Relevant bibliographies by topics / Methylmercury

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Methylmercury'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 February 2023

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Journal articles on the topic "Methylmercury"

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Turner, C. J., M. K. Bhatnagar, and H. Speisky. "Effect of subchronic administration of ethanol and methylmercury in combination on the tissue distribution of mercury in rats." Canadian Journal of Physiology and Pharmacology 68, no. 12 (December 1, 1990): 1558–62. http://dx.doi.org/10.1139/y90-237.

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The effect of oral administration for 14 weeks of 8 g∙kg−1∙day−1 ethanol and 0.5 mg∙kg−1∙day−1 methylmercuric chloride in combination to rats fed isocaloric diets has been investigated. Ethanol, in contrast to published studies, failed to influence the tissue distribution of methylmercury and its inorganic mercury metabolite in brain and kidney, and did not inhibit the increase in kidney weight induced by methylmercury. Ethanol and methylmercury, in combination and individually, reduced the renal but not the hepatic activity of γ-glutamyltransferase, but did not affect the renal and biliary concentration of reduced glutathione. Further study is required to determine the circumstances under which ethanol can influence the tissue distribution of methylmercury and its inorganic mercury metabolite.Key words: toxicology, ethanol, methylmercury.
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Madson, Mark R., and Richard D. Thompson. "Determination of Methylmercury in Food Commodities by Gas-Liquid Chromatography with Atomic Emission Detection." Journal of AOAC INTERNATIONAL 81, no. 4 (July 1, 1998): 808–16. http://dx.doi.org/10.1093/jaoac/81.4.808.

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Abstract A method was developed for determining methylmercury in various food commodities. The organomercurial species was converted to methylmercuric chloride by treatment of a sample homogenized with 1.8M HCI. The resulting chlorinated species was eluted from a Celite 545-sample homogenate column with methylene chloride. The eluate was treated with stannic chloride, and the analyte was isolated from coextractives by using a wide-bore capillary column with microwave-induced plasma atomic emission detection. The method was applied to both high- and low-moisture commodities during analysis of 32 samples of grains, cereal products, fruits, and vegetables. Methylmercury was found at trace levels (i.e., between a signal-to-noise ratio of 3:1 and 10:1) and up to 0.85 ppb. Recoveries of added methylmercury ranged from 70.0 to 114.0℅. Limits of quantitation and detection were 0.63 and 0.24 pg on column, respectively, corresponding to 0.30 and 0.11 ng Hg/g sample for a 40 g sample treated according to the method.
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Jackson, Alan C. "Chronic Neurological Disease Due to Methylmercury Poisoning." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, no. 6 (October 3, 2018): 620–23. http://dx.doi.org/10.1017/cjn.2018.323.

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AbstractOrganic mercury, especially methylmercury, poisoning causes chronic neurological disease predominantly affecting the brain. There have been documented exposures from eating fish from contaminated waters in Japan and in northwestern Ontario and in Iraq from eating bread made from seed wheat treated with methylmercuric fungicide. The neurological disease is called Minamata disease in Japan. Visual field constriction due to involvement of the calcarine cortex, sensory disturbance due to involvement of the somatosensory cortex, and cerebellar ataxia due to involvement of granule cell neurons of the cerebellum are common and characteristic features due to methylmercury poisoning. Other neurological features include dysarthria, postural and action tremor, cognitive impairment, and hearing loss and dysequilibrium. In contrast, peripheral nerve disease is more characteristic of inorganic mercury intoxication. Similarly, psychosis is more typical of exposure to inorganic mercury, which has been documented in the felt hat industry (“mad hatter”). Laboratory tests (e.g., on blood and hair and toenail samples) are of limited value in the assessment of chronic neurological disease due to mercury poisoning because they may not reflect remote neuronal injury due to mercury. Methylmercury also causes injury to fetal brains during development. There is no effective treatment.
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Toyama, Takashi, Sidi Xu, Ryo Nakano, Takashi Hasegawa, Naoki Endo, Tsutomu Takahashi, Jin-Yong Lee, Akira Naganuma, and Gi-Wook Hwang. "The Nuclear Protein HOXB13 Enhances Methylmercury Toxicity by Inducing Oncostatin M and Promoting Its Binding to TNFR3 in Cultured Cells." Cells 9, no. 1 (December 23, 2019): 45. http://dx.doi.org/10.3390/cells9010045.

