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Chemical Compound Review

Caspan     chloro-methyl-mercury

Synonyms: MeHgCl, CH3HgCl, CPD-8865, CCRIS 3968, LS-572, ...
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Disease relevance of chloro-methyl-mercury

  • From the 5th day of life intraperitoneal injections of MeHgCl or Et3PbCl at doses of 0.05 to 5 mg/kg body weight were administered to the rats three times a week [1].
  • In addition, at 10(-6) M, MeHgCl showed pronounced neuron-specific toxicity [2].
  • To determine the implications of subtoxic doses of MeHgCl in the susceptibility of SJL mice to autoimmune disease, Concanavalin A (ConA) stimulated spleen cells from both mouse strains were treated in vitro with MeHgCl concentrations varying between 0.001 and 1.0 microM for 48h [3].
  • Uptake kinetics of monomethylmercury chloride (MeHgCl) were measured for two species of green algae (Selenastrum capricomutum and Cosmarium botrytis), one blue-green algae (Schizothrix calcicola), and one diatom (Thalassiosira weissflogii), algal species that are commonly found in natural surface waters [4].
  • Alpha-tocopherol, alpha-tocopheryl++ succinate and inhibitors of cAMP phosphodiesterase protected glioma cells against the growth-inhibitory effect of CH3HgCl, but they failed to protect NB cells in culture [5].

Psychiatry related information on chloro-methyl-mercury


High impact information on chloro-methyl-mercury

  • Therefore, we analyzed the microglial reaction induced by methylmercury (MeHgCl) using cell cultures of different complexity [7].
  • An association of MeHgCl-induced microglial clusters with astrocytes and neurons was observed in three-dimensional cultures [7].
  • Interleukin-6 release was increased at 10(-7) M of MeHgCl, whereas it was decreased when each of these two cell types was cultured separately [7].
  • Altogether, these results show that microglial cells are directly activated by MeHgCl and that the interaction between activated microglia and astrocytes can increase local IL-6 release, which may cause astrocyte reactivity and neuroprotection [7].
  • IL-6 administered to three-dimensional cultures in the absence of MeHgCl caused astrogliosis, as indicated by increased GFAP immunoreactivity [7].

Chemical compound and disease context of chloro-methyl-mercury


Biological context of chloro-methyl-mercury

  • 3 DMSA was effective in decreasing body burden and the brain concentration of Hg in rats dosed orally with methylmercury (MeHgCl) when intraperitoneal treatment started with 40 mg/kg DMSA 24 h after Hg [11].
  • However, these SJL cells were sensitive to anti-Fas-mediated apoptosis while residual anti-Fas-resistant cells from C57BL/6 mice were, themselves, sensitive to MeHgCl-induced apoptosis [3].
  • We conclude that PARP activation leads to proapoptotic events that contribute to MeHgCl-induced cell death [12].
  • Moreover, these inhibitors blocked MeHgCl-induced oxidative stress as evidenced by a reduction in reactive oxygen species (ROS) generation [12].
  • The chromosome aberrations in human peripheral lymphocytes exposed to various concentrations of CH3HgCl or HgCl2 increased in a concentration-dependent manner and were significantly higher than the control when the cells were incubated with 1 x 10(-5) M (HgCl2) or 2 x 10(-6) M (CH3HgCl) [13].

Anatomical context of chloro-methyl-mercury

  • Isolated microglia were found to be directly activated by MeHgCl (10(-10) to 10(-6) M), as indicated by process retraction, enhanced lectin staining, and cluster formation [7].
  • MeHgCl only induced increased lymphocyte responsiveness at the low-dose exposure [14].
  • Following exposure of human T-cells to 2.5 microM MeHgCl, we observed PARP activation within 45 min [12].
  • The earliest detectable event was at the level of the mitochondrion; in the presence of MeHgCl there was a profound reduction in mitochondrial Deltapsim and a decline in GSH levels within 1 h [15].
  • In the spinal cord following administration of CH3HgCl alone, staining was limited to the gray matter [16].

Associations of chloro-methyl-mercury with other chemical compounds

  • These microspheres also were encapsulated with agarose--a blood compatible polymer--and were tried successfully for plasma perfusion (in 10 min, 40% of CH3HgCl and of HgCl2 were removed from 20 ppm of poisoned plasma) [17].
  • The autometallographic method has been used to determine the precise localization of mercury in the brain and spinal cord of adult Wistar rats which had been treated with repeated ip injections of methylmercuric chloride (CH3HgCl; 0.2 to 10.0 mg) or mercuric chloride (HgCl2; 0.2 to 10.0 mg) [18].
  • Speciation calculations based on our results show that, in absence of substantial concentrations of inorganic sulfides, neutral chloro-complexes (CH3HgCl) and free CH3Hg+ reach concentrations on the order of 10(-17)-10(-18) M at pH 5 in soil solutions with 3 x 10(-5) M of chloride [19].
  • Omission of Ca2+ from the perfusion solution increased the time-dependent MeHgCl-induced D-aspartate release [20].
  • Birds were dosed while in the nest orally every 2.5 days for 15 days with 0.5 mg of methyl mercury chloride (MeHgCl) for an estimated intake of 1.54 mg MeHgCl/kg food intake [21].

