Journal articles: '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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Kuo, TC. "The influence of methylmercury on the nitric oxide production of alveolar macrophages." Toxicology and Industrial Health 24, no. 8 (September 2008): 531–38. http://dx.doi.org/10.1177/0748233708098122.

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Mercury is a global pollutant considered to be a persistent bioaccumulative and toxic chemical. Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes. Methylmercury is more toxic to living organisms than the inorganic forms. In this study, we attempted to elucidate the altered functions of alveolar macrophage including nitric oxide production after methylmercury exposure. Treatment of 7 μM methylmercury for 24 h inhibited lipopolysaccharide-induced nitric oxide and nitric oxide synthase production of alveolar macrophages. The addition of H-89 (PKA inhibitor) significantly decreased the methylmercury inhibition of lipopolysaccharide-mediated nitric oxide production. We found the cell had a calcium-dependent adenylate cyclase, and MeHg could inhibit the phosphorylation of extracellular-signal regulated kinase (ERK). Because methylmercury could increase the intracellular calcium ion concentration, it might activate the adenylate cyclase by increasing [Ca2+]i. Though the interaction of methylmercury with the immune system has been studied by several investigators, the actual mechanisms underlying these interactions are still poorly understood. We discovered that methylmercury could activate protein kinase A, which in turn would inhibit the activation of Raf-1-ERK and so inhibit the release of nitric oxide.

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Karita, Kanae, Toyoto Iwata, Eri Maeda, Mineshi Sakamoto, and Katsuyuki Murata. "Assessment of Cardiac Autonomic Function in Relation to Methylmercury Neurotoxicity." Toxics 6, no. 3 (July 20, 2018): 38. http://dx.doi.org/10.3390/toxics6030038.

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After the European Food Safety Authority reviewed reports of methylmercury and heart rate variability (HRV) in 2012, the panel concluded that, although some studies of cardiac autonomy suggested an autonomic effect of methylmercury, the results were inconsistent among studies and the implications for health were unclear. In this study, we reconsider this association by adding a perspective on the physiological context. Cardiovascular rhythmicity is usually studied within different frequency domains of HRV. Three spectral components are usually detected; in humans these are centered at <0.04 Hz, 0.15 Hz (LF), and 0.3 Hz (HF). LF and HF (sympathetic and parasympathetic activities, respectively) are evaluated in terms of frequency and power. By searching PubMed, we identified 13 studies examining the effect of methylmercury exposure on HRV in human populations in the Faroe Islands, the Seychelles and other countries. Considering both reduced HRV and sympathodominant state (i.e., lower HF, higher LF, or higher LF/HF ratio) as autonomic abnormality, eight of them showed the significant association with methylmercury exposure. Five studies failed to demonstrate any significant association. In conclusion, these data suggest that increased methylmercury exposure was consistently associated with autonomic abnormality, though the influence of methylmercury on HRV (e.g., LF) might differ for prenatal and postnatal exposures. The results with HRV should be included in the risk characterization of methylmercury. The HRV parameters calculated by frequency domain analysis appear to be more sensitive to methylmercury exposure than those by time domain analysis.

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Kuo, Tsun-Cheng. "Methylmercury Induces Alveolar Macrophages Apoptosis." International Journal of Toxicology 27, no. 3 (May 2008): 257–63. http://dx.doi.org/10.1080/10915810802152095.

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Through the use of a scanning electronic microscope, it was found that alveolar macrophages treated with 10 μM of methylmercury for 24 h showed a decrease of surface microvilli, and those treated with 15 μM of methylmercury underwent deformity and subsequent cell death. To investigate their death patterns, DNA was aspirated from alveolar macrophages and analyzed by electrophoresis. It was discovered that the DNA ladder phenomenon became more obvious as the methylmercury increased in concentration. When 5 mM EGTA was used to eliminate calcium ions, a decrease of the ladder phenomenon was observed. Zinc at 1 mM had a similar inhibitory effect. Moreover, an apoptosis peak was observed on flow cytometry analysis of DNA stained with propidium iodide. Alveolar macrophages stained with Hoechst 33342 demonstrated apoptotic bodies induced by methylmercury. The above data indicate that methylmercury can induce a typical apoptosis in alveolar macrophages. Continuing onto the study of the mechanism of apoptosis as induced by methylmercury in alveolar macrophages, it was discovered that methylmercury could increase the intracellular calcium ion concentration and decrease the pH in alveolar macrophages. To find out which endonuclease was responsible for the methylmercury-induced DNA fragmentation of alveolar macrophages, the nuclear proteins of alveolar macrophages was aspirated and tested under different pH values and in conditions with or without calcium ions, and it was discovered that the endonuclease was calcium dependent without relations to pH values.

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Vendrell, Iolanda, Montserrat Carrascal, Maria-Teresa Vilaró, Joaquín Abián, Eduard Rodríguez-Farré, and Cristina Suñol. "Cell viability and proteomic analysis in cultured neurons exposed to methylmercury." Human & Experimental Toxicology 26, no. 4 (April 2007): 263–72. http://dx.doi.org/10.1177/0960327106070455.

