Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Organomercury Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

Binding of tissue inhibitor of metalloproteinases 2 to two distinct sites on human 72-kDa gelatinase. Identification of a stabilization site.

We have identified a binding site for tissue inhibitors of metalloproteinases 2 (TIMP-2) on human 72-kDa gelatinase that is distinct from the active site. 72-kDa progelatinase is found in a complex with TIMP-2 in the medium of cultured cells and can be activated with organomercurial compounds to yield a gelatinolytic proteinase that remains bound to TIMP-2. Removal of TIMP-2 from 72-kDa progelatinase by reverse-phase high performance liquid chromatography, followed by reconstitution of the progelatinase in neutral pH buffer, results in autocatalytic activation. When samples of autoactivated gelatinase were blotted onto nitrocellulose, then probed with 125I-TIMP-2, we found a 29-kDa peptide that was capable of binding TIMP-2. We isolated this fragment and identified it as the region of gelatinase from amino acid 414 to the carboxyl terminus in the primary amino acid sequence of progelatinase. This portion of the molecule does not contain the putative zinc- or gelatin-binding sites and is proteolytically inactive. Incubation of 125I-TIMP-2 with 72-kDa progelatinase-TIMP-2 complexes resulted in a concentration-dependent exchange of labeled TIMP-2 with unlabeled TIMP-2, in both the presence and absence of the metalloproteinase inhibitor 1,10-phenanthroline. Saturation binding kinetics for the active site of 72-kDa gelatinase were measured in pools of the 43-kDa active fragment that results from the autoactivation of 72-kDa progelatinase; this fragment has no carboxyl-terminal TIMP-2 binding capability. Binding of 125I-TIMP-2 to the active site was completely inhibited by 1,10-phenanthroline. Binding kinetics for the putative stabilization site were determined with isolated 72-kDa progelatinase. In the presence of 1,10-phenanthroline, 72-kDa progelatinase bound 125I-TIMP-2 but not 125I-TIMP-1. Scatchard analysis yielded an approximate dissociation constant (Kd) of 0.72 nM for the active site and 0.42 nM for the stabilization site.

Autoradiography↗

[Toxic glomerulonephritis].

Most glomerulopathies are immunologically-mediated. Their pathogenesis is now better understood. The role of cell-mediated immunity has recently been envisaged. The role of circulating antibodies now seems to be more important than that of circulating immune complexes. Antibodies may recognize structural or "planted" antigens in the kidney, the latter being non-renal molecules that may bind renal structures for non-immune reasons. The linear or granular pattern observed at immunofluorescence depends upon the regular or irregular distribution of the antigen. In susceptible individuals, various toxins (heavy metals such as mercury or gold, drugs with an SH group, non-steroidal anti-inflammatory agents) may induce an immune glomerulopathy. It has recently been shown that Brown-Norway rats exposed to one of the above-mentioned agents develop anti-self class II T lymphocytes that are responsible for a polyclonal activation of B cells. Among the various autoantibodies that are produced, some have a nephritogenic potential. Other drugs are responsible for glomerular lesions due to a direct toxic effect of the compound. Doxorubicin induces a nephrotic syndrome in the rabbit, while mitomycin induces a haemolytic uraemic syndrome in humans. Finally, drug addiction often leads to glomerulosclerosis.

Animals↗

Liquid chromatographic-atomic absorption spectrophotometric method for determination of methyl mercury in seafood: collaborative study.

A previously developed method that uses a simplified sample preparation procedure and atomic absorption detection of liquid chromatographic eluates for the determination of methyl mercury in seafood has been collaboratively studied. The unique feature of the method involves the use of a specially designed interface for the generation of mercury vapor. Methyl mercury is isolated from the blended sample by chloroform elution from a diatomaceous earth-hydrochloric acid column. The organomercury compound is then extracted into a small volume of 0.01M sodium thiosulfate solution. An aliquot of this solution is injected onto a Zorbax ODS column and eluted with methanol-ammonium acetate solution (3 + 2), pH 5.7, containing 0.01% mercaptoethanol. Mercury is detected by flameless atomic absorption spectrophotometry using the interface. The samples analyzed in the study were unspiked swordfish, unspiked and spiked lobster, and unspiked and spiked tuna. The spiked samples contained methyl mercury both above and below the U.S. Food and Drug Administration guideline level of 1 microgram Hg/g. Reproducibility relative standard deviations ranged from 10.5% at 1 microgram Hg/g to 18.2% at about 0.1 microgram Hg/g. Accuracy, measured by comparison to reference values obtained by the Associate Referee, ranged from 94.4 to 99.6%. The method has been adopted official first action.

