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At least 19 recordsLinked to original sources
PubMed1993

Carcinogenicity of mercury and mercury compounds.

Mercury and mercury compounds are widely used in modern society, but only sparse data are available on their carcinogenicity. Methylmercury chloride causes kidney tumors in male mice. Mercury chloride has shown some carcinogenic activity in male rats, but the evidence for female rats and male mice is equivocal. Other mercury compounds and metallic mercury have not been tested adequately in experimental animals. Epidemiologic data are available for chloralkali workers, dentists and dental nurses, and nuclear weapons workers, three groups occupationally exposed to low levels of mercury and its compounds, but those highly exposed in the past, such as miners, or populations which have suffered massive environmental exposure have not been adequately studied. However, the sparse epidemiologic data point toward the possibility of a risk of lung, kidney, and central nervous system tumors. Better data are needed on the carcinogenicity of mercury and mercury compounds in humans and experimental animals.

Animals↗
PubMedDate not supplied

[Encephalopathy after poisoning with organic mercury compounds].

Organic mercury compounds have greatest affinity to the central nervous system (cerebellar white matter, basal ganglia, occipital and frontal cortex). Anatomical changes observed in the brain are of degenerative type. Similar changes are found also in the myocardium, liver and kidneys. The authors observed for 2 years a family of three persons who contracted poisoning with organic mercury compounds after easting the meat of pigs and hens fed through negligence with wheat destined for sowing, containing methyl-mercurocyanoguanidine. The level of total mercury determined by the method of cold atomic absorption was in these patients four months after poisoning 650,500 and 175 ng/ml of blood (normal value from 1.56 to 18.72 ng/ml). During the observation it has been established that the severity of poisoning was related to the level of mercury found in the organism. Pharmacological treatment (Cuprenil, Thioctacid, vitamin B complex) and rehabilitation brough slight improvement after 2 years. Two patients with total blood mercury level 650 and 500 ng/ml were completely disabled due to encephalopathy with high grade ataxia, dysarthria and concentric narrowing of the field of vision. In the third patients with less severe poisoning (175 ng/ml) pathological manifestations disappeared completely after short treatment.

Adult↗
PubMed1997

Mercury compounds and the immune system: a review.

This article reviews the literature data concerning the immunologic monitoring of animals and cell cultures exposed to mercury compounds. Mercury is present in nature as metallic mercury, mono- and bivalent inorganic compounds, and organic alkyl, aryl and alloxy-alkyl compounds. Methylmercury is most important in terms of environmental exposure while metallic mercury is the most common form to which workers are exposed. The database on immune function disturbances in human induced by mercury compounds is limited. Immunotoxicity assessment in animals, mainly in rodents, with subsequent extrapolation to man, is the basis of human risk assessment. The strength of in vitro immunotoxicity testing lies in studies aimed at unravelling mechanisms of immunotoxicity. These experimental investigations show clearly that mercury compounds can have immunomodulating activity. Mercuric chloride and methylmercury inhibit most of animal and human lymphocyte functions including proliferation, expression of cell activation markers on cell surface and cytokine production. These cells exhibit a greater sensitivity to the immunotoxic effects of methylmercury than to mercuric chloride. Repeated administration of mercuric chloride to rats, mice and rabbits can induce autoimmune response and a membranous nephropathy. In contrast, Lewis rats injected with mercuric chloride do not develop autoimmunity but exhibit immunosuppression. The immunosuppressive effects associated with exposure to chemical substances are often accompanied by increased susceptibility to challenge with infectious agents or tumour cells. Only few reports are available on animal studies of increased mortality connected with exposure to mercury compounds and challenge with infectious agents. It is difficult to establish a relationship between the observed immunomodulatory properties of mercury compounds and their possible carcinogenicity. In fact, the epidemiological studies performed so far failed to bring any conclusive evidence of carcinogenicity of mercury in animal experiments. The induction of renal tumours in male rodents by methylmercury was observed only.

Animals↗
PubMed1989

[Patch test of mercury compounds and disinfectant solutions and the clinical picture of mercury contact dermatitis].

The results of patch tests with mercury compounds and disinfectant solutions as well as the clinical picture of mercury contact dermatitis are presented and discussed. During the period from Nov. 1983 to Dec. 1986, 686 patients were tested with mercury compounds. During the 13 year period from 1974-1986, 118 patients were tested with disinfectant solutions and 59 patients with mercury contact dermatitis were seen. Among the disinfectant solutions tested, the highest incidence of positive reaction, 11.5%, was obtained with thimersal. Cross sensitization has been shown between mercurochrome and ammoniated mercury, but no statistical correlation existed that demonstrated cross sensitization between mercury and thimerosal until our study. Therefore, the allergen in mercurochrome contact dermatitis is mercury. No statistical correlation could be established between the occurrence of atopic dermatitis and the patch test reactions to mercury compounds. The contactants were mercurochrome, thimerosal, and broken thermometers in 49 out of 59 cases of mercury contact dermatitis. Consequently, the number of occurrence of mercury dermatitis can be reduced by the elimination of the use of these two disinfectant solutions and the substitution of electric thermometers for mercury thermometers.

Adolescent↗
PubMed1983

Mutagenicity and teratogenicity of mercury compounds.