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Homeobox protein B13 (HOXB13), a transcription factor, is related to methylmercury toxicity; however, the downstream factors involved in enhancing methylmercury toxicity remain unknown. We performed microarray analysis to search for downstream factors whose expression is induced by methylmercury via HOXB13 in human embryonic kidney cells (HEK293), which are useful model cells for analyzing molecular mechanisms. Methylmercury induced the expression of oncostatin M (OSM), a cytokine of the interleukin-6 family, and this was markedly suppressed by HOXB13 knockdown. OSM knockdown also conferred resistance to methylmercury in HEK293 cells, and no added methylmercury resistance was observed when both HOXB13 and OSM were knocked down. Binding of HOXB13 to the OSM gene promoter was increased by methylmercury, indicating the involvement of HOXB13 in the enhancement of its toxicity. Because addition of recombinant OSM to the medium enhanced methylmercury toxicity in OSM-knockdown cells, extracellularly released OSM was believed to enhance methylmercury toxicity via membrane receptors. We discovered tumor necrosis factor receptor (TNF) receptor 3 (TNFR3) to be a potential candidate involved in the enhancement of methylmercury toxicity by OSM. This toxicity mechanism was also confirmed in mouse neuronal stem cells. We report, for the first time, that HOXB13 is involved in enhancement of methylmercury toxicity via OSM-expression induction and that the synthesized OSM causes cell death by binding to TNFR3 extracellularly.
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Sakamoto, Mineshi, Nozomi Tatsuta, Kimiko Izumo, Phuong Phan, Loi Vu, Megumi Yamamoto, Masaaki Nakamura, Kunihiko Nakai, and Katsuyuki Murata. "Health Impacts and Biomarkers of Prenatal Exposure to Methylmercury: Lessons from Minamata, Japan." Toxics 6, no. 3 (August 3, 2018): 45. http://dx.doi.org/10.3390/toxics6030045.

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The main chemical forms of mercury are elemental mercury, inorganic divalent mercury, and methylmercury, which are metabolized in different ways and have differing toxic effects in humans. Among the various chemical forms of mercury, methylmercury is known to be particularly neurotoxic, and was identified as the cause of Minamata disease. It bioaccumulates in fish and shellfish via aquatic food webs, and fish and sea mammals at high trophic levels exhibit high mercury concentrations. Most human methylmercury exposure occurs through seafood consumption. Methylmercury easily penetrates the blood-brain barrier and so can affect the nervous system. Fetuses are known to be at particularly high risk of methylmercury exposure. In this review, we summarize the health effects and exposure assessment of methylmercury as follows: (1) methylmercury toxicity, (2) history and background of Minamata disease, (3) methylmercury pollution in the Minamata area according to analyses of preserved umbilical cords, (4) changes in the sex ratio in Minamata area, (5) neuropathology in fetuses, (6) kinetics of methylmercury in fetuses, (7) exposure assessment in fetuses.
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CLARKSON, TOM. "Methylmercury." Toxicological Sciences 16, no. 1 (1991): 20–21. http://dx.doi.org/10.1093/toxsci/16.1.20.

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CLARKSON, T. "Methylmercury." Fundamental and Applied Toxicology 16, no. 1 (January 1991): 20–21. http://dx.doi.org/10.1016/0272-0590(91)90129-r.

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Aschner, Michael, and Tore Syversen. "Methylmercury." Therapeutic Drug Monitoring 27, no. 3 (June 2005): 278–83. http://dx.doi.org/10.1097/01.ftd.0000160275.85450.32.

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Reynolds, J. N., and W. J. Racz. "Effects of methylmercury on the spontaneous and potassium-evoked release of endogenous amino acids from mouse cerebellar slices." Canadian Journal of Physiology and Pharmacology 65, no. 5 (May 1, 1987): 791–98. http://dx.doi.org/10.1139/y87-127.