Animals↗

Effect of organic and inorganic mercury compounds on the growth of incisor and tibia in rats.

The pharmacological effects of methyl mercury chloride (MMC) and mercuric chloride (HgCl2) (2-16 mg/Kg per day subcutaneously, for 6 d) upon the growth were studied in the incisors and proximal tibiae of immature rats histologically. Lead acetate was used as a time marker. 1. Mercury compounds slightly affected the body weight gains of the rats but apparently inhibited the longitudinal growth of proximal tibia and the effect increased with higher dosages. 2. Mercury compounds definitely inhibited not only the longitudinal growth (incisor growth) but also the appositional growth (dentin formation) of incisal dentin. 3. The inhibitory effect on the growth was ranked as follows: bone growth greater than dentin formation greater than incisor growth. 4. The actions of MMC on the growth of incisors and proximal tibiae appeared gradually and the response was biphasic; stimulatory and then inhibitory. The inhibitory effect appeared even after the injection was discontinued and appeared more extremely than during the injections. 5. In HgCl2 groups the inhibitory effect on the growth appeared rapidly. The effect increased with higher dosages and became stronger as the injections were repeated. However, this effect was weakened promptly after the injection was discontinued. 6. The repeated injections of mercury compounds hardly affected the level of serum calcium but disturbed the calcification of incisal dentin. From the above-mentioned results a possible mechanism was discussed. It is suggestive that MMC acts directly upon a cell and is transported into it. Once MMC was introduced into a cell it is slowly demethylated to inorganic Hg and acts as the demethylated mercury. When accumulated mercury is slight in volume, it stimulates and then inhibits the cell function with increasing mercury. However HgCl2 binds directly with an effector cell membrane in loose fashion. This may cause the ready reversibility of the effect.

Animals↗

Organomercury poisoning in Iraq: history prior to the 1971-72 outbreak.

Mercury has been used medically in the Middle East since time immemorial. Organomercury compounds were first used as seed dressings in Iraq in 1955. During the years 1955-59, 200 cases of poisoning occurred. A more clearly defined outbreak occurred in 1960, involving approximately 1000 hospital admissions. Twelve patients from two families affected in this outbreak were re-examined in 1973, and showed considerable improvement.

Disease Outbreaks↗

Purification and characterization of a novel organometallic receptor protein regulating the expression of the broad spectrum mercury-resistant operon of plasmid pDU1358.

The narrow spectrum mercury-resistant (mer) operons of transposons Tn21 and Tn501 are inducible by inorganic mercury salts. The major regulatory gene merR is transcribed divergently from the other mer genes, which are cotranscribed. The MerR protein represses its own expression, as well as the expression of the other mer genes in the absence of the inducers. The synthesis of the polycistronic mer message is stimulated by MerR in the presence of the inducers. The MerRBS protein encoded by the broad spectrum mer operon of plasmid pDU1358 was characterized as a novel organomercurial receptor, distinguishing it from the narrow spectrum MerRNS proteins, described above. Several organomercurial compounds directly effected cellular activation of the mer operon transcription via the receptor protein MerRBS, but not by MerRNS. The merR gene from pDU1358 was cloned under the tac promoter, and the overexpressed MerRBS protein was soluble in buffer solutions containing 0.5 M NaCl at pH 7.5, but precipitated when NaCl concentration was reduced to 0.1 M (MerRBS concentrations at or above 0.1 mg/ml). MerRBS was purified to near homogeneity by selective precipitation and solubilization by varying the salt concentration in buffer solutions, followed by Sephadex G-75 column chromatography. Both MerRBS and Tn21-encoded MerRNS bound with DNA fragments containing the pDU1358 mer operator sequence with comparable affinities. In vitro run-off transcription studies revealed that MerRBS activated mer operon expression in the presence of Hg2+ or phenylmercuric acetate. Phenylmercuric acetate did not induce mer operon expression when the MerRNS was used in the assay.

