Disease relevance of Calo-Gran

• In the nephrotoxic mercury chloride (HgCl(2)) rat model of acute kidney failure systemically administered EP4 agonist reduced the serum creatinine values and increased the survival rate [1].
• The role of G proteins in the functional modulation and potentiation by mercury chloride of the GABA(A) receptor-channel complex in rat dorsal root ganglion neurons was studied by using the whole-cell patch clamp technique [2].
• Simplified X-ray film method for detection of bacterial volatilization of mercury chloride by Escherichia coli [3].
• The rate of vaccinia virus reactivation in cells treated with mercury chloride was reduced, whereas the level of virus mutagenesis did not differ from the control [4].
• Methyl mercury chloride (MMC, 10 mg/kg body weight/day) was subcutaneously injected into rats for 1 week [5].

High impact information on Calo-Gran

• Exposure to low doses of mercury chloride induces autoantibodies to the nucleolar protein fibrillarin in H-2s, but not in H-2b, mice [6].
• The expression of AQP7 in oocytes stimulated the osmotic water permeability by 10-fold which was not inhibited by 0.3 mM mercury chloride [7].
• AB1 derivatives with one or two mutant AP-1-binding elements exhibited reduced but measurable inducer-dependent enhancer activity, but mutation of all three AP-1-binding sites abolished activation by CdCl2 and heme and also by mercury chloride, zinc chloride, H2O2, sodium arsenate, and 12-O-tetradecanoylphorbol-13-acetate [8].
• It was also seen during tubular regeneration after acute tubulotoxic injury induced by mercury chloride poisoning, with vimentin expression being lost in fully regenerated tubular epithelium [9].
• Superoxide dismutase (SOD) was administered to rats prior to mercury chloride injection and renal function, development of lipid peroxidation and renal glutathione level were measured 1 h later [10].

Chemical compound and disease context of Calo-Gran

• Irrigation with mercury chloride and sodium hypochlorite to prevent local recurrence after excision of conjunctival melanoma. An experimental study [11].

Biological context of Calo-Gran

• Inorganic mercury chloride-induced apoptosis in the cultured porcine renal cell line LLC-PK1 [12].
• In conclusion, both PKA and PKC negatively regulate the activity of the GABA(A) receptor-channel complex probably through phosphorylation of the receptor, and the PKA system underlies the mechanism of mercury chloride potentiation of GABA-activated currents [13].
• However, the potentiation was independent of membrane potential suggesting that mercury chloride binds to an external site of the receptor [14].
• Mercury chloride (0.5 mM) reduced osmotic water movement by 31.3 +/- 5.5% in the adult BLMV, but by only 4.0 +/- 4.0% in neonatal vesicles (P < 0.01) [15].
• Also supporting an external binding site is the observation that preapplication of mercury chloride alone for up to 60-sec potentiated GABA-induced currents [14].

Anatomical context of Calo-Gran

• Mercury chloride activates c-Jun N-terminal kinase and induces c-jun expression in LLC-PK1 cells [16].
• Decreased expression of brain nitric oxide synthase in macula densa cells and glomerular epithelial cells of rats with mercury chloride-induced acute renal failure [17].
• After mercury chloride treatment, most of the mercury is localized in lysosomes and is only rarely seen in secretory granules [18].
• Examples of localization of mercury in the central nervous system and various organs from animals exposed to mercury chloride or methyl mercury chloride with or without additional sodium selenide treatment are presented [18].
• The potential immunotoxic effects of mercury chloride on murine bone marrow (bm) cell subpopulations, including analysis of maturation patterns for B-cells, were evaluated by flow cytometric analysis [19].

Associations of Calo-Gran with other chemical compounds

• We found that in oocytes expressing cRNA encoding fUT, a 5-min preincubation in 0.5 mM mercury chloride (HgCl2) also significantly reduced urea uptake [20].
• The optical interconversion of the P-450 and P-420 forms of neuronal nitric oxide synthase: effects of sodium cholate, mercury chloride and urea [21].
• Sodium cholate and mercury chloride induced the conversion of nNOS from the P-450 to the P-420 form in concentration- and incubation time-dependent manners, and the nNOS activity decreased [21].
• However, no reconversion of the mercury chloride-treated P-420 form to the P-450 form was observed in the presence of glycerol, L-arginine, or tetrahydrobiopterin [21].
• 203Hg-labeled methyl mercury chloride was administered via the caudal vein, and bile collected through exteriorized cannulas in the free swimming fish [22].

Gene context of Calo-Gran

• The aquaporin inhibitor mercury chloride blocked water channel activity but had no effect on wild-type yeast [23].
• The human AQP3 stimulated osmotic water permeability by eightfold, which was inhibited by 0.3 mM mercury chloride by 34% and reversed by beta-mercaptoethanol [24].
• The role of protein kinase A (PKA) and protein kinase C (PKC) in the function and modulation by mercury chloride of the GABA(A) receptor-chloride channel complex was studied with rat dorsal root ganglion cells using the whole-cell patch clamp technique [13].
• Injection of AQP9-cRNA into Xenopus oocytes stimulated the osmotic water permeability 7-folds with a low activation energy (4.2 kcal/mol) which was inhibited by 0.3 mM mercury chloride by 48% [25].
• Relationship between expression of HSP70 and metallothionein and oxidative stress during mercury chloride induced acute liver injury in rats [26].

Analytical, diagnostic and therapeutic context of Calo-Gran

• Aquaporin-mediated water transport could be inhibited and consequently ultrafiltration was reduced by i.p. administration of mercury chloride in our rabbit model [27].
• The objective of this study was to investigate the hypothesis that intraperitoneal ampho B increases and mercury chloride inhibits aquaporin-1-mediated water transport in a chronic peritoneal dialysis model in the rabbit [27].
• OBJECTIVE: To evaluate clinical symptoms and urinary mercury before and after chelation therapy in subjects with chronic cutaneous mercurous chloride (HgCl; calomel) exposure [28].
• Acute mercury chloride intoxication. Effects of hemodialysis and plasma exchange on mercury kinetic [29].
• A 27 year-old man developed after ingestion of mercury chloride, 6 g, a hypovolemic shock, an acute renal failure and a necrosis of the stomach which required a total gastrectomy [29].

References