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Methylmercury is an environmental contaminant with special selectivity for cerebellar granule cells. The aim of this study was to determine the effect of long-term methylmercury exposure on cell viability and cellular proteome in cultured cerebellar granule cells. Primary cultures of mice cerebellar granule cells were treated with 0-300 nM methylmercury at 2 days in vitro (div) and afterwards the cells were harvested at 12 div. 100 nM methylmercury produced loss of cell viability, reduced intracellular glutamate content and increased lipid peroxidation. Glutamate transport was not modified by methylmercury treatment. Cell death induced by 300 nM methylmercury at 8 div was apoptotic without producing activation of caspase 3. Extracts of total protein were separated by 2D electrophoresis. Around 800 protein spots were visualized by silver staining in SDS-polyacrylamide gels. Gel images were digitized and protein patterns were analysed by image analysis. Several spots were identified through a combination of peptide mass fingerprinting and matrix-assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS). The mitochondrial protein 3-ketoacid-coenzyme A transferase I was decreased up to 39% of controls at concentrations of methylmercury that did not produce cytotoxic effects, whereas the cytoplasmic proteins lactate dehydrogenase chain B and actin did not change. Human & Experimental Toxicology (2007) 26, 263-272

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Kim, Byoung-Gwon, Young-Seoub Hong, Koichi Haraguchi, Mineshi Sakomoto, Hyoun-Ju Lim, Jeong-Wook Seo, and Yu-Mi Kim. "Comparative Screening Analytic Methods for Elderly of Blood Methylmercury Concentration between Two Analytical Institutions." Computational and Mathematical Methods in Medicine 2018 (June 26, 2018): 1–5. http://dx.doi.org/10.1155/2018/2509413.

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Methylmercury is widely known to be a toxic substance in the human, especially a nervous system. However, it is difficult to accurately measure the amount of methylmercury in blood, and the form of methylmercury is variously presented. The purpose of study was to compare the total mercury and methylmercury measurements techniques and detection levels between analytical institutions in two countries using the same elderly human blood samples. Total mercury using gold amalgamation direct mercury analysis method (both) and methylmercury using the dithizone extraction and gas chromatography-electron capture detector (GC-ECD) method (N Lab in Japan) and the cold vapor atomic fluorescence spectrophotometer (CVAFS) method (D Lab in Korea) were measured in 47 subjects who agreed to participate in this study. Total mercury concentrations in both analytical laboratories were observed at similar levels (9.4 versus 9.5 ug/kg, p=0.898) and the distribution was highly correlated. However, the concentration of methylmercury showed some difference between two laboratories (9.1 versus 8.6 ug/kg, p<0.001). Due to different recovery rates by different analytical methods, it is assumed that the methyl/total mercury ratio in N lab in Japan was higher than D lab in Korea (96.8 versus 90.4%, p<0.001). The GC-ECD was more sensitive method than CVAFS in methylmercury analytic techniques.

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Liu, Yang, Wei Zhang, Jiating Zhao, Xiaoying Lin, Liming Wang, Liwei Cui, Junfang Zhang, Bai Li, and Yu-Feng Li. "Using nanoselenium to combat Minamata disease in rats: the regulation of gut microbes." Environmental Science: Nano 8, no. 5 (2021): 1437–45. http://dx.doi.org/10.1039/d1en00267h.

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Culbreth, Megan, and Michael Aschner. "Methylmercury Epigenetics." Toxics 7, no. 4 (November 9, 2019): 56. http://dx.doi.org/10.3390/toxics7040056.

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Methylmercury (MeHg) has conventionally been investigated for effects on nervous system development. As such, epigenetic modifications have become an attractive mechanistic target, and research on MeHg and epigenetics has rapidly expanded in the past decade. Although, these inquiries are a recent advance in the field, much has been learned in regards to MeHg-induced epigenetic modifications, particularly in the brain. In vitro and in vivo controlled exposure studies illustrate that MeHg effects microRNA (miRNA) expression, histone modifications, and DNA methylation both globally and at individual genes. Moreover, some effects are transgenerationally inherited, as organisms not directly exposed to MeHg exhibited biological and behavioral alterations. miRNA expression generally appears to be downregulated consequent to exposure. Further, global histone acetylation also seems to be reduced, persist at distinct gene promoters, and is contemporaneous with enhanced histone methylation. Moreover, global DNA methylation appears to decrease in brain-derived tissues, but not in the liver; however, selected individual genes in the brain are hypermethylated. Human epidemiological studies have also identified hypo- or hypermethylated individual genes, which correlated with MeHg exposure in distinct populations. Intriguingly, several observed epigenetic modifications can be correlated with known mechanisms of MeHg toxicity. Despite this knowledge, however, the functional consequences of these modifications are not entirely evident. Additional research will be necessary to fully comprehend MeHg-induced epigenetic modifications and the impact on the toxic response.

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Cossa, Daniel. "Methylmercury manufacture." Nature Geoscience 6, no. 10 (September 27, 2013): 810–11. http://dx.doi.org/10.1038/ngeo1967.

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Weihe, Pál, and Philippe Grandjean. "Methylmercury Risks." Science 279, no. 5351 (January 30, 1998): 635.5–635. http://dx.doi.org/10.1126/science.279.5351.635e.

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RITTER, STEVE. "METHYLMERCURY DETOX." Chemical & Engineering News 85, no. 29 (July 16, 2007): 10. http://dx.doi.org/10.1021/cen-v085n029.p010.