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The effects of methylmercury on the spontaneous and potassium-evoked release of endogenous amino acids from mouse cerebellar slices have been examined. Methylmercury induced a concentration-dependent increase in the spontaneous release of glutamate, aspartate, γ-aminobutyric acid, and taurine from mouse cerebellar slices. Glycine release was slightly increased, but not in a concentration-dependent manner. The spontaneous release of glutamine from mouse cerebellar slices was not altered by any concentration of methylmercury examined (10, 20, and 50 μM). The tissue content of glutamate, γ-aminobutyric acid, glutamine, and taurine decreased after exposure to methylmercury. Exposure of cerebellar slices to 20 μM methylmercury resulted in a significant enhancement in glutamate release during stimulation with 35 mM K+. This increase could be accounted for by the methylmercury-induced increase in spontaneous glutamate release. The increase in spontaneous release of glutamate and γ-aminobutyric acid was independent of the availability of extracellular calcium. These results suggest that methylmercury increases the release of neurotransmitter amino acids, particularly γ-aminobutyric acid and glutamate, by acting at intracellular sites to increase release from a neurotransmitter pool. The increase in the potassium-stimulated release of glutamate may reflect an increased sensitivity of the cerebellar granule cell to the effects of methylmercury. It is suggested that alterations in amino acid neurotransmitter function in the cerebellum may contribute to some of the neurological symptoms of methylmercury intoxication.
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Luk, Grace K., and Wai C. Au Yeung. "Modelling Human Exposure of Methylmercury from Fish Consumption." Water Quality Research Journal 41, no. 1 (February 1, 2006): 1–15. http://dx.doi.org/10.2166/wqrj.2006.001.

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Abstract Mercury and its compounds are widely distributed in the environment and the principal cause of methylmercury accumulation in humans is fish consumption. The rate of methylmercury accumulation depends on many factors including the amount, size, type and frequency of fish consumed, as well as contamination levels in the aquatic habitat. The ability to predict accurately human exposure to methylmercury through fish consumption is essential to the setting of public consumption guidelines. This paper describes the development of an innovative method of estimating human exposure to methylmercury through sport fish consumption by mathematical modelling. Through a judicious combination of fish methylmercury bioaccumulation models and survey information on human fish-eating habits, the model allows for a scientifically based estimation of the average daily exposure to methylmercury from fish consumption. It provides a practical tool to estimate the methylmercury uptake from a fish diet as governed by the diet frequency, fish species and fish size. The efficacy of the model is demonstrated by application to six common Lake Ontario fish species. Results showed that the human methylmercury exposure from fish consumption is a serious issue, as demonstrated by the exceedance of the tolerable daily intake levels in many instances. It was also found that the level of human methylmercury uptake depends heavily on the species of fish consumed; among the six species studied, walleye carries the highest risk, followed by yellow perch, while rainbow trout seems to be the safest with the lowest bioaccumulation levels.
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Dissertations / Theses on the topic "Methylmercury"

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Tanner, Kari Christine. "Methylmercury in California Rice Ecosystems." Thesis, University of California, Davis, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10642100.

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Methylmercury (MeHg) is a toxic and bioaccumulative form of mercury that can be produced by bacteria living in water saturated soils, including those found in flooded rice fields. In the Sacramento Valley, California, rice is grown on 240,000 hectares, and mercury is a concern due to a history of mining in the surrounding mountains.

Using unfiltered aqueous MeHg data from MeHg monitoring programs in the Sacramento River watershed from 1996 to 2007, the MeHg contribution from rice systems to the Sacramento River, was assessed. AgDrain MeHg concentrations were elevated compared to upstream river water during November through May, but were not significantly different during June through October. June through October AgDrain MeHg loads (concentration × flow) contributed 10.7–14.8% of the total Sacramento River MeHg load. Missing flow data prevented calculation of the percent contribution of AgDrains in November through May.

Field scale MeHg dynamics were studied in two commercial rice fields in the Sacramento Valley. The Studied fields had soil total mercury concentrations of 25 and 57 ng g-1, which is near the global background level. Surface water and rice grain MeHg and THg concentrations were low compared to previously studied fields. An analysis of surface water drainage loads indicates that both fields were net MeHg importers during the growing season and net MeHg exporters during the fallow season.