Bacterial Proteins↗

Detection of organotin, organomercury, and organolead compounds with a pulsed discharge detector (PDD).

The response of a pulsed discharge detector (PDD) to organometallic compounds in the helium ionization detection (HID) mode was dependant on the number of C atoms in the tested analytes with the limits of detection ranging from 0.7 pg (tetraethyllead (Et(4)Pb)) to 1.2 pg di- n-propyl mercury (Pr(2)Hg)). Response linearity was excellent over three orders of magnitude. Selectivity in the HID mode was enhanced by doping the He discharge gas with argon, although sensitivity dropped threefold. In electron capture detection (ECD) mode, only organolead was detected with a limit of 0.1 pg.

Journal Article↗

Inhibition and uncoupling of photophosphorylation in isolated chloroplasts by organotin, organomercury and diphenyleneiodonium compounds.

1. Trialkyltin, triphenyltin and diphenyleneiodonium compounds inhibited ADP-stimulated O(2) evolution by isolated pea chloroplasts in the presence of phosphate or arsenate. Tributyltin and triphenyltin were the most effective inhibitors, which suggests a highly hydrophobic site of action. Phenylmercuric acetate was a poor inhibitor of photophosphorylation, which suggests that thiol groups are not involved. 2. Triethyltin was a potent uncoupler of photophosphorylation by isolated chloroplasts in media containing Cl(-), but had little uncoupling activity when Cl(-) was replaced by NO(3) (-) or SO(4) (2-), which are inactive in the anion-hydroxide exchange. It is suggested that uncoupling by triethyltin is a result of the Cl(-)-OH(-) exchange together with a natural uniport of Cl(-). Tributyltin, triphenyltin and phenylmercuric acetate had low uncoupling activity, probably because in these compounds the uncoupling activity is partially masked by inhibitory effects. 3. At high concentrations the organotin compounds caused inhibition of electron transport uncoupled by carbonyl cyanide m-chlorophenylhydrazone or NH(4)Cl. At these high concentrations the organotin compounds may be producing a detergent-like disorganization of the membrane structure. In contrast, diphenyleneiodonium sulphate inhibited uncoupled electron transport at low concentrations; however, this inhibition is less than the inhibition of photophosphorylation, which suggests that the compound also inhibits the phosphorylation reactions as well as electron transport. 4. The effects of these compounds on basal electron transport were complex and depended on the pH of the reaction media. However, they can be explained on the basis of three actions: inhibition of the phosphorylation reactions, uncoupling and direct inhibition of electron transport. 5. The inhibition of cyclic photophosphorylation in the presence of phenazine methosulphate by diphenyleneiodonium sulphate shows that it inhibits in the region of photosystem 1.

Adenosine Diphosphate↗

Liquid chromatographic--cold vapour atomic fluorescence spectrometric determination of mercury species.