Gene context of chloro-methyl-mercury

  • Moreover, addition of IL-6 to three-dimensional brain cell cultures treated with 3 x 10(-7) M of MeHgCl prevented the decrease in immunostaining of the neuronal markers MAP-2 and neurofilament-M [7].
  • Similarly, MeHgCl treatment resulted in the release of cytochrome c to the cytoplasm in non-activated T cells but failed to do so in the activated population [22].
  • To investigate the effects of MeHg on the temporal expression of NCAM during development, rat pups were dosed with 7.0 mg/kg MeHgCl (s.c.) on alternate days from postnatal days (PNDs) 3-13 and killed on PNDs 15, 30 and 60 [23].
  • CH3HgCl (MeHg) induced in SJL, A.SW and B10.S mice antinucleolar antibodies (ANoA) targeting the nucleolar 34-kDa protein fibrillarin [24].
  • TPO activities in all cell compartments were inhibited by HgCl2 but not by CH3HgCl [25].

Analytical, diagnostic and therapeutic context of chloro-methyl-mercury

  • Interactions between astrocytes and microglia were studied in cocultures treated for 10 days with MeHgCl [7].
  • A detailed atlas of mercury-containing nuclei following oral administration of HgCl2 (20 mg x liter-1 or CH3HgCl (20 mg x liter-1) was prepared [16].
  • T-cells were exposed to 0.6-5 microM MeHgCl, EtHgCl, or PhHgCl for up to 24 hr and then analyzed by flow cytometry [26].
  • To elucidate the chemical interactions underlying the role of metallothioneins (MTs) in reducing the cytotoxicity caused by MeHg(II), we monitored in parallel by electronic absorption and CD spectroscopies the stepwise addition of MeHgCl stock solution to mammalian Zn(7)-MT1 and the isolated Zn(4)-alphaMT1 and Zn(3)-betaMT1 fragments [27].
  • The level of apoptosis induced by MeHgCl in both regions was verified by AnnexinV-propidium iodide (PI) and TdT-mediated dUTP nick end labeling (TUNEL) immunolabelings [3].


