevant metabolites responsible for the concentration-dependent alterations following methyl mercury chloride treatment could be identified using MS-MS fragmentation analysis. These were gamma-aminobutyric acid, choline, glutamine, creatine and spermine. Their respective mass ion intensities demonstrated metabolic alterations in line with the literature and suggest that the metabolites could be biomarkers for mechanisms of neurotoxicity or neuroprotection. In addition, we evaluated whether the approach could identify neurotoxic potential by testing eight compounds which have target organ toxicity in the liver, kidney or brain at sub-cytotoxic concentrations. PCA revealed cluster formations largely dependent on target organ toxicity indicating possible potential for the development of a neurotoxicity prediction model. With such results it could be useful to perform a validation study to determine the reliability, relevance and applicability of this approach to neurotoxicity screening. Thus, for the first time we show the benefits and utility of in vitro metabolomics to comprehensively detect neurotoxicity and to discover new biomarkers.
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To evaluate their toxicity in the developing brain, eight metal compounds, [bismuth sodium tartrate (BiNA-tartrate), CdCl(2), CoCl(2), HgCl(2), dimethyl mercury, NiCl(2), TlCl and triethyltin chloride (TET)] were tested in aggregating cell cultures of foetal rat telencephalon. The compounds were applied to the cultures continuously, either during an early developmental stage (between days 5 and 14) or during and advanced stage of maturation (between days 24 and 34). Changes in the activities of cell type-specific enzymes were used as a criterion for toxicity. A general cytotoxic effect was observed after treatment with either CdCl(2), HgCl(2) or TET at 10(-6)m, and with TlCl at 10(-5)m. Selective effects were found with BiNa-tartrate and dimethylmercury. CoCl(2) did not modify the parameters tested, whereas a stimulant effect was found with NiCl(2). The effects of several compounds were development dependent: HgCl(2), TET and TlCl were more toxic in immature cultures, whereas BiNa-tartrate, dimethylmercury and NiCl(2) were more effective in differentiated cultures.
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A three-dimensional cell culture system was used as a model to study the influence of low levels of mercury in the developing brain. Aggregating cell cultures of fetal rat telencephalon were treated for 10 days either during an early developmental period (i.e., between days 5 and 15 in vitro) or during a phase of advanced maturation (i.e., between days 25 and 35) with mercury. An inorganic (HgCl2) and an organic mercury compound (monomethylmercury chloride, MeHgCl) were examined. By monitoring changes in cell type-specific enzymes activities, the concentration-dependent toxicity of the compounds was determined. In immature cultures, a general cytotoxicity was observed at 10(-6) M for both mercury compounds. In these cultures, HgCl2 appeared somewhat more toxic than MeHgCl. However, no appreciable demethylation of MeHgCl could be detected, indicating similar toxic potencies for both mercury compounds. In highly differentiated cultures, by contrast, MeHgCl exhibited a higher toxic potency than HgCl2. In addition, at 10(-6) M, MeHgCl showed pronounced neuron-specific toxicity. Below the cytotoxic concentrations, distinct glia-specific reactions could be observed with both mercury compounds. An increase in the immunoreactivity for glial fibrillary acidic protein, typical for gliosis, could be observed at concentrations between 10(-9) M and 10(-7) M in immature cultures, and between 10(-8) M and 3 x 10(-5) M in highly differentiated cultures. A conspicuous increase in the number and clustering of GSI-B4 lectin-binding cells, indicating a microglial response, was found at concentrations between 10(-10) M and 10(-7) M. These development-dependent and cell type-specific effects may reflect the pathogenic potential of long-term exposure to subclinical doses of mercury.