Solvent extraction, sonication, and microwave-assisted extractions in the presence of extraction agents (thioacetic acid, citric acid, cysteine, 2-mercaptoethanol, HCl + NaCl, etc.) were tested for the isolation of mercury species. A mixture of 6 M HCl and 0.1 M NaCl was selected as the most suitable extraction agent. The extraction efficiency was about 10% higher and the RSD below 3.3% when microwave-assisted extraction was applied instead of sonication. The liquid chromatography-cold vapour atomic fluorescence spectrometry (LC/CV-AFS) method was optimised and used for separation and determination of inorganic mercury cations and alkylated and arylated mercury species. Isocratic elution at a flow rate of 0.15 mL/min (with a mobile phase containing 0.05% 2-mercaptoethanol (pH = 5) and 7% methanol and with a stepwise increase of methanol content up to 100% MeOH in the 15th min) was used for separation of mercury species on a Hypersil BDS C18 RP column. The limits of detection of the LC/CV-AFS system were estimated as 0.2 microg/L (3%) for MeHg+, 0.07 microg/L (5.3%) for inorganic Hg, 0.06 microg/L (3.4%) for PhHg+, and 0.12 microg/L (4.4%) for EtHg with the corresponding RSDs at 5 microg/L (n = 10) given in parentheses. The concentrations (2-10 mg/kg fresh weight) of total mercury and methylmercury (90-99% of the total mercury) in selected fish obtained by HPLC/CV-AFS were in good agreement (absolute deviations 0.05 mg/kg) but more precise (RSDs <5.4% at 5 mg/L, n = 10) than those determined by GC coupled to an electron capture detector. The RSDs (3.1-8.2% and 4.1-9.0%) of the overall analytical procedure for the determination of total mercury (AMA 254) and methylmercury (HPLC/CV-AFS) were determined for intra-day and inter-day assays, respectively.

Animals↗

Selective reduction method for separate determination of inorganic and total mercury in mussel tissue by flow-injection cold vapor technique.

A flow-injection cold vapor atomic absorption spectrometry (FI-CV-AAS) method was developed to determine inorganic mercury and total mercury in mussel samples obtained from the Galicia coasts. The mussel samples were digested in a microwave oven using an HNO3/H2O2 mixture and then total mercury was determined using sodium borohydride as reducing agent. In a separate subsample, following ultrasonic extraction in hydrochloric acid medium, inorganic mercury was determined by selective reduction using stannous chloride in acid medium as reducing agent. The accuracy of the digestion method was checked by analyzing BCR Reference Material No. 278 Mussel Tissue (Mytilus edulis). There were no significant differences between the certified and found concentration values. As a certified reference material of mussel tissue containing both methylmercury and inorganic mercury was not available, recovery studies on mussel tissue samples spiked with inorganic mercury and methylmercury were done to check the reliability of the method. The results revealed that the mercury contained in mussel samples was methylmercury.

Animals↗

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↗

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↗

An operationally defined method to determine the speciation of mercury.

This paper presents a modified method of an operationally determined speciation of mercury in soil. The analytical work was mainly concerned to suit properly with inductively coupled plasma-atomic emission spectrometry (ICP-AES). Soil samples analysed in this study were selected from open areas around a crematorium, a waste incinerator, and two power plants. Results show that both topsoil and subsoil samples were dominated by elemental mercury Hg(0) and mercuric sulphide (HgS). The significant correlation between sulphur concentration and HgS was found in topsoil samples.

Geologic Sediments↗

Toxicity of mercury.

A ruling by the European Union heralds the demise of those useful clinical instruments, the mercury thermometer and the mercury sphygmomanometer. The new laws have been passed because of worries about mercury poisoning. Yet you can drink metallic mercury and come to no harm. What does it all mean? There are three forms of mercury from a toxicological point of view: inorganic mercury salts; organic mercury compounds; and metallic mercury. Inorganic mercury salts are water soluble, irritate the gut, and cause severe kidney damage. Organic mercury compounds, which are fat soluble, can cross the blood brain barrier and cause neurological damage. Mercury metal poses two dangers. It can be vaporised: the vapour pressure at room temperature is about 100 times the safe amount, so poisoning can occur if mercury metal is spilled into crevices or cracks in the floorboards. Dentists are occasionally poisoned this way. Mercury easily crosses into the brain, and causes tremor, depression, and behavioural disturbances. A second danger from metallic mercury is that it is biotransformed into organic mercury, by bacteria at the bottom of lakes. This can be passed along the food chain and eventually to man. It was this process that led to the Japanese tragedy at Minimata Bay in the late 1950s when over 800 people were poisoned. It is the need to reduce mercury contamination of the environment which should encourage us to cut the usage of metallic mercury. However, much more metallic mercury is spilled as waste by the chemical industry than is dropped on the floor in the clinic.

Animals↗