Disease relevance of methylmercury chloride

• Neonatal rats received subcutaneous injections of methylmercuric chloride in physiological saline (5 mg Hg/kg/day) beginning on postnatal day 5 and continuing until a given animal demonstrated a persistent loss of body weight during 48 h [1].
• Alterations in gene expression after chronic treatment of glioma cells in culture with methylmercuric chloride [2].
• Sulfur-containing steroids, analogs, and derivatives were synthesized for evaluation in mice suffering acute toxicity from methylmercuric chloride [3].
• Effect of methylmercuric chloride on gangliosides of mouse neuroblastoma cells in culture [4].
• A single oral dose of 75 mumol/kg of methylmercuric chloride (MMC) on day 10, 11 or 12 of gestation caused similar incidences of a cleft palate in the selenium-deficient and selenium-sufficient mice [5].

High impact information on methylmercury chloride

• Paradoxically, we found that addition of methylmercuric chloride can increase the activity of cytochrome c oxidase during its initial substrate utilization [6].
• A stoichiometric amount of methylmercuric chloride substantially inhibits cytochrome c oxidase function under steady-state turnover conditions, where the enzyme is using its substrates, cytochrome c and oxygen, rapidly and continuously [6].
• The interaction of chelating agents with methylmercuric chloride bound to erythrocytes [7].
• Effect of methylmercuric chloride on gene expression in neuroblastoma and glioma cells after acute and chronic treatments [8].
• Cell viability decreased within the 60 min interval from 90% to approx. 80% (controls), <25 (HEMA), <20 (TEGDMA), <20 (H(2)O(2)) <10 (MeHgCl), and <10 (HgCl(2)) [9].

Chemical compound and disease context of methylmercury chloride

• The effect of methylmercuric chloride (CH3HgCl) on the levels of gangliosides in mouse neuroblastoma cells (NBP2) in culture was studied [4].
• There were no differences in the time required to develop clinical signs of methylmercury toxicity, tissue mercury levels or pathology between the groups of cats receiving methylmercury as methylmercuric chloride or as methylmercury-contaminated fish, at either dose level [10].
• Effects of methylmercuric chloride in the presence of cyclic AMP-stimulating agents on glioma and neuroblastoma cells in culture [11].
• The results obtained in this test system are discussed in relation to each of these factors and to the degree of overt toxicity obtained using prenatal treatment with 0, 0.5 or 2.0 mg/kg d-amphetamine sulfate, SC, on gestation days 12-15 (Study 1) or methylmercuric chloride, 0, 2.0 or 6.0 mg/kg by gavage, on gestation days 6-9 (Study 2) [12].
• Effect of sodium selenite & selenomethionine on the accumulation & acute toxicity of mercuric & methylmercuric chloride in the goldfish Carassius auratus [13].

Biological context of methylmercury chloride

• The sensitivity of isolation-induced aggressive behavior to prenatal treatment of 6.0 mg/kg methylmercuric chloride (MMCl) by gavage on gestation days 6-9 was assessed in a subset of animals from the Collaborative Behavioral Teratology Study (CBTS) [14].
• The objective of this investigation was to determine the role of poly(ADP-ribose) polymerase (PARP) in methylmercuric chloride (MeHgCl)-induced T-cell apoptosis [15].
• Depression of frog muscle contraction by methylmercuric chloride and mercuric chloride [16].
• The concentration of mercury in milk and the distribution pattern in the sucking pup was followed over time after administration of a single iv injection of 0.5 mg/kg body wt of 203Hg-labeled methylmercuric chloride or mercuric chloride to lactating mice on Day 10 of lactation [17].
• In this in vitro SCG assay, PY, BaP and CP were positive with exogeneous metabolic activation (rat S9 mix) while 4NQO, BLM, MMC, MTC, hydrogen peroxide, and diepoxbutane were positive in the absence of metabolic activation [18].

Anatomical context of methylmercury chloride

• Tissue concentrations of the neuropeptide somatostatin and the specific activities of glutamic acid decarboxylase (GAD) were measured in several regions of the central nervous system in young rats, following chronic postnatal administration of methylmercuric chloride [19].
• Subcutaneous (s.c.) administration of methylmercuric chloride (MMC, 10 mg kg-1 day-1, 8 days) resulted in significant increases with time of NOS activities in the cerebrum (1. 6-1.9-fold, 5-8 days) and cerebellum (1.4-fold, 8 days) [20].
• A brief exposure of low dose methylmercuric chloride to monolayer cultures of mouse fetal astrocytes caused a marked shift in the distribution of anionic groups on the surface membrane as evidenced by irregular disruption of cationized ferritin [21].
• The cytostatic effect was brought about by the inactivation of the microtubule spindle fiber polymerization mechanism induced by methylmercuric chloride [22].
• Mechanisms involved in methylmercuric chloride (MeHgCl)-induced suppression of human neutrophil apoptosis [23].

Associations of methylmercury chloride with other chemical compounds

• When thiocholesterol is administered as liposomes, it provides significant protection against methylmercuric chloride in mice when given in three intraperitoneal injections, 0.5 hr before and 2 and 8 hr after the methylmercuric chloride [24].
• Biochemical effects of methylmercuric chloride, cadmium chloride, and lead nitrate on embryos and alevins of the brook trout, Salvelinus fontinalis [25].
• We have previously demonstrated that concentrations of 1-10 microM of methylmercuric chloride (MeHgCl) that are cytotoxic to monocytes-macrophages can curiously inhibit neutrophil apoptosis by a yet unknown mechanism [23].
• In an attempt to assess the effects of methylmercury on ethanol metabolism, Sprague-Dawley rats were treated with a daily dose (10 mg/kg i.p.) of methylmercuric chloride for 2 consecutive days and given a test dose (0.4 g/kgi.v.) of ethanol 24 hr after the last treatment [26].
• We studied the uptake mechanism of mercuric chloride (Hg) and methylmercuric chloride (MeHg) in Aedes albopictus C6/36 cells [27].

Gene context of methylmercury chloride

• The specific activities of glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) were measured in 6 regions of the central nervous system in young rats, following chronic postnatal administration of methylmercuric chloride [28].
• The ATPase and transport functions were more sensitive to methylmercuric chloride than to mercuric chloride [29].
• We hypothesized that the resistance of Purkinje cells to methylmercuric chloride reflects their ability to transform organic mercurials to inorganic mercury that, in turn, induces the synthesis of radical-scavenging metallothionein molecules [30].
• The in vitro effect of methylmercuric chloride on superoxide dismutase activity of pig platelets [31].
• A daily dose of 10mg methylmercuric chloride/kg body weight was administered subcutaneously to 15 male Wistar rats for 10 days, and the glutathione peroxidase activity in the liver was measured to compare with the control activity [32].

Analytical, diagnostic and therapeutic context of methylmercury chloride

• Distribution of Mercury in subcellular fractions of brain, liver, and kidney after repeated oral administration of 203Hg-labeled methylmercuric chloride in mice [33].
• Patch test results in 300 consecutive patients to a standard series, to which MeHgCl was added, showed that MeHgCl and TH were never able to give isolated positive reactions, and that the concomitant positive reactions occurred in only 3.6% of subjects [34].

References