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Biomedical subjects

J Chmielnicka

Publications and source records attributed to J Chmielnicka.

At least 55 records · Page 3Linked to original sources
PubMed1985

Comparison of the impact of continuous and intermittent exposure to vinyl chloride, including phenobarbital effect.

Rats were subjected to 4 h continuous and intermittent exposure to vinyl chloride (VC) at the time-weighted average concentration of 50,000 mg/m3. Prior to exposure, half of the animals obtained water, whereas the other half 0.1% sodium phenobarbital (PB) solution for seven consecutive days. The studies were focussed on: body weight, liver weight, activity of enzymes in the blood serum, activity of glutathione S-transferase in the liver cytoplasmatic and microsomal fraction, content of free non-protein sulfhydryl groups (NPSH) in the liver and urinary excretion of thiodiglycolic acid (TDGA). VC exposure, both continuous and intermittent, resulted in a decrease of body weight, NPSH depletion in the liver and TDGA urinary excretion. PB effects were manifested by the persistent decrease in rats' body weight, increase in the liver weight, increase in the cytoplasmatic activity of glutathione S-transferase in the liver and increase in TDGA urinary excretion. With none of the tested parameters, except TDGA, statistically significant differences between the continuous and intermittent VC exposure at the same time-weighted average concentration of 50,000 mg/m3, were found. TDGA urinary excretion was higher in rats poisoned in continuous exposure, as compared to the intermittent one.

Alanine Transaminase↗
PubMed1984

Influence of exposure mode on vinyl chloride action.

Rats were subjected to 4 h continuous or intermittent exposure to vinyl chloride (VC) at different time-weighted average concentrations (15, 50, 150, 500 and 15,000 mg/m3). Hepatic non-protein sulfhydryl content (NPSH) and excretion of thiodiglycolic acid (TdGA) in urine were determined. VC at concentrations from 50 mg/m3 to 15,000 mg/m3 caused a dose-dependent depression of NPSH, but no difference in the magnitude of this depression induced by continuous of VC was noted. At average concentrations of 50 mg/m3 and 150 mg/m3, the urinary excretion of TdGA under continuous exposure did not differ from that under intermittent exposure, whereas at VC concentrations of 500 mg/m3 and 15,000 mg/m3 it was higher following continuous exposure.

Animals↗
PubMed1983

Tissue origin of MDH isozymes in blood serum of rats exposed to alkylmercurials.

Wistar rats were dosed with Hg at 2.5 mg kg-1 intragastrically as methylmercuric chloride (MeHg) or ethylmercuric chloride (EtHg) on alternate days for 6 weeks. Activities of the mitochondrial (m-MDH) and cytosol (c-MDH) isozymes of malate dehydrogenase (MDH: E.C. 1.1.1.37) were studied in the serum, liver and kidneys of rats at 2-week intervals using agar gel electrophoresis. In order to determine the tissue of origin of the MDH isozymes in rat serum, studies were also made on changes in their activities after poisoning the animals with a hepatotoxic (CCl4) or nephrotoxic (HgCl2) agent. The results indicate that the kidneys are responsible for the increase of the c-MDH activity in the serum of rats poisoned with EtHg, while in the case of MeHg this increase results from damage initially to the liver and then also to the kidneys.

Animals↗
PubMed1983

Effect of interaction between 65Zn, mercury and selenium in rats (retention, metallothionein, endogenous copper).

Interaction of zinc with mercuric chloride and sodium selenite was studied in the rat at the organ and subcellular levels (liver and kidneys). Zinc chloride was administered subcutaneously at dose of 5 mg Zn/kg, mercury chloride into the tail vein at a dose of 0.5 mg Hg/kg (both metals every other day during 2 weeks) and sodium selenite intragastrically, at doses of 0.1 mg Se/kg, every day. Zinc retention in the rat did not exceed 20% and was unchanged in the presence of mercury. An interaction effect was reflected by an increased whole-body retention of zinc by selenium, mercury, and selenium. In the presence of selenium no peak of metallothionein-like proteins stimulated by zinc or mercury was found in the soluble fraction of the kidneys. The metallothionein level did not differ from that typical for control group animals, too. A significant increase in the level of endogenous copper was found only in the kidneys of rats exposed to zinc in the presence of mercury and selenium.