Since the microbes that produce MeHg prefer flooded environments, management that dries the soil might reduce MeHg production. Conventional continuously flooded (CF) rice field water management was compared to alternate wetting and drying, where irrigation was stopped twice during the growing season, allowing soil to dry to 35% volumetric moisture content, at which point plots were re-flooded (AWD-35). Compared to CF, AWD-35 resulted in a significant reduction of MeHg concentration in soil, surface water and rice grain.

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Campbell, Sonja Gray. "Methylmercury Neurotoxicity and Interactions with Selenium." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33173.

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Methylmercury (MeHg) is a ubiquitous contaminant and potent neurotoxicant with no completely effective therapy, although selenium antagonises MeHg toxicity. Furthermore, nanoparticles are promising as a novel drug delivery system. We researched the potential of selenium nanoparticles (SeNPs) in antagonising MeHg neurotoxicity compared to selenomethionine (SeMet) using primary astrocyte cell cultures and examining outcomes related to oxidative stress. We found that SeNPs were more toxic than SeMet. Increasing SeNPs significantly decreased MeHg cellular uptake and MeHg significantly decreased uptake of SeNPs at the highest concentration. Finally, SeNPs alone produced significantly higher reactive oxidative species and altered the ratio of reduced-to-oxidised glutathione, but MeHg, SeMet, and co-exposures did not. There were no significant effects on glutathione peroxidase or reductase activity. This suggests that SeNPs are more toxic than MeHg in cerebellar astrocytes and that they may not be suitable as a therapy at the doses and formulation used in this research.
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Heyes, Andrew. "Methylmercury in natural and disturbed wetlands." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40361.

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Methylmercury (MeHg) is the most toxic species of mercury (Hg), and is an important ecosystem contaminant. In wetlands on the Canadian Shield, in NW Ontario, MeHg concentrations in peat and peat porewater ranged from 0.3 to 53 ng $ rm g sp{-1}$ and $<$0.1 to $ rm 7.3 ng l sp{-1},$ respectively. The greatest concentrations of MeHg occurred just below the water table, emphasizing the importance of redox reactions in Hg methylation. Methylmercury partition coefficients between peat and peat porewater ranged from $1.6 times 10 sp3$ to $8.6 times 10 sp5.$ No significant correlations between MeHg and concentrations of $ rm H sp+, NH sb4 sp+, NO sb3 sp-, NO sb2 sp-,$ total dissolved nitrogen (TDN), total dissolved phosphorus (TDP), $ rm SO sb4 sp{2-},$ and dissolved organic carbon (DOC) in the porewater of the wetlands were found.
Following shallow impoundment of a wetland, MeHg concentrations in the upper metre of peat porewater increased from $ rm 0.2 pm 0.2 ng l sp{-1}$ to $ rm 0.8 pm 0.8 ng l sp{-1}.$ Total mercury (T-Hg) and MeHg concentrations were determined in decomposing sedge, spruce needles, and Sphagnum moss, placed in a headwater wetland and the impounded wetland. The amount of T-Hg decreased in all tissues regardless of location. the amount of MeHg increased by as much as an order of magnitude in the tissues placed in the impounded wetland and wet areas (hollows and lawns) of the headwater wetland, but decreased in tissue placed in the dry areas (hummocks) of the headwater wetland. Therefore, it is during anaerobic decomposition of plant material that MeHg is produced in wetlands.
Incubations of peat were performed with addition of Hg, molybdate, $ rm SO sb4 sp{2-}, S sp{2-}, NH sb4NO sb3,$ pyruvate, and upland DOC. Methylmercury production was increased only after addition of $ rm SO sb4 sp{2-}$ and retarded only by $ rm NH sb4NO sb3.$ Although $ rm SO sb4 sp{2-}$ may not be required to methylate Hg, the increased availability of $ rm SO sb4 sp{2-}$ may influence the size and composition of the population of sulfate reducing bacteria in peat, thereby increasing the potential for Hg methylation.
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Hoffman, Nick(Nicholas D. ). "Modeling methylmercury in Maine's tribal meres." Thesis, Massachusetts Institute of Technology, 2018. https://hdl.handle.net/1721.1/122866.