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This paper reports the method development for the simultaneous determination of methylmercury MeHgþ) and inorganic mercury (iHg) species in seafood samples. The study focused on the extraction and quantification of MeHgþ (the most toxic species) by liquid chromatography coupled to on-line UV irradiation and cold vapour atomic fluorescence spectroscopy (LC-UV-CV-AFS), using HCl 4 mol/L as the extractant agent. Accuracy of the method has been verified by analysing three certified reference materials and different spiked samples. The values found for total Hg and MeHgþ for the CRMs did not differ significantly from certified values at a 95% confidence level, and recoveries between 85% and 97% for MeHgþ, based on spikes, were achieved. The detection limits (LODs) obtained were 0.001 mg Hg/kg for total mercury, 0.0003 mg Hg/kg for MeHgþ and 0.0004 mg Hg/kg for iHg. The quantification limits (LOQs) established were 0.003 mg Hg/kg for total mercury, 0.0010 mg Hg/kg for MeHgþ and 0.0012 mg Hg/kg for iHg. Precision for each mercury species was established, being 12% in terms of RSD in all cases. Finally, the developed method was applied to 24 seafood samples from different origins and total mercury contents. The concentrations for Total Hg, MeHg and iHg ranged from 0.07 to 2.33, 0.003-2.23 and 0.006-0.085 mg Hg/kg, respectively. The established analytical method allows to obtain results for mercury speciation in less than 1 one hour including both, sample pretreatment and measuring step.
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Heavy metals have been used in a wide variety of human activities that have significantly increased both professional and environmental exposure. Unfortunately, disasters have highlighted the toxic effects of metals on different organs and systems. Over the last 50 years, the adverse effects of chronic lead, mercury and gadolinium exposure have been underscored. Mercury and lead induce hypertension in humans and animals, affecting endothelial function in addition to their other effects. Increased cardiovascular risk after exposure to metals has been reported, but the underlying mechanisms, mainly for short periods of time and at low concentrations, have not been well explored. The presence of other metals such as gadolinium has raised concerns about contrast-induced nephropathy and, interestingly, despite this negative action, gadolinium has not been defined as a toxic agent. The main actions of these metals, demonstrated in animal and human studies, are an increase of free radical production and oxidative stress and stimulation of angiotensin I-converting enzyme activity, among others. Increased vascular reactivity, highlighted in the present review, resulting from these actions might be an important mechanism underlying increased cardiovascular risk. Finally, the results described in this review suggest that mercury, lead and gadolinium, even at low doses or concentrations, affect vascular reactivity. Acting via the endothelium, by continuous exposure followed by their absorption, they can increase the production of free radicals and of angiotensin II, representing a hazard for cardiovascular function. In addition, the actual reference values, considered to pose no risk, need to be reduced.
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Asha M. R This thesis Entitled Toxicological effects of copper and mercury on the fish macerones gulio (hamiloton – buchanan).Chapter 1. In this chapter, a broad outline of heavy metal uptake, requirement of a suitable bio — monitoring organism, criteria for a standard test fish, and suitability of Macrones gulig for the toxicological study are given. Chapter 2. This chapter deals with the lethal toxicity bioassays to find the 96 hr LC 50 of copper and mercury for the fish Macrones gglig. The experimental results indicated that of the two metals tested, copper was more toxic than mercury.Chapter 3. The effect of copper and mercury on the haemoglobin, haematocrit, erythrocyte count, MCV, MCH and MCHC was studied.Chapter 4. The glycogen and protein contents of liver and muscle after exposure to copper and mercury were studied. There was a significant decrease of glycogen in the liver and muscle of metal treated fishes.Chapter 5. The histopathological changes of the tissues like liver, kidney and gill after exposure to copper and mercury were studied.
