Home About us Contact
|
Home About us Contact | ||
|
|
||
Mercuric Chloride (mercuric + chloride)
Selected AbstractsMercuric Chloride and Iodide Mediated Cyclization of Tethered Alkynedithioacetals as a General Route to Five- and Six-Membered Rings: Tuning of Regioselectivity by Alkyne Substitution.CHEMINFORM, Issue 22 2006Goutam Biswas Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF. [source] Toxicity testing using esterase inhibition as a biomarker in three species of the genus Lecane (Rotifera)ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2002Ignacio Alejandro Pérez-Legaspi Abstract We have developed an esterase inhibition test to investigate the effects of 10 toxicants, including six metals (cadmium, chromium, copper, lead, mercuric chloride, and titanium) and four organics (benzene, ethyl acetate, toluene, and vinyl acetate) in three species of the benthic rotifer genus Lecane (L. hamata, L. luna, and L. quadridentata). Metals affect esterase inhibition by an average value of 4,957-fold greater than the four organics tested for the three rotifer species. Most of the EC50 (effect concentration where a 50% reduction in esterase activity is observed) values correspond to environmentally realistic concentrations. Comparisons of acute-to-chronic ratios among these three species showed that in two species, L. luna and L. quadridentata, esterase inhibition is an outstanding biomarker for most of the toxicants tested. [source] Decay-accelerating factor 1 (Daf1) deficiency exacerbates xenobiotic-induced autoimmunityIMMUNOLOGY, Issue 1 2010Christopher B. Toomey Summary Absence of decay-accelerating factor 1 (Daf1) has been shown to enhance T-cell responses and autoimmunity via increased expression of specific cytokines, most notably interferon (IFN)-,. To determine if Daf1 deficiency can exacerbate IFN-,-dependent murine mercury-induced autoimmunity (mHgIA), C57/BL6 Daf1+/+ and Daf1,/, mice were exposed to mercuric chloride (HgCl2) and examined for differences in cytokine expression, T-cell activation and features of humoral autoimmunity. In the absence of Daf1, mHgIA was exacerbated, with increased serum immunoglobulin G (IgG), anti-nuclear autoantibodies (ANAs) and anti-chromatin autoantibodies. This aggravated response could not be explained by increased T-cell activation but was associated with increased levels of IFN-,, interleukin (IL)-2, IL-4 and IL-10 but not IL-17 in Daf1-deficient mice. Anti-CD3/anti-CD28 costimulation of Daf1,/, CD4+ T cells in vitro was also found to increase cytokine expression, but the profile was different from that of mHgIA, suggesting that the cytokine changes observed in Daf1 deficiency reflect a response to mercury. The role of Daf1 in influencing cytokine expression was further examined by stimulation of CD4+ T cells in the presence of anti-CD3 and CD97, a molecular partner for Daf1. This resulted in increased IL-10, decreased IL-17 and IL-21 and decreased IFN-,. These findings demonstrate that the absence of Daf1 exacerbates mHgIA, with changes in the profile of expressed cytokines. Interaction between Daf1 and its molecular partner CD97 was found to modify expression of mHgIA-promoting cytokines, suggesting a possible approach for the suppression of overaggressive cytokine production in autoimmunity. [source] Diphenyl diselenide protects against hematological and immunological alterations induced by mercury in miceJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2008Ricardo Brandão Abstract Mercury is a heavy metal that can cause a variety of toxic effects on the organism, such as hematological and immunological alterations. In the present investigation, deleterious effects of mercury-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 were studied. Male adult Swiss albino mice received daily a pretreatment with (PhSe)2 (15.6 mg/kg, orally) for 1 week. After this week, mice received daily mercuric chloride (1 mg/kg, subcutaneously) for 2 weeks. A number of hematological (erythrocytes, leukocytes, platelets, hemoglobin, hematocrit, reticulocytes, and leukocytes differential) and immunological (immunoglobulin G and M plasma concentration) parameters were evaluated. Another biomarker