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At least 19 recordsLinked to original sources
PubMed2000

Mercury intolerance and lymphocyte transformation test with nickel sulfate, palladium chloride, mercuric chloride, and gold sodium thiosulfate.

The peripheral lymphocytes of 10 patients referred to as mercury intolerant and 9 patients referred to as tolerant with regard to presence or absence of psychosomatic symptoms when percutaneously exposed to low patch test doses of mercury were stimulated in vitro with four metal salts. In addition, cells from 7 subjects with no anamnestic mercury intolerance or allergy to metals as well as free from dental alloys were included as controls. Lymphocyte transformation test was done by in vitro challenge with five concentrations of gold sodium thiosulfate, nickel chloride, palladium chloride, and seven concentrations of mercuric chloride. Stimulation with palladium chloride and mercuric chloride showed a difference between the mercury-intolerant and -tolerant patients on one hand and the controls on the other, but there was no difference between the two patient groups. With regard to nickel sulfate, there was a significant dose-dependent stimulation in all the three groups but no difference between the groups could be seen. Gold sodium thiosulfate did not stimulate the lymphocytes at all. Based on these results, we therefore conclude that lymphocyte transformation test performed with the four metal salts cannot be used to further differentiate between mercury-intolerant and -tolerant patients.

Adult↗
PubMed1996

Expression of the 25-kDa heat-shock protein (HSP27) correlates with resistance to the toxicity of cadmium chloride, mercuric chloride, cis-platinum(II)-diammine dichloride, or sodium arsenite in mouse embryonic stem cells transfected with sense or antisense HSP27 cDNA.

Embryonic stem (ES) cells were transfected with the protein-coding region of rat HSP27 cDNA placed in sense or antisense orientation in vector pcDNA3 under the control of the constitutive cytomegalovirus (CMV) promoter. Compared with nontransfected ES cells, five sense HSP27 cDNA-transfected ES cell clones displayed up to fourfold increases in expression of HSP27 mRNA and up to sixfold increases in expression of HSP27 protein, whereas four antisense HSP27 cDNA-transfected ES cell lines exhibited synthesis of antisense HSP27 RNA and a 50-85% decrease in HSP27 protein expression. Compared to the parental ES cell lines or ES cells transfected with the vector lacking any HSP27 sequence, all ES cell lines overexpressing HSP27 were resistant to killing by cadmium chloride (CdCl2), mercuric chloride (HgCl2), cis-platinum(II)-diammine dichloride (cDDP), sodium arsenite (NaAsO2), and heat while ES cell lines expressing reduced HSP27 were more sensitive to metal toxicity and heat. The relative toxicities of the tested metals to ES cells were cDDP > NaAsO2 > HgCl2 > CdCl2. Protection of ES cells against metal or heat toxicity was positively correlated with the level of HSP27. These data confirm in ES cells previous reports of the ability of HSP27 to protect other cell types against heat and demonstrate that HSP27 protects mammalian cells against the toxic effects of diverse metals.

Animals↗
PubMed1987

Influence of cadmium chloride, mercuric chloride, and sodium vanadate on the glutathione-conjugating enzyme system in liver, kidney, and brain of mice.

Sublethal doses of CdCl2 (3 mg/kg iv), HgCl2 (2 mg/kg iv), or NaVO3 (6 mg/kg iv) did not alter the content of reduced glutathione (GSH) in the livers of mice during the 24-h observation period. In the kidneys, a tendency to increased GSH content was seen, especially after HgCl2 treatment; in lung and brain the GSH levels were significantly lowered upon the treatment with all three metals. The activities of GSH S-transferase toward an aryl substrate (CDNB; 1-chloro-2,4-dinitrobenzene) was enhanced in all tissues by the administration of HgCl2 greater than NaVO3 greater than CdCl2. The activity of GSH S-transferase toward an epoxide substrate [1,2-epoxy-3-(p-nitrophenoxy)propane was only measurable in the livers and was inhibited 1 and 2 h after the administration of HgCl2 and NaVO3. It is concluded that sublethal doses of CdCl2, HgCl2, or NaVO3 do not impair the GSH concentration and GSH-conjugating enzyme activities toward the aryl substrate in different target organs of their toxicity, which is in contrast to results obtained in vitro.

Animals↗
PubMed1997

Heavy-metal toxicity in an insect cell line. Effects of cadmium chloride, mercuric chloride and methylmercuric chloride on cell viability and proliferation in Aedes albopictus cells.