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Tiekink, Edward R. T. "Methylmercury xanthates." Inorganica Chimica Acta 112, no. 1 (February 1986): L1—L2. http://dx.doi.org/10.1016/s0020-1693(00)85646-7.

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Chauhan, Shubhangi, Kriya Dunlap, and Lawrence K. Duffy. "Effects of Methylmercury and Theaflavin Digallate on Adipokines in Mature 3T3-L1 Adipocytes." International Journal of Molecular Sciences 20, no. 11 (June 5, 2019): 2755. http://dx.doi.org/10.3390/ijms20112755.

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Diabetes is a contributor to morbidity across the globe and is often associated with obesity, metabolic syndrome and other inflammatory diseases associated with aging. In addition to genetic and lifestyle factors, environmental factors such as metals and persistent organic pollutants may increase the severity or lower the threshold of these conditions. In cell culture, methylmercury is toxic to adipocytes and may impact adipokine secretions. In this study, we determined the effects of different concentrations of theaflavin digallate on methylmercury exposed 3T3-L1 adipocytes in cell culture. Secretions of resistin, adiponectin and lipid peroxidation product, 4-hydroxynonenal (4-HNE) were monitored using ELISA assays. Cell morphology of methylmercury and theaflavin-3,3′-digallate treated adipocytes was assessed using Lipid (Oil Red O) staining. Exposure to methylmercury increased the levels of resistin and adiponectin as well as 4-HNE when compared to the control cells. Methylmercury treated cells resulted in smaller number of adipocytes and clumped lipid droplets. These results suggest that methylmercury induces reactive oxygen species leading to development of an inflammatory response. Theaflavin-3,3′-digallate reduced the impact of methylmercury by maintaining the adipocytes morphology and secretion patterns of adiponectin, resistin and 4-hydroxynonenal. With this experimental model system other anti-inflammatory and signaling agents could be tested at the biochemical level before eventually leading to studies in animal models.

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Tatsuta, Nozomi, Kunihiko Nakai, Mineshi Sakamoto, Katsuyuki Murata, and Hiroshi Satoh. "Methylmercury Exposure and Developmental Outcomes in Tohoku Study of Child Development at 18 Months of Age." Toxics 6, no. 3 (August 21, 2018): 49. http://dx.doi.org/10.3390/toxics6030049.

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Seafood is an important component in a healthy diet and may contain methylmercury or other contaminants. It is important to recognize the risks and benefits of consuming seafood. A longitudinal prospective birth cohort study has been conducted to clarify the effects of neurotoxicants on child development—the Tohoku Study of Child Development (TSCD) in Japan. TSCD comprises two cohorts; a polychlorinated biphenyls (PCB) cohort (urban area) and a methylmercury cohort (coastal area). Our previous results from the coastal area showed prenatal methylmercury exposure affected psychomotor development in 18-month-olds, and boys appear to be more vulnerable to the exposure than girls. In this report, we have added the urban area cohort and we reanalyzed the impact of prenatal exposure to methylmercury, which gave the same results as before. These findings suggest prenatal exposure to low levels methylmercury may have adverse effects on child development, especially in boys.

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Silbernagel, Susan M., David O. Carpenter, Steven G. Gilbert, Michael Gochfeld, Edward Groth, Jane M. Hightower, and Frederick M. Schiavone. "Recognizing and Preventing Overexposure to Methylmercury from Fish and Seafood Consumption: Information for Physicians." Journal of Toxicology 2011 (2011): 1–7. http://dx.doi.org/10.1155/2011/983072.

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Fish is a valuable source of nutrition, and many people would benefit from eating fish regularly. But some people eat a lot of fish, every day or several meals per week, and thus can run a significant risk of overexposure to methylmercury. Current advice regarding methylmercury from fish consumption is targeted to protect the developing brain and nervous system but adverse health effects are increasingly associated with adult chronic low-level methylmercury exposure. Manifestations of methylmercury poisoning are variable and may be difficult to detect unless one considers this specific diagnosis and does an appropriate test (blood or hair analysis). We provide information to physicians to recognize and prevent overexposure to methylmercury from fish and seafood consumption. Physicians are urged to ask patients if they eat fish: how often, how much, and what kinds. People who eat fish frequently (once a week or more often) and pregnant women are advised to choose low mercury fish.

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Baxter, Douglas C., Ilia Rodushkin, Emma Engström, Dennis Klockare, and Hans Waara. "Methylmercury Measurement in Whole Blood by Isotope-Dilution GC-ICPMS with 2 Sample Preparation Methods." Clinical Chemistry 53, no. 1 (January 1, 2007): 111–16. http://dx.doi.org/10.1373/clinchem.2007.072520.

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Abstract Background: Despite its known toxicity, methylmercury is rarely measured directly in clinical studies; instead, conclusions are based on total mercury measurements. We have developed isotope–dilution-based methods for methylmercury-specific analysis of whole blood by coupled gas chromatography–inductively coupled plasma mass spectrometry (GC-ICPMS). Methods: We analyzed animal and human blood samples after alkaline digestion or extraction of methylmercury into dichloromethane and back extraction into water. Methylmercury was converted to the volatile ethyl derivative, purged, and trapped on a solid-phase collection medium, and then introduced into the GC-ICPMS system. Results: Limits of quantification were 0.4 and 0.03 μg/L at a signal-to-noise ratio of 10 with the alkaline digestion and extraction methods, respectively. Extraction met our selected acceptable total error criterion, with an SD of 0.58 μg/L at the critical maternal blood concentration of 5.8 μg/L. Results obtained with alkaline digestion indicated the need for improved random analytical uncertainty, which was achieved by increasing the enrichment of the isotope dilution. For 37 blood samples, the mean (SD) proportion of total mercury present as methylmercury was 60 (27)%, range 6%–100%. Conclusions: The combination of extraction and isotope-dilution GC-ICPMS meets the requirements for use as a reference method for measuring methylmercury in whole blood.