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Thesis: S.B., Massachusetts Institute of Technology, Department of Earth, Atmospheric, and Planetary Sciences, 2018
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 59-76).
Methylmercury (MeHg) concentrations in the fish of twenty Maine lakes were projected for the year 2035 under three different policy scenarios. A mechanistic model of Hg fate and transport was calibrated for Maine's environment using four parameters: volumetric outflow rate, settling velocity, burial velocity, and Hg(II) biotic solids partitioning coefficient. The model was evaluated through comparison with measured results from the year 1993. The model results showed that the strictest global Hg regulations will lead to the greatest decreases in MeHg concentration. No piscivore will be safe for frequent consumption, even under the strictest regulations in the cleanest lakes. The Wabanaki traditional-subsistence diet will continue to entail unsafe MeHg exposures.
by Nick Hoffman.
S.B.
S.B. Massachusetts Institute of Technology, Department of Earth, Atmospheric, and Planetary Sciences
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Loseto, Lisa Lucia. "Methylmercury sources in the Canadian High Arctic." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26515.

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Mercury is increasing to toxic levels in Arctic biota living at the top of food webs. The rapid bioaccumulation and biomagnification of methylmercury (MeHg) in food chains, and the subsistence lifestyle of northern populations, has resulted in high levels of Hg in their blood. No prior measurements of MeHg sources to Arctic ecosystems have been made. In southern latitudes wetlands are considered important sources of MeHg with sulfate-reducing bacteria (SRB) thought to be responsible. Thus, the production of MeHg in Arctic wetlands was evaluated as well as SRB presence. Arctic wetlands were further evaluated as sources of MeHg in Arctic ecosystems, as well since snowmelt water provides 60 to 80% of water to Arctic terrestrial systems it was also evaluated as a source of MeHg. This was the first study to evaluate sources of MeHg entering Arctic ecosystems, and showed that although wetlands produced MeHg, the export to downstream lakes was dependant on site characteristics such as DOC levels, furthermore snowmelt water was the most significant source of MeHg to Arctic ecosystems measured here. (Abstract shortened by UMI.)
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Ruck, Philip Lawrence. "Cycling and Speciation of Mercury in Soils and Cadillac Brook and Hadlock Brook Watersheds, Acadia National Park, Maine." Fogler Library, University of Maine, 2002. http://www.library.umaine.edu/theses/pdf/RuckPL2002.pdf.

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Johnson, Kenneth B. "Fire and its Effects on Mercury and Methylmercury Dynamics for Two Watersheds in Acadia National Park, Maine." Fogler Library, University of Maine, 2002. http://www.library.umaine.edu/theses/pdf/JohnsonKB2002.pdf.

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Kaur, Parvinder. "Cellular and Molecular Mechanisms Behind Methylmercury-Induced Neurotoxicity." Doctoral thesis, Norwegian University of Science and Technology, Department of Neuroscience, 2008. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-2225.

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Bellum, Sairam. "Neurotoxic mechanisms of methylmercury: cellular and behavior changes." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4992.