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This thesis Entitled studies on the effect of toxic heavy metal mercury on the physiology and biochemistry of an estuarine crab scylla serrata (Forskal). Evaluate the toxicity of three sub lethal concentrations of mercury, viz., 0.009 mg/l, 0.02 mg/1, and 0.04 mg/l on the mud crab, Scylla serrata through bioaccumulation, and depuration studies. To characterize the biochemical responses to the sub-lethal stress of mercury in chelate muscles, abdominal muscles, hepatopancreas and gills. To study the activity pattern of acid and alkaline phosphatases in mercury-exposed crabs. To evaluate the induced changes in these tissues through histopathological studies,The Cochin backwaters is one of the most productive and biologically active backwater systems, and is the habitat of varieties of fishes, mollusks, and crustaceans, though this water body also receives tons of effluents from factories located on the banks of the river, Periyar.To study the activity levels of acid and alkaline phosphatases in crabs, at three time periods, exposed to three sub lethal concentration of mercury,
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fish bioassays are valuable tools that can be used to elucidate the toxicological potential of numerous substances that are present in the aquatic environment. In this study, we assessed the antagonistic action of selenium (Se) against the toxicity of mercury (Hg) in fish (Oreochromis niloticus). Six experimental groups with six fish each were defined as follows: (1) control, (2) mercury (HgCl2), (3) sodium selenite (Na2Se4O3), (4) sodium selenate (Na2Se6O4), (5) mercury + sodium selenite (HgCl2 + Na2Se4O3), and (6) mercury + sodium selenate (HgCl2 + Na2Se6O4). Hematological parameters [red blood cells (RBC), white blood cells (WBC), and erythroblasts (ERB)] in combination with cytogenotoxicity biomarkers [nuclear abnormalities (NAs) and micronuclei (MN)] were examined after three, seven, ten, and fourteen days. After 7 days of exposure, cytogenotoxic effects and increased erythroblasts caused by mercury, leukocytosis triggered by mercury + sodium selenite, leukopenia associated with sodium selenate, and anemia triggered by mercury + sodium selenate were observed. Positive correlations that were independent of time were observed between WBC and RBC, ERB and MN, and NA and MN. The results suggest that short-term exposure to chemical contaminants elicited changes in blood parameters and produced cytogenotoxic effects. Moreover, NAs are the primary manifestations of MN formation and should be included in a class characterized as NA only. Lastly, the staining techniques used can be applied to both hematological characterization and the measurement of cytogenotoxicity biomarkers.
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Mercury (Hg) pollution is a global environmental problem. Numerous Hg-contaminated sites exist in the world and new techniques for remediation are urgently needed. Phytoremediation, use of plants to remove pollutants from the environment or to render them harmless, is considered as an environment-friendly method to remediate contaminated soil in-situ and has been applied for some other heavy metals. Whether this approach is suitable for remediation of Hg-contaminated soil is, however, an open question. The aim of this thesis was to study the fate of Hg in terrestrial plants (particularly the high biomass producing willow, Salix spp.) and thus to clarify the potential use of plants to remediate Hg-contaminated soils. Plants used for phytoremediation of Hg must tolerate Hg. A large variation (up to 30-fold difference) was detected among the six investigated clones of willow in their sensitivity to Hg as reflected in their empirical toxicity threshold (TT95b), the maximum unit toxicity (UTmax) and EC50 levels. This gives us a possibility to select Hg-tolerant willow clones to successfully grow in Hgcontaminated soils for phytoremediation. Release of Hg into air by plants is a concern when using phytoremediation in practice. No evidence was found in this study that Hg was released to the air via shoots of willow, garden pea (Pisum sativum L. cv Faenomen), spring wheat (Triticum aestivum L. cv Dragon), sugar beet (Beta vulgaris L. cv Monohill), oil-seed rape (Brassica napus L. cv Paroll) and white clover (Trifolium repens L.). Thus, we conclude that the Hg burden to the atmosphere via phytoremediation is not increased. Phytoremediation processes are based on the ability of plant roots to accumulate Hg and to translocate it to the shoots. Willow roots were shown to be able to efficiently accumulate Hg in hydroponics, however, no variation in the ability to accumulate was found among the eight willow clones using CVAAS to analyze Hg content in plants. The majority of the Hg accumulated remained in the roots and only 0.5-0.6% of the Hg accumulation was translocated to the shoots. Similar results were found for the five common cultivated plant species mentioned above. Moreover, the accumulation of Hg in willow was higher when being cultivated in methyl-Hg solution than in inorganic Hg solution, whereas the translocation of Hg to the shoots did not differ. The low bioavailability of Hg in contaminated soil is a restricting factor for the phytoextraction of Hg. A selected tolerant willow clone was used to study whether iodide addition could increase the plant-accumulation of Hg from contaminated soil. Both pot tests and field trials were carried out. Potassium iodide (KI) addition was found to mobilize Hg in contaminated soil and thus increase the bioavailability of Hg in soils. Addition of KI (0.2–1 mM) increased the Hg concentrations up to about 5, 3 and 8 times in the leaves, branches and roots, respectively. However, too high concentrations of KI were toxic to plants. As the majority of the Hg accumulated in the roots, it might be unrealistic to use willow for phytoextraction of Hg in practice, even though iodide could enhance the phytoextraction efficiency. In order to study the effect of willow on various soil fractions of Hg-contaminated soil, a 5-step sequential soil extraction method was used. Both the largest Hg-contaminated fractions, i.e. the Hg bound to residual organic matter (53%) and sulphides (43%), and the residual fraction (2.5%), were found to remain stable during cultivations of willow. The exchangeable Hg (0.1%) and the Hg bound to humic and fulvic acids (1.1%) decreased in the rhizospheric soil, whereas the plant accumulation of Hg increased with the cultivation time. The sum of the decrease of the two Hg fractions in soils was approximately equal to the amount of the Hg accumulated in plants. Consequently, plants may be suitable for phytostabilization of aged Hg-contaminated soil, in which root systems trap the bioavailable Hg and reduce the leakage of Hg from contaminated soils.