We evaluated the toxicity of CdCl2, HgCl2, and MeHgCl on the C6/36 cell line of Aedes albopictus. This cell line proved to be a suitable tool for studying heavy-metal toxicity in insect cells. Since data on heavy-metal toxicity in invertebrate cell cultures are almost nonexistent, our results are discussed in relation to in vivo invertebrate and in vitro vertebrate studies. Viability and proliferation were assessed by dye exclusion and DNA quantification, respectively. Viability tests were carried out with and without 5% fetal calf serum in the medium. The three metal species decreased viability to different extents (MeHgCl > HgCl2 > CdCl2), and fetal calf serum had a protective effect. In serum-deprived cultures, LD50 values were 140.20, 2.51, and 2.08 mumol/L for CdCl2, HgCl2, and MeHgCl, respectively. For cultures with fetal calf serum, LD50 values were 149.71, 12.01, and 5.47 mumol/L, respectively. The viability curve for CdCl2 under serum-free conditions suggests the induction of a cell defense system. The three metal species also inhibited cell proliferation (MeHgCl > CdCl2 > HgCl2). The IC50 values were 1.75, 18.36, and 0.96 mumol/L for CdCl2, HgCl2, and MeHgCl, respectively. In summary, low MeHgCl concentrations caused both cell death and inhibition of cell proliferation; HgCl2 primarily disrupted the plasma membrane, whereas CdCl2 primarily inhibited cell proliferation.

Aedes↗
PubMed1991

Ultrastructural demonstration of mercury in Sertoli and Leydig cells of the rat following methyl mercuric chloride or mercuric chloride treatment.

The autometallographic silver enhancement technique has been used to demonstrate the ultrastructural localization of mercury in the testes of adult rats. Administration of mercuric chloride or methyl mercuric chloride in the drinking water (20 mg/L for 12 weeks) resulted in intracellular accumulations of mercury in the interstitial Leydig cells as well as in the Sertoli cells of the seminiferous tubules.

Animals↗
PubMed2002

Potentized Mercuric chloride and Mercuric iodide enhance alpha-amylase activity in vitro.

Mercuric chloride 30c and Mercuric iodide 30c were prepared by successive dilution in 30 steps of 1:100 followed by sonication at 20KHz for 30s at each step. Both were prepared in two media: 90% ethanol and distilled water. Three preparations of Mercuric chloride 30 in water were used: 12-month old, 1-month old and 4-day old. The controls for the water and ethanol-water preparations were pure water 30c and 90% ethanol 30c, respectively. For the three water preparations there were three matched controls of water 30c of the same ages. Each potentized substance or its control was mixed with distilled water 1:100 before testing. Hydrolysis of starch by alpha-amylase was measured by the standard procedure after incubation for 15 min at 27 degrees C. Mercuric chloride 30c and Mercuric iodide 30c in both water and aqueous ethanol media, enhanced enzyme activity significantly, compared to their respective controls. Mercuric chloride 30c, prepared in water 12 months previously, produced no significant change in the enzyme activity compared to its control. We hypothesize that the structure of the active molecule imprinted on water polymers during the process of dynamization. The specifically structured water interacts with the active sites of alpha-amylase, modifying its activity. Ethanol molecules have large non-polar part stabilizing the water structure and thus retaining activity for a longer time.

Disinfectants↗
PubMed1990

Antinucleolar autoantibody induced in mice by mercuric chloride.

Mercuric chloride (MC) was administered to mice subcutaneously 3 times a week for 4 weeks. When inbred BALB/c, CBA/JN, C3H/He, C57BL/6 and DBA/2 and outbred ICR female mice were given 1 mg/kg MC, 8 of 10 ICR mice developed antinucleolar autoantibodies (AnuA) of the IgG class but none of the inbred mice produced AnuA. So the ICR mice were used in the following experiments. In a kinetic study, in which mice were given 1.5 mg/kg MC, the positivities and titers of AnuA increased time-dependently, and were kept at high levels until 8 weeks after the final treatment. The AnuA titers of mice receiving 0.5-2.0 mg/kg increased dose-dependently, while the positivity was similar at all dosages. The antibody titers were higher in mice pretreated with an intramuscular injection of either complete or incomplete Freund's adjuvant. The titer increase was more prominent in mice administered doses lower than 0.5 mg/kg. Neither nude mice nor mice treated with a monoclonal antibody to L3T4 (GK1.5) developed AnuA. These results indicate that the induction of AnuA by MC depend primarily on L3T4-positive T cells.

Animals↗
PubMed1991

Increased urinary calcium and magnesium excretion in rats injected with mercuric chloride.

