Disease relevance of MERCURIC CHLORIDE

• Administration of HgCl2 to naive BN rats induced marked autoantibody production, systemic vasculitis and lymphocytic infiltration of the kidneys, liver and skin in all of the animals and a 47% mortality [1].
• In the present study, the pathophysiologic role of glomerular hemodynamic factors in the early phase of HgCl2-induced acute renal failure is evaluated in the dog [2].
• HgCl2 toxicity appears to be a consequence of inhibition of oxidative phosphorylation leading to ATP depletion and cell death [3].
• These experiments demonstrate that HgCl2 induces autoreactive T cells and suggest that these cells may be responsible for the autoimmune disease [4].
• Previous studies have established that in susceptible mouse strains, such as A.SW (H-2s), repeated injections of subtoxic doses of HgCl2 induce increased serum levels of total IgE and IgG1, high serum titers of antinuclear autoantibodies (ANo1A), and immune-complex glomerulonephritis [5].

Psychiatry related information on MERCURIC CHLORIDE

• The results indicate a role for HgCl2 in the stimulation of natural antibodies producing cells and the existence of interspecies cross-reactive Id among mouse and rat natural antibodies [6].
• In time-response studies, animals were administered 5 mg Hg/kg as HgCl2 and sacrificed after 3, 9, 18, 24, and 48 h [7].

High impact information on MERCURIC CHLORIDE

• The cationic conductance was also induced by direct injection of protein kinase A (PKA) catalytic subunit, reduced by the kinase inhibitor H7, and blocked by HgCl2, an inhibitor of aquaporin 1 [8].
• The aim of this work was to investigate, using T cell lines derived from HgCl2-injected LEW rats (LEWHg), the effect of these autoreactive T cells on the development of Th2-mediated autoimmunity [9].
• Protection from the experimental autoimmunity was associated with signs of low grade activation of the BN immune system, which included: increased numbers of circulating B and activated T cells before administration of HgCl2, and less autoreactivity and spontaneous proliferation in vitro after HgCl2 [1].
• In contrast, BN rats pretreated with HgCl2-resistant allogeneic Lewis bone marrow and transient FK506 showed less clinical disease and were completely protected from mortality [1].
• Unfractionated BN rat splenocytes and purified T cells exposed to HgCl2 expressed high levels of IL-4 mRNA [10].

Chemical compound and disease context of MERCURIC CHLORIDE

• We previously have shown that chronic sodium chloride (NaCl) loading protects against HgCl2-induced acute renal failure (ARF) in dogs [11].
• Facilitated diffusion of [14C]lactose into inverted membrane vesicles of Escherichia coli was measured using HgCl2 as a stopping reagent and polylysine to flocculate the vesicles for filtration [12].
• Cross-linking of proteins to DNA in live, intact Novikoff ascites hepatoma cells exposed in vitro to different concentrations of CuSO4, Pb(NO3)2, HgCl2, and AlCl3 was studied [13].
• Hexachlorobutadiene and HgCl2 produced severe glycosuria and transient enzymuria [14].
• Blocking of glutathione synthesis increased the toxicity of HgCl2, but also abolished any sensitizing effect on mediator release [15].

Biological context of MERCURIC CHLORIDE

• The five LEWHg T cell lines obtained protect against Th2-mediated autoimmunity induced by HgCl2 in (LEW x BN)F1 hybrids [9].
• The early effect on IL-4 production observed on BN rat spleen cells and T cells may explain that the autoreactive anti-class II T cells that are found in HgCl2-injected BN rats have a Th2 phenotype [10].
• Transcripts encoded by the endogenous PAL genes and GUS transcripts from the PAL1-GUS gene fusion were induced by wounding, HgCl2-stress, and light [16].
• This model of moderate ARF is characterized by a parallel fall in glomerular filtration rate (delta GFR, -43%) and renal blood flow (delta RBF, -38%) within the first three hours after HgCl2 administration [2].
• HgCl2 was not able to attenuate TNF-alpha-mediated apoptosis in U-937 cells, or ceramide-C6-mediated apoptosis in Jurkat cells, suggesting that mercury acts upstream of, or does not involve, these signals [17].