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The organic or methylated form of mercury (Hg), consisting of one methyl group bound to each atom of Hg, (methylmercury; MeHg), accounts for most of the Hg to which humans are exposed. MeHg, by virtue of its lipophilicity is highly neurotoxic to both the developing and mature central nervous system (CNS). Historically, MeHg has been implicated in high morbidity and mortality rates over the last 40 years in Japan, Iraq, Pakistan and Guatemala. The most common symptom exhibited in these exposure episodes was cerebellar ataxia. Recent in vitro studies using cultured granule cells showed that MeHg alters intracellular calcium ion ([Ca2+]i) homeostasis, potentiates reactive oxygen species (ROS) generation and loss of mitochondrial membrane potential leading to apoptotic death of cerebellar granule neurons. To better understand the neurotoxic mechanisms of MeHg on cerebellum, changes with respect to biochemical processes in cerebellar granule cells and associated behavior changes were investigated. The aims of this dissertation were: (1) to assess mercury concentrations in mouse brain using different routes of administration and different tissue preparations, (2) to determine the behavior effects of in vivo MeHg exposure in young adult mice. (3) to understand specific biochemical processes leading to granule cell death/dysfunction due to in vivo MeHg toxicity in mice, and (4) to determine the toxic effects of in vivo MeHg exposure on mice aged between 16-20 months. The present results showed that repeated oral exposure to MeHg results in greater accumulation of Hg in brain tissue when compared to single oral or subcutaneous exposures at the same concentration of MeHg. Behavior analysis revealed that MeHg at the concentrations used in this study had profound effects on motor coordination and balance in young adult and aged mice. Investigation of biochemical processes in cerebellar granule cells of mice exposed to MeHg showed an increase in ROS generation, alteration of ([Ca2+]i (in young adult mice) and loss of MMP in young adult and aged mice. However, these changes did not lead to apoptotic cell death of granule cells at the concentrations of MeHg used and at the specific time point it was investigated in young adult mice.
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Gibson, Jennifer C. W. "The effects of methylmercury ingestion on amphibian tadpoles." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27137.

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Methylmercury (MeHg) is a toxic heavy metal and a health threat to wildlife and humans, however nothing is known about its effects on amphibians. MeHg is produced from inorganic Hg in the aquatic environment, and bioaccumulates in the food chain. This exposes tadpoles to elevated levels of MeHg in their diet, and may pose a risk to development. Tadpoles of the North American species Bufo americanus and Rana pipiens as well as the African frog model species Xenopus tropicalis were subchronically exposed to dietary McHg ranging in concentration from 1ng/g to 1000 ng/g to determine LC50s and species sensitivity differences. A developmental differences study was also performed with B. americanus. The 33-day LC50 estimates indicate that Gosner stage 25 tadpoles of both B. americanus and R. pipiens were the most sensitive, and they exhibited a similar sensitivity to McHg toxicity. The X. tropicales LC50 estimate is significantly higher (p=0.05) than those calculated for B. americanus and R. pipiens Gosner stage 25, and the developmentally advanced B. americanus Gosner stage 27-30 LC50 estimate is also significantly higher (p=0.05) than the B. americanus Gosner stage 25 LC50. (Abstract shortened by UMI.)
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Books on the topic "Methylmercury"

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Ceccatelli, Sandra, and Michael Aschner, eds. Methylmercury and Neurotoxicity. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6.

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Clampet, Andrew P. Methylmercury: Formation, sources, and health effects. New York: Nova Science Publishers, 2011.

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Hoffman, Ray J. Methylmercury in water and bottom sediment along the Carson River system, Nevada and California, September 1998. Carson City, Nev: U.S. Dept. of the Interior, U.S. Geological Survey, 2000.

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Yamashita, Michiaki. Gyoshoku to kenkō: Mechiru suigin no seibutsu eikyō. Tōkyō-to Minato-ku: Kōseisha Kōseikaku, 2014.

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1921-, Tsubaki Tadao, and Takahashi Hitoshi 1926-, eds. Recent advances in minamata disease studies: Methylmercury poisoning in Minamata and Niigata, Japan. Tokyo: Kodansha, 1986.

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Carmouze, Jean-Pierre, Marc Lucotte, and Alain Boudou. Le mercure en Amazonie: Rôle de l'homme et de l'environnement, risques sanitaires. Paris: IRD éditions, 2001.

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Office, Canada Environment Canada National Guidelines and Standards. Canadian tissue residue guidelines for the protection of consumers of aquatic life: Methylmercury. Ottawa: The Office, 2001.

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DeWild, John F. Determination of methyl mercury by aqueous phase ethylation, followed by gas chromatographic separation with cold vapor atomic fluorescence detection. Middleton, Wis: U.S. Dept. of the Interior, U.S. Geological Survey, 2002.

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Hoffman, Ray J. Methylmercury in water and bottom sediment along the Carson River system, Nevada and California, September 1998. Carson City, Nev: U.S. Dept. of the Interior, U.S. Geological Survey, 2000.