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Love, Tanzy MT, Sally W. Thurston, and Philip W. Davidson. "Finding vulnerable subpopulations in the Seychelles Child Development Study: effect modification with latent groups." Statistical Methods in Medical Research 26, no. 2 (December 14, 2014): 809–22. http://dx.doi.org/10.1177/0962280214560044.

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The Seychelles Child Development Study is a research project with the objective of examining associations between prenatal exposure to low doses of methylmercury from maternal fish consumption and children’s developmental outcomes. Whether methylmercury has neurotoxic effects at low doses remains unclear and recommendations for pregnant women and children to reduce fish intake may prevent a substantial number of people from receiving sufficient nutrients that are abundant in fish. The primary findings of the Seychelles Child Development Study are inconsistent with adverse associations between methylmercury from fish consumption and neurodevelopmental outcomes. However, whether there are subpopulations of children who are particularly sensitive to this diet is an open question. Secondary analysis from this study found significant interactions between prenatal methylmercury levels and both caregiver IQ and income on 19-month IQ. These results are sensitive to the categories chosen for these covariates and are difficult to interpret collectively. In this paper, we estimate effect modification of the association between prenatal methylmercury exposure and 19-month IQ using a general formulation of mixture regression. Our mixture regression model creates a latent categorical group membership variable which interacts with methylmercury in predicting the outcome. We also fit the same outcome model when in addition the latent variable is assumed to be a parametric function of three distinct socioeconomic measures. Bayesian methods allow group membership and the regression coefficients to be estimated simultaneously and our approach yields a principled choice of the number of distinct subpopulations. The results show three groups with different response patterns between prenatal methylmercury exposure and 19-month IQ in this population.

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Schartup, Amina T., Prentiss H. Balcom, Anne L. Soerensen, Kathleen J. Gosnell, Ryan S. D. Calder, Robert P. Mason, and Elsie M. Sunderland. "Freshwater discharges drive high levels of methylmercury in Arctic marine biota." Proceedings of the National Academy of Sciences 112, no. 38 (September 8, 2015): 11789–94. http://dx.doi.org/10.1073/pnas.1505541112.

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Elevated levels of neurotoxic methylmercury in Arctic food-webs pose health risks for indigenous populations that consume large quantities of marine mammals and fish. Estuaries provide critical hunting and fishing territory for these populations, and, until recently, benthic sediment was thought to be the main methylmercury source for coastal fish. New hydroelectric developments are being proposed in many northern ecosystems, and the ecological impacts of this industry relative to accelerating climate changes are poorly characterized. Here we evaluate the competing impacts of climate-driven changes in northern ecosystems and reservoir flooding on methylmercury production and bioaccumulation through a case study of a stratified sub-Arctic estuarine fjord in Labrador, Canada. Methylmercury bioaccumulation in zooplankton is higher than in midlatitude ecosystems. Direct measurements and modeling show that currently the largest methylmercury source is production in oxic surface seawater. Water-column methylation is highest in stratified surface waters near the river mouth because of the stimulating effects of terrestrial organic matter on methylating microbes. We attribute enhanced biomagnification in plankton to a thin layer of marine snow widely observed in stratified systems that concentrates microbial methylation and multiple trophic levels of zooplankton in a vertically restricted zone. Large freshwater inputs and the extensive Arctic Ocean continental shelf mean these processes are likely widespread and will be enhanced by future increases in water-column stratification, exacerbating high biological methylmercury concentrations. Soil flooding experiments indicate that near-term changes expected from reservoir creation will increase methylmercury inputs to the estuary by 25–200%, overwhelming climate-driven changes over the next decade.

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Aždajić, Mija, Emmanuel Yumvihoze, Jules M. Blais, and Alexandre J. Poulain. "The effect of legacy gold mining on methylmercury cycling and microbial community structure in northern freshwater lakes." Environmental Science: Processes & Impacts 23, no. 8 (2021): 1220–30. http://dx.doi.org/10.1039/d1em00129a.

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Historical smelting pollution gradient at Giant Mine (Yellowknife, NWT, Canada) affects rate of methylmercury production in sediments and final methylmercury concentrations in water columns of nearby lakes.

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29

McKay, S. J., J. N. Reynolds, and W. J. Racz. "Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices." Canadian Journal of Physiology and Pharmacology 64, no. 12 (December 1, 1986): 1507–14. http://dx.doi.org/10.1139/y86-254.