Anatomical context of MERCURIC CHLORIDE

• We conclude that HgCl2 induces CD4+ autoreactive T cells that proliferate in the presence of class II+ cells in susceptible BN as well as in resistant LEW rats [18].
• Resistance to HgCl2-induced autoimmunity is not due to these suppressor cells since treatment with an anti-CD8 monoclonal antibody (mAb) did not allow autoimmunity to appear [18].
• Expression of in vitro transcribed mRNA encoding CHIP28k in Xenopus oocytes increased oocyte osmotic water permeability (Pf) from (4 +/- 1) x 10(-4) to (33 +/- 4) x 10(-4) cm/s at 10 degrees C; the increase in oocyte Pf was weakly temperature dependent and inhibited by HgCl2 [19].
• Liposomes reconstituted with HPLC-purified CHIP28 from human erythrocytes had a high osmotic water permeability (Pf0.04 cm/s) that was inhibited by HgCl2 [20].
• Conversely, carbachol evoked an HgCl2-sensitive increase in [Ca(2+)] (average approximately 400 microM, but as large as 520 microM) in the lumen of single gastric glands [21].

Associations of MERCURIC CHLORIDE with other chemical compounds

• Mercuric chloride (HgCl2) induced autoimmunity in the Brown Norway (BN) strain but an immuno-suppression in the Lewis strain with, however, autoreactive anti-class II T cells present in both strains [10].
• Russell's viper venom, a control Factor X-activating serine protease, was not inhibited by either 0.1 mM HgCl2 or 1 mM iodoacetamide [22].
• In addition, expression of a direct Factor X activator developed under hypoxic conditions; the activator was membrane-associated and expressed on the surface of intact cultures, Ca-dependent, inhibited by HgCl2 but not PMSF, and had Km approximately 25 micrograms/ml for the substrate at pH 7 [23].
• Fluorescence quenching measurements showed that the isolated vesicles maintained a high, HgCl2-sensitive water permeability, consistent with the presence of vasopressin-sensitive water channels [24].
• The increase in osmotic water permeability was inhibited by HgCl2, and this effect was reversed by a reducing agent, 2-mercaptoethanol [25].

Gene context of MERCURIC CHLORIDE

• HgCl2 reversibly reduced the Lp of AQP3 and increased sigmaglyc to 1 and sigmaform to 0 [26].
• The redistribution of AQP2 in CD8 cells was accompanied by an approximately 6-fold increase in osmotic water permeability coefficient (Pf), which was inhibited by 0.3 m HgCl2 [27].
• It was concluded that HgCl2-induced ARF is amenable to improvement by IGF-1 infusion and that the increase in renal IGFBP-1 mRNA may be an important modulator in the recovery of the kidney [28].
• We have previously shown, by fully quantitative polymerase chain reaction (PCR), up-regulation of interleukin-4 (IL-4) gene expression in HgCl2-treated BN rats, implicating Th2 cells in the autoimmune syndrome [29].
• Involvement of the reciprocal Th1 subset, producing interferon-gamma (IFN-gamma), in resistance of LEW rats to HgCl2 has been suggested [29].

Analytical, diagnostic and therapeutic context of MERCURIC CHLORIDE

• Brown-Norway (BN) rats were pretreated with a syngeneic or allogeneic bone marrow infusion under transient FK506 immunosuppression before receiving HgCl2 [1].
• In the present study we looked at modifications of cytokine production by PCR and cytofluorometric analyses in normal BN and Lewis rat splenocytes, cultured with or without HgCl2 [10].
• Moreover, exogenous HGF stimulated DNA synthesis of renal tubular cells after renal injuries caused by HgCl2 administration and unilateral nephrectomy and induced reconstruction of the normal renal tissue structure in vivo [30].
• No loss of cellular integrity or major mitochondrial structural alterations occurred within the first 3 h after a subcutaneous injection of 5 mg/kg of HgCl2 [31].
• Rats treated with HgCl2 received antibody by intravenous injection at various time points [32].

References