  1. UDPgalactose:ceramide galactosyltransferase and 2',3'-cyclic-nucleotide 3'-phosphodiesterase activities in rat brain after long-term exposure to methylmercury or triethyllead. Grundt, I.K., Neskovic, N.M. Exp. Neurol. (1985) [Pubmed]
  2. Comparison of the developmental effects of two mercury compounds on glial cells and neurons in aggregate cultures of rat telencephalon. Monnet-Tschudi, F., Zurich, M.G., Honegger, P. Brain Res. (1996) [Pubmed]
  3. Sensitivity to methylmercury-induced autoimmune disease in mice correlates with resistance to apoptosis of activated CD4+ lymphocytes. Pheng, S.R., Auger, C., Chakrabarti, S., Massicotte, E., Lamontagne, L. J. Autoimmun. (2003) [Pubmed]
  4. Kinetics and uptake mechanisms for monomethylmercury between freshwater algae and water. Moye, H.A., Miles, C.J., Phlips, E.J., Sargent, B., Merritt, K.K. Environ. Sci. Technol. (2002) [Pubmed]
  5. New opportunities with neuronal cultures to study the mechanisms of neurotoxic injuries. Prasad, K.N. Neurotoxicology (1991) [Pubmed]
  6. Lipid peroxidation in liver of rats administrated with methyl mercuric chloride. Lin, T.H., Huang, Y.L., Huang, S.F. Biological trace element research. (1996) [Pubmed]
  7. Microglial reaction induced by noncytotoxic methylmercury treatment leads to neuroprotection via interactions with astrocytes and IL-6 release. Eskes, C., Honegger, P., Juillerat-Jeanneret, L., Monnet-Tschudi, F. Glia (2002) [Pubmed]
  8. Cell death effects of resin-based dental material compounds and mercurials in human gingival fibroblasts. Reichl, F.X., Esters, M., Simon, S., Seiss, M., Kehe, K., Kleinsasser, N., Folwaczny, M., Glas, J., Hickel, R. Arch. Toxicol. (2006) [Pubmed]
  9. Methylmercury stimulates the exhalation of volatile selenium and potentiates the toxicity of selenite. Yonemoto, J., Webb, M., Magos, L. Toxicol. Lett. (1985) [Pubmed]
  10. Voltage-activated calcium channel currents of rat DRG neurons are reduced by mercuric chloride (HgCl2) and methylmercury (CH3HgCl). Leonhardt, R., Pekel, M., Platt, B., Haas, H.L., Büsselberg, D. Neurotoxicology (1996) [Pubmed]
  11. The effects of dimercaptosuccinic acid on the excretion and distribution of mercury in rats and mice treated with mercuric chloride and methylmercury chloride. Magos, L. Br. J. Pharmacol. (1976) [Pubmed]
  12. Inhibition of poly(ADP-ribose) polymerase rescues human T lymphocytes from methylmercury-induced apoptosis. Guo, T.L., Miller, M.A., Datar, S., Shapiro, I.M., Shenker, B.J. Toxicol. Appl. Pharmacol. (1998) [Pubmed]
  13. A comparison of the 8-hydroxydeoxyguanosine, chromosome aberrations and micronucleus techniques for the assessment of the genotoxicity of mercury compounds in human blood lymphocytes. Ogura, H., Takeuchi, T., Morimoto, K. Mutat. Res. (1996) [Pubmed]
  14. Neuroimmunological effects of exposure to methylmercury forms in the Sprague-Dawley rats. Activation of the hypothalamic-pituitary-adrenal axis and lymphocyte responsiveness. Ortega, H.G., Lopez, M., Takaki, A., Huang, Q.H., Arimura, A., Salvaggio, J.E. Toxicology and industrial health. (1997) [Pubmed]
  15. Induction of apoptosis in human T-cells by methyl mercury: temporal relationship between mitochondrial dysfunction and loss of reductive reserve. Shenker, B.J., Guo, T.L., O, I., Shapiro, I.M. Toxicol. Appl. Pharmacol. (1999) [Pubmed]
  16. Localization of mercury in CNS of the rat. IV. The effect of selenium on orally administered organic and inorganic mercury. Møller-Madsen, B., Danscher, G. Toxicol. Appl. Pharmacol. (1991) [Pubmed]
  17. A novel approach for heavy metal poisoning treatment, a model. Mercury poisoning by means of chelating microspheres: hemoperfusion and oral administration. Margel, S. J. Med. Chem. (1981) [Pubmed]
  18. Localization of mercury in CNS of the rat. II. Intraperitoneal injection of methylmercuric chloride (CH3HgCl) and mercuric chloride (HgCl2). Møller-Madsen, B. Toxicol. Appl. Pharmacol. (1990) [Pubmed]
  19. Bonding of ppb levels of methyl mercury to reduced sulfur groups in soil organic matter. Karlsson, T., Skyllberg, U. Environ. Sci. Technol. (2003) [Pubmed]
  20. The role of -SH groups in methylmercuric chloride-induced D-aspartate and rubidium release from rat primary astrocyte cultures. Mullaney, K.J., Fehm, M.N., Vitarella, D., Wagoner, D.E., Aschner, M. Brain Res. (1994) [Pubmed]
  21. Effects of mercury on health and first-year survival of free-ranging great egrets (Ardea albus) from southern Florida. Sepúlveda, M.S., Williams, G.E., Frederick, P.C., Spalding, M.G. Arch. Environ. Contam. Toxicol. (1999) [Pubmed]
  22. Activated human T lymphocytes exhibit reduced susceptibility to methylmercury chloride-induced apoptosis. Close, A.H., Guo, T.L., Shenker, B.J. Toxicol. Sci. (1999) [Pubmed]
  23. Developmental methylmercury administration alters cerebellar PSA-NCAM expression and Golgi sialyltransferase activity. Dey, P.M., Gochfeld, M., Reuhl, K.R. Brain Res. (1999) [Pubmed]
  24. Methyl mercury-induced autoimmunity in mice. Hultman, P., Hansson-Georgiadis, H. Toxicol. Appl. Pharmacol. (1999) [Pubmed]
  25. Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells. Nishida, M., Muraoka, K., Nishikawa, K., Takagi, T., Kawada, J. J. Histochem. Cytochem. (1989) [Pubmed]
  26. Induction of apoptosis in human T-cells by organomercuric compounds: a flow cytometric analysis. Shenker, B.J., Datar, S., Mansfield, K., Shapiro, I.M. Toxicol. Appl. Pharmacol. (1997) [Pubmed]
  27. Chemical foundation of the attenuation of methylmercury(II) cytotoxicity by metallothioneins. Leiva-Presa, A., Capdevila, M., Cols, N., Atrian, S., González-Duarte, P. Eur. J. Biochem. (2004) [Pubmed]
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