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The effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices have been examined. All mercury compounds examined produced concentration-dependent increases in the spontaneous release of [3H]dopamine, with an order of potency of methylmercury > mercuric (Hg2+) mercury >p-choloromercuribenzene sulfonic acid. Methylmercury had no effect on the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium. However, in calcium-free conditions, methylmercury significantly increased the potassium-evoked release of [3H]dopamine. Mercuric mercury significantly reduced the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium, and this response was not reversible with brief washing of the tissue. In calcium-free conditions, mercuric mercury significantly elevated the evoked release of [3H]dopamine, similar to the result obtained with methylmercury. It is suggested that mercury compounds alter dopaminergic synaptic function, possibly by disrupting calcium homeostasis or calcium-dependent processes, and that methylmercury and mercuric mercury can have differential effects to alter dopaminergic neurotransmission.

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30

Bowles, Karl C., Simon C. Apte, William A. Maher, Matthew Kawei, and Ross Smith. "Bioaccumulation and biomagnification of mercury in Lake Murray, Papua New Guinea." Canadian Journal of Fisheries and Aquatic Sciences 58, no. 5 (May 1, 2001): 888–97. http://dx.doi.org/10.1139/f01-042.

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The bioaccumulation of mercury in the food webs incorporating the major piscivorous fish species of Lake Murray, Papua New Guinea, has been characterised. Methylmercury concentrations increased with trophic level and the proportion of total mercury present as methylmercury increased from <1% in plants to 94% in piscivorous fish. Methylmercury bioaccumulation factors (BAFs) were similar to those found in temperate environments, with a typical increase of 1 log unit between planktivore and piscivore trophic levels. The greatest bioaccumulation of methylmercury occurred between seston and the water column (log BAF of 5.36). The bioaccumulation of mercury to levels of regulatory concern by the lake's piscivores was attributable to the biomagnification power of the plankton-based food chain comprising four trophic levels (phytoplankton, zooplankton, planktivore, piscivore) rather than any elevated concentrations of mercury in waters or sediments. The methylmercury concentrations of individual piscivores were positively correlated with both trophic position, as indicated by δ15N measurements, and fish size. Stable-isotope measurements were used to identify fish species where dietary changes occurring with age significantly augmented age-related bioaccumulation of mercury.

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31

Liu, Yongwen, Yunhui Zai, Xijun Chang, Yong Guo, Shuangming Meng, and Feng Feng. "Highly selective determination of methylmercury with methylmercury-imprinted polymers." Analytica Chimica Acta 575, no. 2 (August 2006): 159–65. http://dx.doi.org/10.1016/j.aca.2006.05.081.

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32

Maršálek, P., and Z. Svobodová. "Rapid determination of methylmercury in fish tissues." Czech Journal of Food Sciences 24, No. 3 (November 12, 2011): 138–42. http://dx.doi.org/10.17221/3309-cjfs.

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The aim of the present study was to develop a rapid and inexpensive method for the determination of methylmercury in fish tissues based on GC/ECD instrumentation. The new method is based on acidic digestion in hydrochloric acid and subsequent extraction with toluene. Methylmercury is determined by the GC/ECD technique using a DB-608 capillary column. The following parameters of the method were established: detection limit 13 μg/kg, limit of quantification 22 μg/kg, linearity 0.2–200 ng/ml, reproducibility 9.4%, and recovery 90%. The method was developed and verified using CRM 464 reference material and was successfully tested in inter-laboratory comparisons IMEP – 20 “Trace elements in tuna fish” organised by the Joint Research Centre – Institute for Reference Materials and Measurements (Belgium), with the success rate of En=0.43.

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Bubb, J. M., T. P. Williams, and J. N. Lester. "The Behaviour of Mercury within a Contaminated Tidal River System." Water Science and Technology 28, no. 8-9 (October 1, 1993): 329–38. http://dx.doi.org/10.2166/wst.1993.0631.

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The historical emission of mercury from a municipal sewage treatment works, which discharges to a lowland river, has resulted in a 17 km contamination plume, the nature of which is strongly dependent upon river bed morphology. Significant variations occur in the spatial distribution of mercury concentrations over very short distances as dictated by sediment type, channel morphology, hydrology and sedimentation rates. The major sedimentalogical process is one of net deposition of paniculate matter rather than downstream transportation, which has buried contaminated sediment beneath a cleaner overlay. The behaviour of methylmercury within the sediment system is not dependent solely upon total mercury concentrations but instead is governed by a complex interplay between sediment redox potential, temperature, sulphur chemistry and the nature of bacterial communities. Detectable levels of methylmercury were confined to the uppermost 40 cm of sediment with peak loadings occurring 4-8 cm from the sediment/water interface. Methylmercury concentrations vary seasonally with minimum loadings in the autumn and highest concentrations in the summer. The distribution of methylmercury within the sediment compartment closely mirrors that of the mercury tolerant bacteria but in-situ and laboratory based experiments have also linked seasonal variations in methylmercury levels to changes in temperature.

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34

Chen, Long, Feng Li, Wenrou Huang, Zhi Li, and Mingguang Chen. "Evaluation of Mercury Transformation and Benthic Organisms Uptake in a Creek Sediment of Pearl River Estuary, China." Water 11, no. 6 (June 25, 2019): 1308. http://dx.doi.org/10.3390/w11061308.