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Maryland. Monitoring and Non-Tidal Assessment Division. An examination of the factors that control methylmercury production and bioaccumulation in Maryland reservoirs: Final report. Annapolis, Md: Maryland Dept. of Natural Resources, Monitoring and Non-Tidal Assessment Division, 2008.

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Book chapters on the topic "Methylmercury"

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Clarkson, Thomas W. "Methylmercury Toxicity." In Trace Elements in Clinical Medicine, 465–70. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68120-5_60.

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Bach, Robert D., Harsha B. Vardhan, Donald W. Goebel, and John P. Oliver. "Methylmercury(II) Nitrate and Methylmercury (II) Trifluoroacetate." In Inorganic Syntheses, 143–46. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470132555.ch43.

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Hachiya, Noriyuki. "Epidemiological Update of Methylmercury and Minamata Disease." In Methylmercury and Neurotoxicity, 1–11. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_1.

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Onishchenko, Natalia, Nina N. Karpova, and Eero Castrén. "Epigenetics of Environmental Contaminants." In Methylmercury and Neurotoxicity, 199–218. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_10.

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Costa, Lucio G., and Gennaro Giordano. "Methylmercury Neurotoxicity: A Synopsis of In Vitro Effects." In Methylmercury and Neurotoxicity, 219–27. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_11.

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Usuki, Fusako, and Masatake Fujimura. "Effects of Methylmercury on Cellular Signal Transduction Systems." In Methylmercury and Neurotoxicity, 229–40. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_12.

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Kaur, Parvinder, Michael Aschner, and Tore Syversen. "Methylmercury Neurotoxicity: Why Are some Cells more Vulnerable than Others?" In Methylmercury and Neurotoxicity, 241–58. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_13.

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Suñol, Cristina, and Eduard Rodríguez-Farré. "In Vitro Models for Methylmercury Neurotoxicity: Effects on Glutamatergic Cerebellar Granule Neurons." In Methylmercury and Neurotoxicity, 259–70. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_14.

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Zhaobao, Yin, Marcelo Farina, João B. T. Rocha, Parvinder Kaur, Tore Syversen, and Michael Aschner. "Methylmercury and Glia Cells." In Methylmercury and Neurotoxicity, 271–85. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_15.

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Edoff, Karin, and Sandra Ceccatelli. "Methylmercury and Neural Stem Cells." In Methylmercury and Neurotoxicity, 287–302. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6_16.

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Conference papers on the topic "Methylmercury"

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Zhang, Yanxu. "Bioaccumulation of Methylmercury in a Marine Plankton Ecosystem." In Goldschmidt2020. Geochemical Society, 2020. http://dx.doi.org/10.46427/gold2020.3140.

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JOHNS, N., J. KURTZMAN, Z. SHTASEL-GOTTLIEB, S. RAUCH, and D. I. WALLACE. "THE BIOACCUMULATION OF METHYLMERCURY IN AN AQUATIC ECOSYSTEM." In BIOMAT 2010 - International Symposium on Mathematical and Computational Biology. WORLD SCIENTIFIC, 2011. http://dx.doi.org/10.1142/9789814343435_0017.

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Gu, Baohua, Xujun Liang, Pei Lei, Huan Zhong, Alexander Johs, Lijie Zhang, Jiating Zhao, Dale Pelletier, and Eric Pierce. "Phytoplankton Demethylation: An Unexplored Pathway of Methylmercury Detoxification." In Goldschmidt2022. France: European Association of Geochemistry, 2022. http://dx.doi.org/10.46427/gold2022.12142.

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Sun, Ruoyu, Jingjing Yuan, Jeroen Sonke, Wang Zheng, Mei Meng, JiuBin Chen, Yi Liu, Xiaotong Peng, and Cong-Qiang Liu. "Marinana Trench Fauna Accumulate Methylmercury Produced in Upper Oceans." In Goldschmidt2020. Geochemical Society, 2020. http://dx.doi.org/10.46427/gold2020.2504.

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Pierce, Caroline, Stephen Sebestyen, Randall Kolka, Natalie Griffiths, Edward Nater, and Brandy M. Toner. "The Effect of Climate Change on Methylmercury in Boreal Peatlands." In Goldschmidt2020. Geochemical Society, 2020. http://dx.doi.org/10.46427/gold2020.2084.