Mercuric chloride (HgCl2) is a classic nephrotoxic agent. While it is well established that HgCl2 can induce metallothionein synthesis in the kidney and also cause damage to the pars recta region of the renal tubule, the urinary losses of essential elements like calcium (Ca) and magnesium (Mg) probably related to this process, have not been described. In this study, calcium, magnesium, metallothionein (MT), as well as sodium (Na) and potassium (K) in urine, kidney cortex and liver were measured in male Wistar rats after two daily injections of HgCl2 (0.5 or 1.0 mg Hg/kg body weight intraperitoneally). As compared with controls, there was a significant 3-4-fold increase in calcium excretion which reached its maximum at 8-12 and 32-36 hr after treatment with 1.0 mg Hg/kg. Urinary magnesium excretion was also increased in a similar way as the calcium excretion. At 12-16 hr, urinary magnesium in the 1.0 mg Hg/kg dose group was 3.4 times higher than that of the controls. Urinary MT level in HgCl2 treated rats was much higher than that in the controls, the maximum excretion was between 24-28 and 32-36 hrs preceeded by the peak of Hg in urine. Na and K concentrations in urine decreased significantly in rats treated with HgCl2. The present study thus demonstrates that increases of urinary calcium and magnesium excretion are early toxic effects of HgCl2 on the kidney. It gives support to the hypotheses implying these ion imbalances in the mechanism of elicitation of renal toxicity by mercury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The comparative effects of methylmercuric chloride and mercuric chloride upon DNA synthesis in mouse fetal astrocytes in vitro.

The relative effects of direct exposure to methylmercuric chloride (MMC) and mercuric chloride (MC) upon [3H]thymidine incorporation were determined using cultured mouse fetal astrocytes. The labeling indices of cells exposed to MMC were significantly lower than those of cells exposed to equimolar concentrations of MC. These results indicate that on a mole-for-mole basis, MMC is much more deleterious upon DNA synthesis of mouse fetal astrocytes than those of MC.

Animals↗
PubMed1991

Rapid changes in concentrations of essential elements in organs of rats exposed to methylmercury chloride and mercuric chloride as shown by simultaneous multielemental analysis.

An in vivo study of rats given a dominant lethal dose of methylmercury chloride (MMC) or mercuric chloride (HgCl2) was conducted to elucidate the rapid biotransformation of essential elements. The elements were measured by inductively coupled plasma atomic emission spectrometry. For the rat brain Zn concentrations were higher in the MMC group than in the HgCl2 and control groups. The highest Cu concentration was found in HgCl2 dosed rat liver. For the rat kidney the highest Zn concentration was seen in the MMC group. From principal component analysis on the time dependent behaviour of each element in rat organs, characteristics specific to Cu in the liver and kidney and Mn in the brain were found after exposure to HgCl2 and Ca and Zn in the brain after exposure to MMC.

Animals↗
PubMed1990

The cytotoxic effects of cadmium chloride and mercuric chloride mixtures in rat primary hepatocyte cultures.

The toxic effects of Cd and Hg mixtures were studied using primary monolayer cultures of rat hepatocytes. Cytotoxicity was assessed by measuring the release of lactic dehydrogenase from the cells. Cytotoxic and non-cytotoxic metal levels were used. At the higher exposure concentrations (0.2 micrograms Cd.ml-1 and 2.0 micrograms Hg.ml-1), Cd was very toxic to hepatocytes whereas Hg was only marginally toxic. The combination of Cd and Hg was more toxic than predicted by summation of the individual metal toxicities. The incorporation of [35S]cysteine into protein of the cytosol and insoluble cell fraction was increased in response to Cd or Hg exposure and was directly related to cell 35S accumulation. Combinations of Cd and Hg significantly increased the proportion of total 35S which was incorporated in cell protein, an effect that was attributed to the accumulation of protein in the insoluble cell fraction. Cd uptake by hepatocytes was related to exposure concentration but was lower when Hg was also present in the incubation medium. Gel chromatography of the cytosol from Cd-exposed cells showed 3 Cd containing fractions which corresponded to the elution positions of high Mr proteins, metallothionein (MT) and low Mr molecules. When hepatocytes were exposed to Hg in combination with Cd, the MT-like fraction was no longer evident and Cd in the low Mr fraction was greatly reduced. Regardless of the presence or absence of Cd in the exposure medium, 98% of cytosol Hg in Hg-exposed cells was found to elute after the low Mr fraction, at a position equivalent to inorganic salts. This indicates that the enhanced cytotoxicity of Cd and Hg may be related to a decrease in the MT-like protein in the cytosol and not due to a direct competitive binding interaction in relation to the protein.

Animals↗
PubMed1984

[Inhibition by methyl mercury chloride and mercuric chloride of the in vitro polymerization of microtubules].

Mercury was tested at the same concentration but under two different forms, organic CH3HgCl and inorganic HgCl2, in order to compare its relative inhibitory effect on in vitro microtubules polymerization. Induced by GTP and glycerol 8 M, tubulin polymerization was completely inhibited by HgCl2 10(-3) M while a 75.8% inhibition was measured for CH3HgCl2 10(-3) M.

In Vitro Techniques↗
PubMed1990

Differential effects of methylmercuric chloride and mercuric chloride on oxidation and iodination reactions catalyzed by thyroid peroxidase.

