Disease relevance of methylmercury

• A role of selenium against methylmercury toxicity [1].
• Five monkeys were treated from birth with oral doses of mercury as methylmercury (50 micrograms per kilogram of body weight per day); concentrations in the blood peaked at 1.2 to 1.4 parts per million; and declined after weaning from infant formula to a steady level of 0.6 to 0.9 part per million [2].
• Is chemical neurotransmission altered specifically during methylmercury-induced cerebellar dysfunction [3]?
• Impaired biliary excretion and whole body elimination of methylmercury in rats with congenital defect in biliary glutathione excretion [4].
• Acute and chronic intoxications of rhesus monkeys with methylmercury produced lesions in the central nervous system (CNS) with different distributions [5].

Psychiatry related information on methylmercury

• Methylmercury and neurodevelopment: reanalysis of the Seychelles Child Development Study outcomes at 66 months of age [6].
• Methylmercury (MeHg) is a potent neurotoxin that in high exposures can cause mental retardation, cerebral palsy, and seizures [7].
• The methylmercury-exposed groups showed a lower level of exploratory behavior as well as an impairment in habituation and working memory when subjected to the novel object exploration task [8].
• Does methylmercury have a role in causing developmental disabilities in children [7]?
• Prenatal methylmercury exposure and children: neurologic, developmental, and behavioral research [9].

High impact information on methylmercury

• In addition, electrophoresis of oviduct nuclear RNA on agarose gels containing methylmercury hydroxide reveals multiple species of RNA that are from 1.3 to over 4 times larger than ovalbumin mRNA and hybridize to both structural and intervening sequences of the ovalbumin gene [10].
• Methylmercury and selenium in umbilical cords of inhabitants of the Minamata area [11].
• As in liver, cytochrome P-450 in brain is degraded in vitro to its inactive form, cytochrome P-420 by methylmercury chloride [12].
• Algal blooms reduce the uptake of toxic methylmercury in freshwater food webs [13].
• Mercury accumulation in fish is a global public health concern, because fish are the primary source of toxic methylmercury to humans [13].

Chemical compound and disease context of methylmercury

• The disposition and toxicity of methylmercury, a ubiquitous environmental pollutant, is modulated by binding to the endogenous tripeptide glutathione (GSH) and metabolism of the resulting methylmercury-glutathione complex by the ectoproteins gamma-glutamyl transpeptidase (GGT) and dipeptidase [14].
• Exposure of mammalian cells to ultraviolet light, nutrient deprived culture media, hypoxia, environmental toxicants such as methyl mercury, methyl methanesulfonate, crocodilite asbestos or the agents that disrupt the function of endoplasmic reticulum (ER) leads to activation of the pro-apoptotic transcription factor GADD153/CHOP [15].
• The interaction of methylmercury (MeHg) with neuronal Ca2+ channels in rat forebrain synaptosomes and dihydropyridine (DHP)-sensitive Ca2+ channels in rat pheochromocytoma (PC12) cells was examined using radiotracer flux assays and radioligand binding analyses [16].
• For initial study, triethyltin was chosen as an agent producing demyelination of nerves, acrylamide as an agent producing "dying-back" neuropathy, and methylmercury as an agent producing mixed central and peripheral neuropathies [17].
• The effects of methylmercury (CH3Hg) or mercuric chloride (HgCl(2)) on neurite outgrowth and cell viability were quantified using undifferentiated (unprimed) and differentiated (primed) pheochromocytoma (PC12) cells [18].

Biological context of methylmercury

• After exposure to H(2)O(2) or methylmercury, both inducing oxidative stress, the number of apoptotic cells was significantly higher in DEX- than in control-CGC [19].
• Since inorganic mercury crosses the blood-brain barrier poorly, biotransformation of methyl to inorganic mercury may have occurred after methylmercury crossed the blood-brain barrier, accounting for its persistence in brain and causing part of the brain damage [20].
• Using a genomic library constructed from Saccharomyces cerevisiae, we have identified a gene GFA1 that confers resistance to methylmercury toxicity [21].
• These findings provide direct evidence for a major role of GGT in regulating the tissue distribution and elimination of methylmercury and inorganic mercury and provide additional support for the use of NAC as an antidote in methylmercury poisoning [14].
• Conalbumin mRNA is also a poor template for the synthesis of full length cDNA synthesis by avian myeloblastosis virus reverse transcriptase, and treatment of this mRNA with methylmercury hydroxide increases the size of DNA sequences synthesized [22].