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A large fraction of mercury contaminant in the environment is from industrial production, and it potentially impairs human health once entering the food chain. Millions of people reside in the Pearl River Delta region, and water quality in the estuary directly affects their drinking water safety. Considering the highly intense anthropogenic activities and industrial productions, we attempted to measure the sediment mercury concentration in the Pearl River estuary. In this work, samples of a creek sediment within this region were collected and mercury concentrations were quantified. Total mercury, simultaneously extracted mercury, methylmercury, and bio-accumulated mercury were individually assayed. Results indicated that total mercury concentrations of investigated sites ranged from 1.073 to 4.450 µg/g dry sediment. The mercury in the sediment also transformed into more toxic methylmercury, which then adversely affected benthos biodiversity. Correlation analysis revealed that, mercury was accumulated into benthic microorganisms, mainly through the uptake of methylmercury. High concentrations of acid-volatile sulfide in the sediment indicated the presence of active sulfate-reducing bacteria, which could also catalytically transform inorganic mercury into methylmercury. Correlation analysis further showed that sulfate-reducing bacteria activity accounted for methylmercury formation.

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35

Kružíková, K., Z. Svobodová, O. Valentová, T. Randák, and J. Velíšek. "Mercury and methylmercury in muscle tissue of chub from the Elbe River main tributaries." Czech Journal of Food Sciences 26, No. 1 (February 19, 2008): 65–70. http://dx.doi.org/10.17221/1140-cjfs.

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The aim of the present study was to investigate the concentrations of total mercury and methylmercury in muscle of 55 chub (Leuciscus cephalus) from seven main tributaries (Orlice, Chrudimka, Cidlina, Jizera, Vltava, Ohře, Bílina) of the Elbe River and to evaluate the health risks of eating fish from the tributaries monitored. Mercury was determined by means of cold vapour atomic absorption spectrometry using AMA-254, methylmercury in the form of CH3HgCl by gas chromatography. The highest mean concentrations of total mercury and methylmercury were found in the Jizera (0.27 ± 0.19 mg/kg and 0.23 ± 0.15 mg/kg, respectively) and the lowest mean concentrations of total mercury and methylmercury were found in the chub from the Cidlina (0.07 ± 0.05 mg/kg and 0.06 ± 0.04 mg/kg, respectively). The average methylmercury-to-total mercury ratio was 83 ± 15%. The fish intake hazard indexes calculated for the individual tributaries monitored were between 0.01 and 0.03. The results of this study show that the Elbe River is not significantly affected by mercury contamination from its main tributaries

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Knoblauch, Stephan, H. Fred Koch, Catherine Polydore, and D. Max Roundhill. "A computational approach to seeking methylmercury(II) thiolate calix[4]arene hosts for both octasulfur and organosulfur compounds as guests." Canadian Journal of Chemistry 79, no. 5-6 (May 1, 2001): 977–82. http://dx.doi.org/10.1139/v00-197.

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Calculations have been carried out on the conformational preferences of calix[4]arene thiols and their methylmercury(II) derivatives. Calculations have also been carried out on hostguest combinations of methylmercury(II) ethanethiolate calix[4]arenes and 1,4-dithiacyclohexane, octasulfur, thiacyclopropane, and thiophene. For the 1,4-dithiacyclohexane, thiacyclopropane, and thiophene guests, calculations have been carried out for both 1:1 and 1:4 ratios of the methylmercury(II) ethanethiolate calix[4]arene to the sulfur containing guests. For octasulfur only the 1:1 hostguest ratio has been considered because it has four sulfurs that are conformationally arranged to bind to the four mercury(II) centers. The computational results generally show that hostguest formation is enthalpically favored over the separated molecules in cases where adducts with mercury-sulfur donor atom interactions are allowed to reach energy minima.Key words: calixarene, methylmercury, octasulfur, organosulfur compounds.

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37

Rutchik, Jonathan. "Methylmercury and Neurotoxicity." Journal of Occupational and Environmental Medicine 55, no. 1 (January 2013): 111. http://dx.doi.org/10.1097/jom.0b013e318278260a.

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38

Kakita, Akiyoshi, Koichi Wakabayashi, Mu Su, Yuichiro Yoneoka, Mineshi Sakamoto, Fusahiro Ikuta, and Hitoshi Takahashi. "Intrauterine methylmercury intoxication." Brain Research 877, no. 2 (September 2000): 322–30. http://dx.doi.org/10.1016/s0006-8993(00)02717-7.

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39

DALTON, LOUISA WRAY. "METHYLMERCURY TOXICOLOGY PROBED." Chemical & Engineering News 82, no. 3 (January 19, 2004): 70–71. http://dx.doi.org/10.1021/cen-v082n003.p070.

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40

Marsh, David O. "Fetal Methylmercury Poisoning." Archives of Neurology 44, no. 10 (October 1, 1987): 1017. http://dx.doi.org/10.1001/archneur.1987.00520220023010.

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41

Bloom, Nicolas. "Determination of Picogram Levels of Methylmercury by Aqueous Phase Ethylation, Followed by Cryogenic Gas Chromatography with Cold Vapour Atomic Fluorescence Detection." Canadian Journal of Fisheries and Aquatic Sciences 46, no. 7 (July 1, 1989): 1131–40. http://dx.doi.org/10.1139/f89-147.