Agriculture, consumption of fossil fuels and, to a lesser extent, industry, are the main sources of pollution by mercury which is discharged into the environment as metallic mercury, as inorganic mercury compounds, or as organic compounds. Once in the environment, mercury compounds are capable of a variety of transformations. Some professional or accidental mercury poisonings have been reported in human populations, but they can easily be minimized by appropriate preventive measures. Production of C-mitosis in plant material is the most noticeable genetic effect of mercury compounds. No positive report that mercury could be carcinogenic in man has appeared up to now and animal experiments have also provided negative results. Although placenta may represent a certain barrier to mercury, embryotoxicity and teratogenicity of organic mercury compounds have been observed in numerous systems such as fish, birds and mammals.

Animals↗
PubMed1996

Comparison of the developmental effects of two mercury compounds on glial cells and neurons in aggregate cultures of rat telencephalon.

A three-dimensional cell culture system was used as a model to study the influence of low levels of mercury in the developing brain. Aggregating cell cultures of fetal rat telencephalon were treated for 10 days either during an early developmental period (i.e., between days 5 and 15 in vitro) or during a phase of advanced maturation (i.e., between days 25 and 35) with mercury. An inorganic (HgCl2) and an organic mercury compound (monomethylmercury chloride, MeHgCl) were examined. By monitoring changes in cell type-specific enzymes activities, the concentration-dependent toxicity of the compounds was determined. In immature cultures, a general cytotoxicity was observed at 10(-6) M for both mercury compounds. In these cultures, HgCl2 appeared somewhat more toxic than MeHgCl. However, no appreciable demethylation of MeHgCl could be detected, indicating similar toxic potencies for both mercury compounds. In highly differentiated cultures, by contrast, MeHgCl exhibited a higher toxic potency than HgCl2. In addition, at 10(-6) M, MeHgCl showed pronounced neuron-specific toxicity. Below the cytotoxic concentrations, distinct glia-specific reactions could be observed with both mercury compounds. An increase in the immunoreactivity for glial fibrillary acidic protein, typical for gliosis, could be observed at concentrations between 10(-9) M and 10(-7) M in immature cultures, and between 10(-8) M and 3 x 10(-5) M in highly differentiated cultures. A conspicuous increase in the number and clustering of GSI-B4 lectin-binding cells, indicating a microglial response, was found at concentrations between 10(-10) M and 10(-7) M. These development-dependent and cell type-specific effects may reflect the pathogenic potential of long-term exposure to subclinical doses of mercury.

Animals↗
PubMed1998

Induction of apoptosis by mercury compounds depends on maturation and is not associated with microglial activation.

The earliest sign of neurotoxicity observed after exposure of three-dimensional brain cell cultures to low concentrations of mercury compounds is a microglial reaction. We hypothesized that an induction of apoptosis by mercury compounds could be an activating signal of the microglial reaction. Aggregating brain cell cultures of fetal rat telencephalon were treated for 10 days with either mercury chloride or monomethylmercury chloride at noncytotoxic concentrations during two developmental periods: from day 5 to 15, corresponding to an immature stage, and from day 25 to 35 corresponding to a mature stage. Apoptosis was evaluated by the TUNEL technique. It was found that both mercury compounds caused a significant increase in the number of apoptotic cells, but exclusively in immature cultures exhibiting also spontaneous apoptosis. Double staining by the TUNEL technique combined with either neuronal or astroglial markers revealed that the proportion of cells undergoing apoptosis was highest for astrocytes. Furthermore neither an association nor a colocalization was found between apoptotic cells and microglial cells. In conclusion, it appears that the induction of apoptosis by mercury compounds in immature cells is only an acceleration of a spontaneously occurring process, and that it is not a directly related to the early microglial reaction.

Animals↗
PubMed1985

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↗
PubMed1986

Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices.

The effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices have been examined. All mercury compounds examined produced concentration-dependent increases in the spontaneous release of [3H]dopamine, with an order of potency of methylmercury greater than mercuric (Hg2+) mercury greater than p-choloromercuribenzene sulfonic acid. Methylmercury had no effect on the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium. However, in calcium-free conditions, methylmercury significantly increased the potassium-evoked release of [3H]dopamine. Mercuric mercury significantly reduced the 25 mM potassium evoked release of [3H]dopamine in the presence of 1.3 mM calcium, and this response was not reversible with brief washing of the tissue. In calcium-free conditions, mercuric mercury significantly elevated the evoked release of [3H]dopamine, similar to the result obtained with methylmercury. It is suggested that mercury compounds alter dopaminergic synaptic function, possibly by disrupting calcium homeostasis or calcium-dependent processes, and that methylmercury and mercuric mercury can have differential effects to alter dopaminergic neurotransmission.

4-Chloromercuribenzenesulfonate↗
PubMed1980

The inhibition of cerebral high affinity receptor sites by lead and mercury compounds.

The effect of various concentrations of several lead and mercury compounds upon various high affinity receptor sites within discrete brain regions has been measured. The specific binding of radioactive spiroperidol and quinuclidinyl benzilate to striatal and cortical membranes respectively, was much more severely inhibited in the presence of tri-n-butyl lead acetate than by lead acetate. This suggested that the hydrophobic organic lead derivative was able to interfere with receptor structure more readily than the lead acetate. On the other hand mercuric chloride was more effective in blocking these two neurotransmitter receptor sites than was the organic methylmercuric chloride. This implied that sulfhydryl groups may be within, or proximal to the allosteric binding site. The relative ineffectiveness of all heavy metal compounds studied in blocking the glycine. GABA or the diazepam receptors indicated that the mechanism of binding may not be similar with different receptor proteins. Since micromolar concentrations of some lead and mercury compounds suffice to severely inhibit neurotransmitter binding sites, such a direct interference with postsynaptic events may in part account for the neurological consequences of heavy metal poisoning.

Animals↗