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The influence of selenium on the level of mercury and metallothionein in rat kidneys in prolonged exposure to different mercury compounds.

Mercuric chloride, phenylmercuric chloride, ethylmercuric chloride /0,23 mg Hg/kg/ and methylmercurycyan guanidine /0,46 mg Hg/kg/ were orally administered to rats every second day for 14 weeks. The same doses of the above mentioned mercury compounds were administered alternately with sodium selenite /0,18 mg Se/kg/ to parallel groups of rats at the same time. The level of total and inorganic mercury and of metallothionein was determined. All mercury compounds increased the level of metallothionein in rat kidneys. In rats which received only selenium the level of metallothionein was twice lower in the kidneys in relation to the physiological level of this protein. Selenium eliminated the stimulation of biosynthesis of metallothionein by mercury.

Animals↗

[Regeneration of freshwater planarians Dugesia tigrina and Polycelis tenuis under the influence of methyl mercury compounds of natural origin].

We studied the effects of methyl mercury compounds of natural origin on regeneration of the planarians Dugesia tigrina and Polycelis tenuis. Accumulation of methyl mercury in the planarian body leads to a delayed formation of photoreceptor organs in planarians of both species. After a significant traumatic load, the regeneration is suppressed and the death of some control and most experimental animals was observed. The intensity of joining additional cuts depends on the localization of body fragment with a cut and localization of a cut itself.

Animals↗

The influence of dissolved selenium compounds on the accumulation of inorganic and methylated mercury compounds from solution by the mussel Mytilus edulis and the plaice Pleuronectes platessa.

In laboratory experiments, the effects of dissolved selenate and selenite (2 and 200 micrograms Se l-1) on the accumulation of inorganic and methylated mercury (1 microgram l-1) from solution by mussels (Mytilus edulis) and plaice (Pleuronectes platessa) have been studied. In mussels, selenate, and to a lesser extent selenite, markedly reduced the accumulation of inorganic mercury in gills, mantle, kidney and digestive gland. Selenate at 2 micrograms Se l-1 inhibited methylmercury accumulation in most organs, but the same effect was not observed at 200 micrograms l-1. Selenite had little effect on methylmercury accumulation. In plaice, selenate (2 and 200 micrograms l-1) and selenite (200 micrograms l-1) enhanced the accumulation of inorganic mercury in muscle only, but neither compound had any effect on the accumulation of methylated mercury.

Animals↗

The octanol/water distribution of mercury compounds.

Lipophilicity plays an important role in the biological action of mercurials. The distribution of one inorganic and five organic mercury compounds was determined in an n-octanol/water system. Lipophilicity decreased in the order CH3HgCl, bromomercurihydroxypropane, HgCl2, chlormerodrin, p-chloromercuribenzoic acid (PCMB), p-chloromercuriphenylsulfonic acid (PCMBS). The toxicity of mercurials, as reported in the literature, appears to parallel their lipophilicity.

Chemical Phenomena↗

The assessment of the condition of the liver in patients chronically exposed to mercury compounds in the place of settlement.

Problems with the assessment of organ damage caused by toxic substances in places of residence have recently appeared with increasing frequency. In spite of this there have been so far no uniform, objective research methods which could allow their accurate evaluation. This is why the attempt has been made to assess morphological and functional condition of the liver in patients chronically exposed to mercury compounds in the place of settlement. The research group consisted of 62 patients exposed to metallic mercury at a yearly rate exceeding 24 kg for average duration of 16 years. Patients with the liver or biliary tract diseases, symptoms of chronic circulatory insufficiency, Australia (HBs+) antigen carriers and alcoholics were excluded from the research group. The control group consisted of 29 males. AST and ALT activity, prothrombin level, bilirubin and protein concentration in blood serum were measured and scintigraphic and USG examinations of the liver were performed. Mercury concentrations were also established. Scintigraphic examination yielded an abnormal image of the liver in 52% of the exposed patients. The differences in frequency and intensity of scintigraphic changes in comparison with the control group were of statistical significance. No pathological changes were found in USG examination. Significantly higher ALT activity and bilirubin concentration and significantly lower total protein concentration were found in the exposed group. The correlation between the intensity of scintigraphic changes and mercury concentration were noted. Liver scintigraphic examination combined with biochemical analysis allows an assessment of the liver condition in chronic exposure to mercury compounds in the place of settlement.

Adolescent↗

Distinct genotoxicity of phenylmercury acetate in human lymphocytes as compared with other mercury compounds.

