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

• In time-response studies, animals were administered 5 mg Hg/kg as CH3HgCl and sacrificed after 24 and 48 h [6].

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

• The sensitivity of splenic lymphoid cells to apoptosis induced by low concentrations of methylmercury (MeHgCl) has been examined in C57BL/6 and SJL mice, which are, respectively, resistant and sensitive to a genetically determined autoimmune disease induced by subtoxic doses of MeHgCl [3].
• Following relative toxicities were found: HEMA 1; TEGDMA 3; UDMA 109; BisGMA 133; HgCl2 887; MeHgCl 2306 [8].
• The aim of the present experiments was to investigate whether a single dose of 24 mumol/kg methylmercuric chloride (MeHgCl) in rats can influence the effect of an equimolar dose of sodium selenite (Na2SeO3) on body weight or the exhalation of dimethylselenide, a volatile metabolic product of selenium [9].
• The actions of bath applied mercuric chloride (HgCl2) and methylmercury (CH3HgCl) on voltage-activated calcium channel currents (VACCCs) were tested, using the whole cell patch clamp recording technique with cultured dorsal root ganglion (DRG) neurons from 2-4 day old rat pups [10].
• Glioma factors, sodium ascorbate, non-inhibitory concentrations of prostaglandins E1 (PGE1), and glutamate enhanced the growth-inhibitory effect of CH3HgCl on both NB and glioma cells in culture [5].

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].

References