of tissue damage, lactate dehydrogenase (LDH), was also determined. The results demonstrated that mercury exposure caused a reduction in the erythrocyte, hematocrit, hemoglobin, leukocyte, and platelet counts and an increase in the reticulocyte percentages. (PhSe)2 was effective in protecting against the reduction in hematocrit, hemoglobin, and leukocyte levels. (PhSe)2 ameliorated reticulocyte percentages increased by mercury. However, (PhSe)2 was partially effective in preventing against the decrease in erythrocyte and platelet counts. Immunoglobulin G and M concentrations and LDH activity were increased by mercury exposure, and (PhSe)2 was effective in protecting against these effects. In conclusion, (PhSe)2 was effective in protecting against hematological and immunological alterations induced by mercury in mice. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:311,319, 2008; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20242 [source] Mercury compounds disrupt neuronal glutamate transport in cultured mouse cerebellar granule cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2005Elena Fonfría Abstract Cerebellar granule cells are targeted selectively by mercury compounds in vivo. Despite the affinity of mercury for thiol groups present in all cells, the molecular determinant(s) of selective cerebellar degeneration remain to be elucidated fully. We studied the effect of mercury compounds on neuronal glutamate transport in primary cultures of mouse cerebellar granule cells. Immunoblots probed with an antibody against the excitatory amino acid transporter (EAAT) neuronal glutamate transporter, EAAT3, revealed the presence of a specific band in control and mercury-treated cultures. Micromolar concentrations of both methylmercury and mercuric chloride increased the release of endogenous glutamate, inhibited glutamate uptake, reduced mitochondrial activity, and decreased ATP levels. All these effects were completely prevented by the nonpermeant reducing agent Tris-(2-carboxyethyl)phosphine (TCEP). Reduction of mitochondrial activity by mercuric chloride, but not by methylmercury, was inhibited significantly by 4,4,-diisothiocyanato-stilbene-2,2,-disulfonic acid (DIDS) and by reduced extracellular Cl, ion concentration. In addition, DIDS and low extracellular Cl, completely inhibited the release of glutamate induced by mercuric chloride, and produced a partial although significant reduction of that induced by methylmercury. We suggest that a direct inhibition of glutamate uptake triggers an imbalance in cell homeostasis, leading to neuronal failure and Cl, -regulated cellular glutamate efflux. Our results demonstrate that neuronal glutamate transport is a novel target to be taken into account when assessing mercury-induced neurotoxicity. © 2005 Wiley-Liss, Inc. [source] Mercury hinders recovery of shoot hydraulic conductivity during grapevine rehydration: evidence from a whole-plant approachNEW PHYTOLOGIST, Issue 3 2006Claudio Lovisolo Summary ,,This experiment aimed to test whether recovery of shoot hydraulic conductivity after drought depends on cellular metabolism in addition to xylem hydraulics. ,,We rehydrated droughted grapevines (Vitis vinifera) after treating intact plants through the root with 0.5 mm mercuric chloride (a metabolic inhibitor) at the end of the stress period, before rehydration. The contribution of mercury-inhibited water transport in both shoot and root, and the extent of shoot vessel embolization, were assessed. ,,Drought stress decreased plant water potential and induced embolization of the shoot vessels. The rehydration in Hg-untreated plants re-established both shoot water potential and specific shoot hydraulic conductivity (Kss) at levels comparable with watered controls, and induced recovery of most of the embolisms formed in the shoot during the drought. In contrast, in plants treated with HgCl2, recovery of Kss and root hydraulic conductance were impaired. In rehydrated, Hg-treated plants, the effects of Hg on Kss were reversed when either the shoot or the root was treated with 60 mm,-mercaptoethanol as a mercuric scavenger. ,,This work suggests that plant cellular metabolism, sensitive to