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Since it is very toxic and accumulates in organisms, particularly in fish, mercury is a very important pollutant and one of the most studies. And this concern over the toxicity and human health risks of mercury has prompted efforts to regulate anthropogenic emissions. As mercury pollution problem is getting increasingly serious, we are curious about how serious this problem will be in the future. What is more, how the climate change in the future will affect the mercury concentration in the atmosphere. So we investigate the impact of climate change on mercury concentration in the atmosphere. We focus on the comparison between the mercury data for year 2000 and for year 2050. The GEOS-Chem model shows that the mercury concentrations for all tracers (1 to 3), elemental mercury (Hg(0)), divalent mercury (Hg(II)) and primary particulate mercury (Hg(P)) have differences between 2000 and 2050 in most regions over the world. From the model results, we can see the climate change from 2000 to 2050 would decrease Hg(0) surface concentration in most of the world. The driving factors of Hg(0) surface concentration changes are natural emissions(ocean and vegetation) and the transformation reactions between Hg(0) and Hg(II). The climate change from 2000 to 2050 would increase Hg(II) surface concentration in most of mid-latitude continental parts of the world while decreasing Hg(II) surface concentration in most of high-latitude part of the world. The driving factors of Hg(II) surface concentration changes is deposition amount change (majorly wet deposition) from 2000 to 2050 and the transformation reactions between Hg(0) and Hg(II). Climate change would increase Hg(P) concentration in most of mid-latitude area of the world and meanwhile decrease Hg(P) concentration in most of high-latitude regions of the world. For the Hg(P) concentration changes, the major driving factor is the deposition amount change (mainly wet deposition) from 2000 to 2050.
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Mercury (Hg) contamination is a global issue due to its anthropogenic release, long-range transport, and deposition in remote areas. In Kejimkujik National Park and National Historic Site, Nova Scotia, Canada, high concentrations of total mercury (THg) were found in tissues of yellow perch (Perca flavescens). The aim of this study was to evaluate a possible relationship between THg concentrations and the morphology of perch liver as a main site of metal storage and toxicity. Yellow perch were sampled from five lakes known to contain fish representing a wide range in Hg concentrations in fall 2013. The ultrastructure of hepatocytes and the distribution of Hg within the liver parenchyma were analyzed by transmission electron microscopy (TEM) and electron energy loss spectrometry (EELS). The relative area of macrophage aggregates (MAs) in the liver was determined using image analysis software and fluorescence microscopy. No relation between general health indicators (Fulton's condition index) and THg was observed. In line with this, TEM examination of the liver ultrastructure revealed no prominent pathologies related to THg accumulation. However, a morphological parameter that appeared to increase with muscle THg was the relative area of MAs in the liver. The hepatic lysosomes appeared to be enlarged in samples with the highest THg concentrations. Interestingly, EELS analysis revealed that the MAs and hepatic lysosomes contained Hg.