Anatomical context of methylmercury

• The globin transcripts from one cell line are polyadenylylated and migrate as 9S RNA on methylmercury gels [23].
• This report is the first to identify the target molecule of methylmercury toxicity in eukaryotic cells [21].
• The effects of methylmercury on the intestinal epithelium were studied in 14 adolescent male Macaca mulatta monkeys weighing 3 to 5 kg [24].
• Thus, the cultured cells which are free from the influence of whole body complexities, such as absorption, distribution, metabolism, etc., which complicate the interpretation of in vivo experimental results, attract the attention of many scientists who are interested in clarifying the mode of toxic action of methylmercury [25].
• Taxol protects the microtubules of concanavalin A-activated lymphocytes from disassembly by methylmercury, but DNA synthesis is still inhibited [26].

Associations of methylmercury with other chemical compounds

• Nuclear magnetic resonance studies of the solution chemistry of metal complexes. XI. The binding of methylmercury by sulfhydryl-containing amino acids and by glutathione [27].
• Yeast strains transformed with the CDC34 gene were resistant not only to methylmercury but also to mercuric chloride and p-chloromercuribenzoate [28].
• Handling of cysteine S-conjugates of methylmercury in MDCK cells expressing human OAT1 [29].
• Selective preconcentration of methylmercury (MeHg) in the presence of Hg(II), ethylmercury (EtHg), and phenylmercury (PhHg) was achieved at pH 6.8 through loading the sample solution onto the microcolumn due to a displacement reaction between MeHg and the presorbed Cu-DDTC [30].
• The interactions of inorganic mercury Hg(II), methylmercury (MeHg(I)), ethylmercury (EtHg(I)), and phenylmercury (PhHg(I)) with DNA have been probed by capillary electrophoresis with on-line electrothermal atomic absorption spectrometric detection (CE-ETAAS) in combination with circular dichroism and Fourier transform infrared spectroscopy [31].

Gene context of methylmercury

• Overexpression of the ubiquitin-conjugating enzyme Cdc34 confers resistance to methylmercury in Saccharomyces cerevisiae [28].
• Overexpression of UBC4 and of UBC7, two other genes for ubiquitin-conjugating enzymes, also conferred resistance to methylmercury [28].
• On the basis of these results, we conclude that met2 and met17 (met15) cause accumulation of hydrosulfide ions in the cell and that the increased level of hydrosulfide is responsible for detoxification of methylmercury [32].
• Foreign metallothionein-I expression by transient transfection in MT-I and MT-II null astrocytes confers increased protection against acute methylmercury cytotoxicity [33].
• Overexpression of Msn2 conferred a much greater sensitivity to methylmercury in yeast, while deletion of the corresponding gene lowered the degree of resistance to methylmercury induced by overexpression of Bop3 [34].

Analytical, diagnostic and therapeutic context of methylmercury

• The relationship between increased intracellular calcium concentration ([Ca(2+)](i)) and changes in spontaneous synaptic current frequency caused by the neurotoxicant methylmercury (MeHg) was examined in Purkinje cells of cerebellar slices using confocal microscopy and whole-cell recording [35].
• Application of isotopically labeled methylmercury for isotope dilution analysis of biological samples using gas chromatography/ICPMS [36].
• Changes in fatty acid composition of myelin cerebrosides after treatment of the developing rat with methylmercury chloride and diethylmercury [37].
• Using whole-cell recording techniques we compared effects of the environmental cerebellar neurotoxicant methylmercury (MeHg) on spontaneous IPSCs (sIPSCs) of both Purkinje and granule cells in cerebellar slices of the rat [38].
• This decrease in [3H]GABA uptake is consistent with the results of previous studies using this animal model, which demonstrated a preferential degeneration of GABAergic neurons in the cerebral cortex and caudate-putamen of methylmercury-treated animals [39].

References