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A technique is presented, which allows the rapid and precise determination of methylmercury in aqueous samples. The sample is first reacted with sodium tetraethylborate, to convert the nonvolatile monomethyl mercury to gaseous methylethylmercury. The volatile adduct is then purged from solution, and recollected on a graphitic carbon column at room temperature. The methylethylmercury is then thermally desorbed from the column, and analyzed by cryogenic gas chromatography with cold vapour atomic fluorescence detection. The method allows the simultaneous determination of labile Hg(II) species, through the formation of diethylmercury, and of dimethylmercury, which is not ethylated. The methylmercury detection limit is about 0.6 pg Hg, or 0.003 ng∙L−1 for a 200-mL sample. The technique has been successfully applied directly to a wide variety of freshwater samples and alkaline tissue digestates. Seawater is analyzed following a simple extraction step to separate the methylmercury from the interfering chloride matrix. Analyses of natural surface waters have shown methylmercury levels typically in the range of 0.02–0.10 ng∙L−1, with values as high as 0.64 ng∙L−1 in a polluted urban lake. Waters collected from the anoxic bottom waters of a stratified remote lake have shown methylmercury levels as high as 4 ng∙L−1 as Hg.

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42

Aschner, M., N. B. Eberle, and H. K. Kimelberg. "Interactions of methylmercury with rat primary astrocyte cultures: methylmercury efflux." Brain Research 554, no. 1-2 (July 1991): 10–14. http://dx.doi.org/10.1016/0006-8993(91)90165-r.

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43

Kenšová, R., K. Kružíková, and Z. Svobodová. "Mercury speciation and safety of fish from important fishing locations in the Czech Republic." Czech Journal of Food Sciences 30, No. 3 (April 27, 2012): 276–84. http://dx.doi.org/10.17221/239/2011-cjfs.

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The aim of the study was to describe the distribution of total mercury in the tissues of fish originating from important Czech fishing locations and to determine the level of methylmercury as a percentage of total mercury (Hg speciation). At six important fishing locations a total of 144 fishes of 13 species were caught and analysed. Samples of muscle, liver, gonads and scales were analysed for total mercury and in the case of muscles for methylmercury concentrations. Total mercury was determined by AAS using an AMA 254 analyser, and methylmercury determination was performed by GC/ECD using a GC-2010A chromatograph. Total mercury concentrations in muscle and other tissues of all the fish from all fishing locations were below 0.5 mg/kg, with the exception of 6 asps (Aspius aspius). A significant (P < 0.05) correlation was found between the total mercury concentrations in scales and other tissues. Methylmercury made up about 46–100% of total mercury in muscle. The overall results confirmed the good hygienic quality of fish from important Czech fishing locations.

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44

Ahmad Khan, Waqar. "New Information on the Mechanisms Underlying the Neurotoxicity Caused by Methylmercury and Manganese." International Journal of Advances in Biology 9, no. 3 (August 31, 2022): 15–26. http://dx.doi.org/10.5121/ijab.2022.9302.

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Toxic elements are extensively distributed in the Earth’s crust and individuals may be exposed to several of them. Indeed, exposure to toxic elements such as mercury (Hg) can be a potential health risk factor of health, mainly by ingestion of fish containing methylmercury (MeHg). On the other hand, essential elements such as manganese (Mn) play an important role in physiological process in human body. In this regard, it is well known that MeHg and Manganese have neurotoxic effects on the developing brain. Therefore, we discuss the effects of Methylmercury and Manganese on cell signaling pathways in this review, as these effects may contribute to the molecular mechanisms underlying Methylmercury and Manganese -induced neurotoxicity.

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45

Öller, Hans-Jürgen, Paul Kiprof, and Hubert Schmidbaur. "Flexible ein-und zweikernige Aralkyl-und Aralkoxyquecksilberverbindungen als Modelle zum Nachweis von Hg(II)-Hg(II)-W echselwirkungen / Flexible Mono-and Dinuclear Aralkyl and Aralkoxy Mercury Compounds for Detection of Hg (II)-Hg (II) Interactions." Zeitschrift für Naturforschung B 47, no. 3 (March 1, 1992): 333–43. http://dx.doi.org/10.1515/znb-1992-0306.

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The aralkyl and aralkoxy mercury(II) compounds 1-(chloromercury(II)methyl)naphthalene (1), bis[1-naphthylmethyl]mercury(II) (2), 1-naphthyl(1-naphthylmethyl)mercury(II) (3), 1,8-bis[chloromercury(II)methyl]naphthalene (4), methylmercury(II)-benzylate (5), methylmercury( II)-1-naphthylmethylate (6) and bis[methylmercury(II)]μ-1,8-naphthalenediyl-bismethylate (7) have been prepared and characterized by means of NMRspectroscopy, mass spectrometry and elemental analysis. The molecular structure of compound 2 has been determined by single X-ray crystallography. The unit cell of 2 contains two crystallographically independent molecules, one of which is disordered. The interatomic distances and angles meet the expectations with Hg ⋯ Hg separations larger than 5.60 Å, indicating the absence of metal metal interactions.

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46

Kružíková, Kamila, Renáta Kenšová, Jana Blahová, and Zdeňka Svobodová. "Assessment of mercury contamination of the Svitava and Svratka rivers and muscle of chub (Leuciscus cephalus L.) in the urban agglomeration of Brno in the Czech Republic." Acta Veterinaria Brno 80, no. 2 (2011): 227–33. http://dx.doi.org/10.2754/avb201180020227.

