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PubMed1990

Mercury compounds: lipophilicity and toxic effects on isolated myocardial tissue.

Lipophilicity is suggested to modulate the diffusion and the cytotoxic effects of mercury compounds. To investigate this, the positive inotropic effect of four Hg compounds (HgCl2, CH3HgCl, chlormerodrin, bromomercurihydroxypropane) was studied in catecholamine-depleted isolated heart muscle preparations. The rate of development of the positive effect was inversely correlated to the concentration in the case of HgCl2 and chlormerodrin, i.e. the product of concentration (c) and time to half-maximal effect (t50) remained constant. This was in accordance with the assumption of a permeation-controlled rate of action, as was shown earlier for p-chloromercuriphenyl-sulfonic acid. In addition, the c X t50 values of the individual mercurials decreased hyperbolically with the increase in lipophilicity as measured by the octanol/water partition. The results support the view that the toxicity of mercurials increases with their lipid solubility. In conjunction with the previously reported negative inotropic effect of Hg compounds, a model is proposed allocating thiol groups responsible for the negative inotropic action to lipid compartments within the cell membrane, while SH groups conveying the increase in contraction force are thought to be situated at the internal surface of the sarcolemma.

Animals↗
PubMed1992

Resolution of oral lichenoid lesions after replacement of amalgam restorations in patients allergic to mercury compounds.

The significance of contact allergy in patients with various oral symptoms was studied. Positive patch-test reactions to mercury compounds were found in 21/91 patients. Of these, 18 had lichenoid lesions in oral mucosa in close contact to amalgam fillings, and three patients with contact allergy had neither amalgam fillings in their teeth nor visible oral lesions. Amalgam replacement was carried out in 15/18 symptomatic patients. The fillings were replaced with gold in three cases, composite resin fillings in six, glass ionomer in three and both gold and composite materials in three cases. In 10 patients there was complete replacement and in five it was restricted to the fillings adjacent to the mucosal lesions. After a mean follow-up period of 3.2 years a complete cure was seen in seven patients, each of whom had had all their fillings changed. A marked improvement occurred in six patients, and there was no change in two.

Adult↗
PubMed1998

Modification of sulfhydryls of the skeletal muscle calcium release channel by organic mercurial compounds alters Ca2+ affinity of regulatory Ca2+ sites in single channel recordings and [3H]ryanodine binding.

The actions of two organic mercurial compounds, 4-(chloromercuri)phenyl-sulfonic acid (4-CMPS) and p-chloromercuribenzoic acid (p-CMB) on the calcium release channel (ryanodine receptor) from rabbit skeletal muscle were determined by single channel recordings with the purified calcium release channel, radioligand binding to sarcoplasmic reticulum vesicles (HSR) and calcium release from HSR. p-CMB or 4-CMPS (20-100 microM) increased the mean open probability (Po) of the calcium channel at subactivating (20 nM), maximally activating (20-100 microM and inhibitory (1-4 mM) Ca2+ concentrations, with no effect on unitary conductance. This activation was partly reversed by 2 mM DTT. Both compounds affected the channels only from the cytosolic side, but not from the trans side. 100 microM 4-CMPS caused a transient increase in Po, followed by a low activity state within 1 min. At inhibitory Ca2+ concentrations Po was increased to values observed with maximally activating Ca2+ or lower, inhibitory Ca2+ concentrations. The p-CMB/4-CMPS modified channels were ryanodine sensitive and blocked by ruthenium red. [3H]Ryanodine binding was increased up to four-fold with 3-15 microM 4-CMPS/p-CMB (Hill coefficient 1.7-2.0) at 4 microM Ca2+ and reduced at high concentrations (50-200 microM). The increase in [3H]ryanodine binding by 10 microM 4-CMPS was completely inhibited by 2 mM DTT. 4-CMPS significantly increased the affinity for the high affinity calcium activation sites and decreased the affinity of low affinity calcium inhibitory sites of specific [3H]ryanodine binding. 4-CMPS increased the affinity of the ryanodine receptor for high affinity ryanodine binding without a change in receptor density. 4-CMPS induced a rapid, concentration-dependent, biphasic calcium release from passively calcium-loaded HSR vesicles at subactivating Ca2+ concentrations (20 nM), which was partly inhibited by 4 mM DTT and completely blocked by 20 microM ruthenium red. It is suggested that the 4-CMPS-induced modulation of essential sulfhydryls involved in the gating of the calcium release channel results in a modulation of the apparent calcium affinity of the activating high affinity and inhibitory low affinity calcium binding sites of the calcium release channel.