mercuric chloride, affects the recovery of shoot hydraulic conductivity during grapevine rehydration by interfering with embolism removal, and that it involves either the root or the shoot level. [source] Protective effects of Ginkgo biloba extract against mercury(II)-induced cardiovascular oxidative damage in ratsPHYTOTHERAPY RESEARCH, Issue 1 2007Tugba Tunali-Akbay Abstract This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) against Hg II-induced oxidative damage and also thromboplastic activity in the aorta and heart tissues. Wistar albino rats of either sex (200,250 g) were divided into four groups. Rats were injected intraperitoneally with (1) control (C) group: 0.9% NaCl; (2) EGb group: Ginkgo biloba extract (Abdi Ibrahim Pharmaceutical Company, Istanbul, Turkey) at a dose of 50 mg/kg/day; (3) Hg group: a single dose of 5 mg/kg mercuric chloride (HgCl2); and (4) Hg + EGb group: First day EGb at a dose of 50 mg/kg/day, i.p., 1 hour after HgCl2 (5 mg/kg) injection; following four days EGb at a dose 50 mg/kg/day, i.p. After decapitation of the rats, trunk blood was obtained and serum tumor necrosis factor- , (TNF- ,), lactate dehydrogenase (LDH) activity, and malondialdehyde (MDA) and glutathione (GSH) levels were analysed. In the aorta and heart tissues total protein, MDA, GSH levels and thromboplastic activity were determined. The results revealed that HgCl2 induced oxidative tissue damage, as evidenced by increases in MDA levels and decreased GSH levels both in serum and tissue samples. Thromboplastic activity was increased significantly following Hg administration, which verifies the cardiotoxic effects of HgCl2. Serum LDH and TNF- , were elevated in the Hg group compared with the control group. Since EGb treatment reversed these responses, it seems likely that Ginkgo biloba extract can protect the cardiovascular tissues against HgCl2 -induced oxidative damage. Copyright © 2006 John Wiley & Sons, Ltd. [source] Maximum limits of organic and inorganic mercury in fish feedAQUACULTURE NUTRITION, Issue 2 2004M.H.G. Berntssen Abstract The relatively high levels of mercury found in fish feeds might form a fish health and food safety risk. The present study aims to establish sublethal toxic threshold levels in fish and assess feed-fillet transfer of dietary mercury. Atlantic salmon (Salmo salar L.) parr were fed for 4 months on fish meal-based diets supplemented with mercuric chloride (0, 0.1, 1, 10 or 100 mg Hg kg,1 dry weight (DW)) or methylmercuric chloride (0, 0.1, 0.5, 5 or 10 mg MeHg kg,1 DW). At the end of the experiment, dietary inorganic mercury mainly accumulated in intestine (80% of body burden) and assimilation was low (6%). In contrast, methylmercury readily accumulated in internal organs and muscle (80% of body burden) and had a relatively high assimilation (23%). Highest accumulation of dietary inorganic mercury was observed in the gut and kidney. Fish fed 10 mg Hg kg,1 had an early (after 2 months) significant increase in renal metallothionein (MT) level and intestinal cell proliferation, followed by intestinal pathological conditions after 4 months of exposure. At 100 mg Hg kg,1, intestinal and renal function were reduced as seen from the significantly reduced protein and glycogen digestibility and increased plasma creatinine levels. For dietary methylmercury (MeHg), highest accumulation was found in blood and muscle. Intestinal cell proliferation and liver MT significantly increased at 5 mg MeHg kg,1 after 2 months of exposure. At the end of the experiment, blood haematology was significantly affected in fish fed 5 mg MeHg kg,1 and these fish exceeded the current food safety limit for mercury. Tissue MT induction and intestinal cell proliferation appeared to be useful and quantifiable early indicators of toxic mercury exposures. Based on the absence of induction of these early biological markers such as MT and cell proliferation, nonobserved effect levels (NOELs) could be set to 0.5 mg Hg kg,1 for dietary methylmercury and 1 mg Hg kg,1 for inorganic mercury. Lowest observed effect levels (LOELs) levels could be set to 5 mg kg,1 for methylmercury and 10 mg Hg kg,1 for inorganic mercury. [source] | ||||||||||||||||