In the present study, the frequency of sister chromatid exchanges (SCEs) was assayed to evaluate the genotoxic effects of mercury nitrate (Hg2+), methylmercury chloride (CH3HgCl and phenylmercury acetate (PMA) on human lymphocytes. The free radical scavengers, catalase (CA) and superoxide dismutase (SOD) were tested for their antigenotoxic effects toward PMA. PMA (1-30 microM) increased SCE frequency in a concentration-dependent manner. However, CH3HgCl significantly increased SCE frequency only at a concentration of 20 microM, and all concentrations treated with Hg2+ did not induce a positive effect. On the other hand, we first reported that 30 microM Hg2+, 20 microM CH3HgCl and (3-30 microM) PMA significantly increased the frequency of endoreduplicated mitosis. PMA was about 3- or 5-fold more effective in inducing endoreduplication than CH3HgCl or Hg2+ at equivalent toxic concentrations, respectively. However, neither CA nor SOD in concentrations of 75 and 150 microg/ml showed antagonistic action on the genotoxic effects of PMA. The results suggest that the mechanism of PMA-induced genotoxicity is not mediated by superoxide anion nor H2O2. It is concluded that PMA, which was more effective in inducing the elevation of both SCEs and endoreduplication, may be especially hazardous of the three mercury compounds tested.

Adult↗

Comparison of cytotoxicity of mercury-selenium and mercury compounds on cultured cells.

In vitro effects of mercury-selenium (Hg-Se) compounds, as compared with their original mercury compounds, against growth and viability of HeLa cells were studied. A water-soluble, ethanol-insoluble black complex (GX) formed from HgCl2, Na2SeO3 and GSH was less toxic than HgCl2, but the cytotoxicity of bis(methylmercuric) selenide (BMS) seemed to be similar to that of methylmercury. This may be due to the instability of BMS; i.e., there is a possibility that BMS decomposed to methylmercury and selenium under our culture conditions.

Cell Survival↗

The action of organic mercury compounds on the function of isolated mammalian heart muscle.

The effects of four organic mercury compounds (methylmercuric chloride; bromomercurihydroypropane, BMHP; chlormerodrin; p-chloromercuribenzoic acid, PCMB) on mechanical and electrical functions of guinea-pig papillary muscles were investigated. An initial decline in contraction force was followed by a transient positive inotropic response. The first was accompanied by a shortening of the action-potential duration and by a reduction of the depolarization velocity and the duration of the Ca2+-dependent slow response. The latter was characterized by an indirect component (release of noradrenaline) and by a direct component, which was dependent on the stimulation rate and on the extracellular concentration of Na+ and K+. The direct positive effect, therefore, was likely to have resulted from inhibition of the sarcolemmal Na+ + K+-ATPase. This notion was confirmed by experiments with isolated membrane particles. The prevalence of the negative or positive inotropic action of these compounds could be ascribed to their lipophilic or hydrophilic properties, respectively.

Action Potentials↗

Neurotological studies upon intoxication by organic mercury compounds.

In 1965, a strange illness, which afterwards was diagnosed as the intoxication caused by organic mercury compounds, began to affect the inhabitants of the riverside areas of the Aganogawa River, Niigata, Japan. The authors have investigated the neurotological disturbances, which occurred in 144 cases intoxicated with organic mercurials. The results obtained are summarized as follows: (1) Recruitment (in SISI and other tests) was negative in all the cases except for 32 with inner ear deafness, and Békèsy's AUDIOMETRY (TTS) showed type II: unsettled wide amplitude in 17 cases and severe abnormal adaptation characterizing the type III pattern in nine cases. (2) Spontaneous and positional nystagmus were recorded with ENG in 94 of 144 cases. In 62 of 144 cases, pathological findings of horizontal optokinetic nystagmus were recorded, and those of vertical optokinetic nystagmus were frequently observed in 81 of the 118 cases tested (69 percent). Judging from the authors' observations, neurotological disturbances due to chronic mercurial intoxication may be considered mainly as lesions of the retrocochlea and of the oculomotor system in the brain stem and the cerebellum.

Adolescent↗

Studies on the reaction between pyridine nucleotides and mercury compounds in artificial intracellular and extracellular fluids.

The strong complex formations of pyridine nucleotides with mercury compounds were demonstrated in artificial intracellular fluid containing oxianions (HPO42-, HCO3-), while those in artificial extracellular fluid were considerably weaker. Dissociation constants (K) of the complexes of [MC.NADP], [MC.NADPH], [MC.NAD], [MC.NADH], [MC.adenine], and [MC.nicotinamide mononucleotide] were found to be 1.0 x 10(-4), 2.6 x 10(-5), 1.2 x 10(-4), 2.9 x 10(-5), 7.2 x 10(-6), and 3.8 x 10(-3), respectively in phosphate buffer (43 mM, pH 8.0).

Extracellular Space↗