4-Chloromercuribenzenesulfonate↗
PubMedDate not supplied

Peripheral neurotoxicity in workers exposed to inorganic mercury compounds.

Nerve conduction velocity (NCV) of the median motor, median sensory, and sural nerves was assessed in 16 workers chronically exposed to various inorganic mercury compounds. Exposed workers were compared with an unexposed control group using t test analyses. Slowing of the median motor nerve NCV was found, which was correlated with both increased levels of mercury in blood and urine, and with increased number of neurologic symptoms. Sensitive evaluation of neural function was found to be practical and informative for investigating mercury toxicity. Such evaluation can help determine safe mercury levels at the workplace.

Adult↗
PubMed1977

Interactions of acetylcholine receptors with organic mercury compounds.

Micromolar concentrations of methylmercury and several organic mercury fungicides were found to block binding of [3H]acetylcholine (ACh) to the ACh-receptor of the electric organ of the electric ray, Torpedo ocellata. The same compounds had little or no effect on the catalytic activity of ACh-esterase of the same tissue. [14C]Methyl-mercury bound to the purified ACh-receptor with high affinity (Kd=7micrometer) and there were 6.5 +/- 0.5 binding sites for each ACh-binding site. Binding of methylmercury was highly cooperative with a Hill coefficient of 2.6. This binding was irreversible by redialysis in methylmercury - free medium, however, the bound [14C]methylmercury was easily displaced from the receptor protein with micrometer concentrations of BAL or penicillamine. Methylmercury also blocked binding of [3H] nicotine and [3H]pilocarpine to the nicotinic and muscarinic ACh-receptors of the rat brain, respectively. The data suggest that the ACh-receptor may be a target for methylmercury and other organic mercury compounds.

Acetylcholine↗
PubMed1986

Quenching of red cell tryptophan fluorescence by mercurial compounds.

Intrinsic tryptophan fluorescence in red cell ghost membranes labeled with N-ethylmaleimide (N-EM) is quenched in a dose-dependent manner by the organic mercurial p-chloromercuribenzene sulfonate (p-CMBS). Fluorescence lifetime analysis shows that quenching occurs by a static mechanism. Binding of p-CMBS occurs by a rapid (less than 5 s) biomolecular association (dissociation constant K1 = 1.8 mM) followed by a slower unimolecular transition with forward rate constant k2 = 0.015 s-1 and reverse rate constant k-2 = 0.0054 s-1. Analysis of the temperature dependence of k2 gives delta H = 6.5 kcal/mol and delta S = -21 eu. The mercurial compounds p-chloromercuribenzoic acid, p-aminophenylmercuric acetate, and mercuric chloride quench red cell tryptophan fluorescence by the same mechanism as p-CMBS does; the measured k2 value was the same for each compound, whereas K1 varied. p-CMBS also quenches the tryptophan fluorescence in vesicles reconstituted with purified band 3, the red cell anion exchange protein, in a manner similar to that in ghost membranes. These experiments define a mercurial binding site on band 3 in ghosts treated with N-EM and establish the binding mechanism to this site. The characteristics of this p-CMBS binding site on band 3 differ significantly from those of the p-CMBS binding site involved in red cell water and urea transport inhibition.

Anion Exchange Protein 1, Erythrocyte↗
PubMedDate not supplied

Tissue distribution of different mercurial compounds analyzed by the improved FI-CVAAS.

Mercury contents in biological samples can be measured by cold vapor atomic absorption spectroscopy combined with the flow-injection analysis system. However, water vapor in the absorption cell attenuated and distorted the signals. This study described the strategy to overcome this problem by adding an additional gas-liquid separator after the mixing/separator assembly. This modification can efficiently minimize the moisture in the transfer line and in the absorption cell. This improved technique was adopted to study the differential tissue distribution of methylmercury and HgS after oral administration to mice for five consecutive days. The present study suggests that the insoluble HgS (the main constituent of a Chinese mineral drug, cinnabar, used as a sedative) can still be absorbed from gastrointestinal tract and distributed to various tissues including the brain. As compared with methylmercury, the total amount of HgS accumulated in the tissues ranging about one five-thousandth of methylmercury, which is well correlated with the biological activity of HgS reported previously.

Administration, Oral↗