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Riva Murray, Karen. "TOTAL MERCURY AS A SURROGATE FOR METHYLMERCURY IN AQUATIC MACROINVERTEBRATES." In 51st Annual Northeastern GSA Section Meeting. Geological Society of America, 2016. http://dx.doi.org/10.1130/abs/2016ne-272542.

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Baêta, A. P., H. A. Kehrig, O. Malm, and I. Moreira. "Total mercury and methylmercury in fish from a tropical estuary." In ENVIRONMENTAL TOXICOLOGY 2006. Southampton, UK: WIT Press, 2006. http://dx.doi.org/10.2495/etox060181.

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Rocha, João, Laura Orian, Pablo Nogara, Andrea Madabeni, and Marco Bortoli. "Dehydroalanine Formation from GPx Inhibited by Methylmercury: A DFT Study." In 1st International Electronic Conference on Catalysis Sciences. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/eccs2020-07554.

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Gallorini, Andrea, and Jean-Luc Loizeau. "Methylmercury in suspended particles of a peri-alpine deep lake." In Goldschmidt2021. France: European Association of Geochemistry, 2021. http://dx.doi.org/10.7185/gold2021.7340.

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Schwartz, Grace, Scott Painter, Katherine Muller, and Scott Brooks. "Using Transient Availability Kinetics to Scale Methylmercury Production from Microcosms to Watersheds." In Goldschmidt2020. Geochemical Society, 2020. http://dx.doi.org/10.46427/gold2020.2321.

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Reports on the topic "Methylmercury"

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Meagher, Richard B. Phytoremediation of ionic and methylmercury pollution. Office of Scientific and Technical Information (OSTI), April 2010. http://dx.doi.org/10.2172/1122083.

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Meagher, Richard B. Phytoremediation of ionic and methylmercury pollution. Office of Scientific and Technical Information (OSTI), June 2002. http://dx.doi.org/10.2172/835409.

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Meagher, Richard B. Phytoremediation of ionic and methylmercury pollution. Office of Scientific and Technical Information (OSTI), June 2003. http://dx.doi.org/10.2172/835410.

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Richard Meagher. Phytoremediation of Ionic and Methylmercury Pollution. Office of Scientific and Technical Information (OSTI), January 2006. http://dx.doi.org/10.2172/877184.

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Richard Meagher, Sarah Marshburn, Andrew Heaton, Anne Marie Zimer, and Raoufa Rahman. The Engineered Phytoremediation of Ionic and Methylmercury Pollution. Office of Scientific and Technical Information (OSTI), June 2003. http://dx.doi.org/10.2172/812002.

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Meagher, Richard B. The engineered phytoremediation of ionic and methylmercury pollution 70054yr.2000.doc. Office of Scientific and Technical Information (OSTI), June 2000. http://dx.doi.org/10.2172/833502.

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Meagher, Richard B. The engineered phytoremediation of ionic and methylmercury pollution 70054yr.2001.doc. Office of Scientific and Technical Information (OSTI), June 2001. http://dx.doi.org/10.2172/833503.

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Oji, L. N., and C. A. Langton. Methylmercury Speciation and Retention Evaluation to Support Saltstone Waste Acceptance Criteria. Office of Scientific and Technical Information (OSTI), February 2019. http://dx.doi.org/10.2172/1505946.

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Looney, Brian, Holly Vermeulen, J. Dickson, Thomas White, Andrew Boggess, Thomas Peters, and Emily Fabricatore. Vapor-Liquid Partitioning of Methylmercury Compounds: Fundamental Data to Support the Savannah River Site Liquid Waste System: Henry's Law, Solubility and Vapor Pressure Determination for Representative Methylmercury Compounds. Office of Scientific and Technical Information (OSTI), June 2021. http://dx.doi.org/10.2172/1804664.

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Boggess, A. Speciation of methylmercury and ethylmercury by gas chromatography cold vapor atomic fluresence spectroscopy. Office of Scientific and Technical Information (OSTI), September 2017. http://dx.doi.org/10.2172/1395978.

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