Thyroid peroxidase (TPO), the major enzyme in the thyroid hormone synthesis, multifunctionally catalyzes (1) iodide oxidation, (2) iodination of the precursor protein, and (3) a coupling reaction of iodotyrosyl residues. The present study was carried out to examine the mercurial effects on the iodination, the second step of TPO. Purified porcine thyroglobulin or bovine serum albumin as acceptor protein was iodinated with [125I]NaI and H2O2 by purified porcine TPO. Iodinated protein was separated by acid precipitation on membrane filter or paper chromatography. Both CH3HgCl and HgCl2 dose-dependently inhibited the iodination, but HgCl2 was more potent to inhibit the iodination than CH3HgCl. These mercurial effects on the second step resemble the effects on the third step which were already reported; but are in marked contrast to the effects on the first step, where TPO was inhibited by HgCl2 but never by CH3HgCl.

Animals↗
PubMed1986

Differential effects of methylmercuric chloride and mercuric chloride on the L-glutamate and potassium evoked release of [3H]dopamine from mouse striatal slices.

The effects of CH3HgCl and HgCl2 on the evoked release of 3H from mouse striatal slices prelabelled with [3H]dopamine have been examined. CH3HgCl (10 microM) was observed to increase the L-glutamate-evoked release of [3H]dopamine, while HgCl2 (10 microM) had no effect. In contrast, CH3HgCl at concentrations up to 100 microM had no effect on the 25 mM K+-stimulated release of [3H]dopamine, whereas HgCl2 (100 microM) significantly reduced the 25 mM K+-stimulated release of [3H]dopamine. Thus CH3HgCl and HgCl2 have differential effects on the L-glutamate- and K+-stimulated release of [3H]dopamine from mouse striatal slices, suggesting that these compounds may have different sites and (or) mechanisms of action in altering neurotransmitter release. It is suggested that CH3HgCl may act predominantly at intracellular sites or at the level of the L-glutamate receptor, whereas the major site of action of HgCl2 may be the voltage-operated calcium channel.

Animals↗
PubMed1989

Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells.

This study was designed to characterize the interaction of CH3HgCl or HgCl2 with thyroid peroxidase (TPO). Two types of experiments were performed. First, the thyroids from rats that were given 5.6 mg/kg/day of either CH3HgCl or HgCl2 for 2 weeks by intubation were subjected to histochemical treatment and then to electron microscopy. TPO activities in all cell compartments were inhibited by HgCl2 but not by CH3HgCl. Morphological observation showed that taller epithelia were induced by HgCl2, whereas flattened epithelia forming large follicles were induced by CH3HgCl. The serum thyrotropin level was substantially lowered by CH3HgCl but was unchanged by HgCl2. Second, the guaiacol oxidation by TPO in isolated and ruptured pig thyroid cells was spectrophotometrically monitored in the presence of either CH3HgCl or HgCl2. The TPO was not inhibited by CH3HgCl but was inhibited by HgCl2. These results indicated that CH3HgCl induced a hypothyroid state without affecting TPO, whereas HgCl2 inhibited TPO and induced a hypertropic state owing to compensation for loss of enzyme activity, and that the lack of inhibitory activity of CH3HgCl was not due to the inability to penetrate the cells. Therefore, there appeared to be a differential interaction of organic and inorganic forms of mercurials with the thyroid.

3,3'-Diaminobenzidine↗
PubMed1986

Subacute toxicity of methylmercuric chloride and mercuric chloride on mouse thyroid.

Intoxication effect on mouse thyroid by prolonged administration of either CH3HgCl or HgCl2 was studied. It was found by giving CH3 203HgCl and 203HgCl2 through stomach intubation at either a single or a 30 d treatment that thyroid is a moderately susceptible organ to both mercurials. Animals were given 50, 100 and 150 micrograms/d of either mercurial in drinking water for a month. At the lowest amount of HgCl2, body weight was increased, whereas at the highest dose, there was a transient delay in growth. With lower amounts of CH3HgCl, no change in growth was observed. However, at the highest amount, a severe growth inhibition occurred. The thyroid weight was unaffected by lower amounts, but was significantly reduced by 150 micrograms/d of either mercurial. The 24 h radioiodide uptake in the thyroid, expressed by cpm/mg organ weight, was reduced by lower levels of mercurials. CH3HgCl and HgCl2 suppressed the rate of radioiodide incorporation into the iodothyronine fraction, but not into the iodotyrosine fractions, indicating that mercurials do not interfere with organification of iodide but do inhibit the coupling process. Serum thyroxine (T4) level was affected by mercurials, but serum triiodothyronine (T3) was not. This result suggested that even thyroidal secretion of T4 was inhibited by mercurials, but the peripheral conversion of T4 to T3 may not be affected in the maintenance of an active hormone level.

Animals↗