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This study focused on the total mercury and methylmercury content in the muscle of chub (Leuciscus cephalusL.), the total mercury in the river sediments and the evaluation of health risks associated with fish contamination. Chub were caught at seven localities on the Svratka and Svitava rivers in the agglomeration of Brno in 2008. The results were compared to those obtained from the same sites in 2007. Total mercury was determined by atomic absorption spectrophotometry using an AMA 245 analyzer, and methylmercury was determined by gas chromatography (using an electron-capture detector) after acid digestion and toluene extraction in chub muscle. The highest concentrations of total mercury and methylmercury (0.12 ± 0.14 and 0.07 ± 0.02 mg·kg-1fresh weight, respectively) were found in Svratka before junction (south of Brno), whereas the lowest concentration of mercury and methylmercury in chub (0.06 ± 0.01 and 0.04 ± 0.01 mg·kg-1) was detected in Svitava before junction with the Svratka River. Total mercury in sediments ranged from 0.01 to 1.05 mg·kg-1dry weight, the highest value was detected in the sediment from Rajhradice. The lowest content (0.01 mg·kg-1) was at Kníničky. Hazard indices calculated for the selected localities showed no health risk for either a standard consumer or a fishing family. Fish from the Svitava and Svratka rivers show very low mercury concentration and hazard index and their consumption poses no health risk from total mercury and methylmercury contamination.

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Baldi, Franco, Milva Pepi, and Marco Filippelli. "Methylmercury Resistance in Desulfovibrio desulfuricans Strains in Relation to Methylmercury Degradation." Applied and Environmental Microbiology 59, no. 8 (1993): 2479–85. http://dx.doi.org/10.1128/aem.59.8.2479-2485.1993.

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Ignatavičius, Gytautas, Murat H. Unsal, Peter E. Busher, Stanisław Wołkowicz, Jonas Satkūnas, Giedrė Šulijienė, and Vaidotas Valskys. "Geochemistry of mercury in soils and water sediments." AIMS Environmental Science 9, no. 3 (2022): 261–81. http://dx.doi.org/10.3934/environsci.2022019.

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<abstract> Our paper reviews the current understanding of mercury in the environment of soil and sediment, including sampling, mobilization phases and analyzing methods. As a dangerous trace element, mercury has been shown to have several harmful effects on the environment. Mercury is released into the environment in a variety of chemical forms by both geogenic and human activities, with the majority of it coming from anthropogenic sources. It is affected by environmental conditions such as pH, redox potential, light and temperature-all of which determine its final chemical form-reactivity and toxicity. Methylmercury is considered one of the most poisonous forms found in nature. Considering the methodologies of the studies carried out we have found that the best technique for preserving methylmercury in soil and sediment samples is to freeze it immediately after collection. Organically rich soils are related to higher total mercury levels. Plants, such as Solanum nigrum (BR3) and Cynodon dactylon (BR2), can play an important role in mercury transport and accumulation. Solid-phase selenium causes faster demethylation and slower methylation of mercury. Methylmercury can increase by climate change and thawing; arctic permafrost is a potential source of Hg. Chemical vapor generation inductively coupled plasma mass spectrometry was used to develop a simple and quick method for measuring methylmercury; ultrasonic agitation and HNO3 were used for the process, the last of which proved to be the most efficient for selective extraction of methylmercury. </abstract>

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Ekstrom, Eileen B., François M. M. Morel, and Janina M. Benoit. "Mercury Methylation Independent of the Acetyl-Coenzyme A Pathway in Sulfate-Reducing Bacteria." Applied and Environmental Microbiology 69, no. 9 (September 2003): 5414–22. http://dx.doi.org/10.1128/aem.69.9.5414-5422.2003.

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ABSTRACT Sulfate-reducing bacteria (SRB) in anoxic waters and sediments are the major producers of methylmercury in aquatic systems. Although a considerable amount of work has addressed the environmental factors that control methylmercury formation and the conditions that control bioavailability of inorganic mercury to SRB, little work has been undertaken analyzing the biochemical mechanism of methylmercury production. The acetyl-coenzyme A (CoA) pathway has been implicated as being key to mercury methylation in one SRB strain, Desulfovibrio desulfuricans LS, but this result has not been extended to other SRB species. To probe whether the acetyl-CoA pathway is the controlling biochemical process for methylmercury production in SRB, five incomplete-oxidizing SRB strains and two Desulfobacter strains that do not use the acetyl-CoA pathway for major carbon metabolism were assayed for methylmercury formation and acetyl-CoA pathway enzyme activities. Three of the SRB strains were also incubated with chloroform to inhibit the acetyl-CoA pathway. So far, all species that have been found to have acetyl-CoA activity are complete oxidizers that require the acetyl-CoA pathway for basic metabolism, as well as methylate mercury. Chloroform inhibits Hg methylation in these species either by blocking the methylating enzyme or by indirect effects on metabolism and growth. However, we have identified four incomplete-oxidizing strains that clearly do not utilize the acetyl-CoA pathway either for metabolism or mercury methylation (as confirmed by the absence of chloroform inhibition). Hg methylation is thus independent of the acetyl-CoA pathway and may not require vitamin B12 in some and perhaps many incomplete-oxidizing SRB strains.

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Miura, Kyoko, Nobumasa Imura, and Thomas W. Clarkson. "Mechanism of Methylmercury Cytotoxicity." CRC Critical Reviews in Toxicology 18, no. 3 (January 1987): 161–88. http://dx.doi.org/10.3109/10408448709089860.

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Journal articles on the topic 'Methylmercury'

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