Animals↗
PubMed1983

Organ and subcellular distribution of cadmium in rats exposed to cadmium, mercury, and selenium.

Four groups of rats were given: cadmium chloride (Cd), cadmium chloride and mercuric chloride (Cd + Hg), cadmium chloride and sodium selenite (Cd + Se), or cadmium chloride, mercuric chloride, and sodium selenite (Cd + Hg + Se). All animals received subcutaneous doses of 115mCdCl2 (0.3 mg Cd/kg) every other day for 2 weeks. Mercuric chloride was administered intravenously at doses of 0.5 mg Hg/kg every other day, and Na2 75SeO3 intragastrically at doses of 0.1 mg Se/kg every day for a fortnight. The whole-body and organ retention of cadmium changed slightly with the type of exposure. A significant interaction effect of the examined elements was noted in the nuclear and soluble fractions of the liver and kidneys. Mercury decreased the cadmium concentration in both the nuclear and soluble fractions of the kidneys and diminished the effect of selenium on the cadmium level in the soluble fraction of the kidneys. In the liver the presence of mercury contrary to selenium, lowered the cadmium level in the nuclear fraction. The pattern of cadmium binding to proteins of the soluble fraction of the kidneys and liver remained the same in all groups of animals.

Animals↗
PubMed1983

Organ and subcellular distribution of selenium in rats exposed to cadmium, mercury, and selenium.

Three groups of rats were given sodium selenite (Se), sodium selenite and cadmium chloride (Se + Cd), or sodium selenite, cadmium chloride, and mercuric chloride (Se + Cd + Hg), respectively. All animals received subcutaneous doses of 115CdCl2 (0.3 mg Cd/kg) every other day for a fortnight. Mercuric chloride was administered intravenously at doses of 0.5 mg Hg/kg every other day and Na2 75SeO3 intragastrically at doses of 0.1 mg Se/kg every other day for 2 weeks. The whole-body retention of selenium was slightly elevated by cadmium and increased threefold by cadmium with mercury (mainly blood, liver, and kidneys). Cadmium did not affect subcellular levels of selenium in the kidneys and slightly increased the selenium content in the soluble fraction of the liver. On the other hand, combined administration of mercury and cadmium induced a significant elevation of the selenium content in all subcellular fraction of the kidneys and in the nuclear and mitochondrial fractions of the liver. In all animal groups selenium was bound in the soluble fractions of both the liver and kidneys by high-molecular-weight proteins.

Animals↗
PubMed1983

Activity of chosen indicator enzymes in blood serum of guinea pigs exposed to ethyl- and phenylmercuric chloride alone or jointly with sodium selenite.

The effect of sodium selenite on the activity of the selected enzymes in blood serum and on mercury concentration in some tissues of guinea pigs exposed to ethyl- (EtHg) or phenylmercuric chloride (PhHg) was investigated. Every second day for a 3-month period animals were given intragastrically a solution of mercuric compounds (2.5 mg Hg/kg) with or without sodium selenite (1 mg Se/kg). The activity of malate dehydrogenase (MDH, EC 1.1.1.37), phosphohexoizomerase (PHI, EC 5.3.1.9), and gamma-glutamyltranspeptidase (GGTP, EC 2.3.2.2) in blood serum of control animals was ca. 3.8, 325, and 48 IU. After 10 weeks of exposure to EtHg and PhHg, the activities (IU) of the above enzymes were, respectively, 5.9 and 6.5 (MDH), 585 and 600 (PHI) and 211 and 86.5 (GGTP). Sodium selenite administered with mercuric compounds did not prevent in increases in enzyme activity. During the experiment the level of inorganic as well as organic mercury accumulated in kidneys and liver was estimated. After a 12-week exposure, sodium selenite decreased the level of total mercury in the liver (in the case of both EtHg and PhHg: from 47.0 to 31.8 and from 41.3 to 25.4 micrograms Hg/g tissue, respectively). It also slightly decreased the mercury level in the kidneys of animals exposed to PhHg (from 889 to 73.3 micrograms Hg/g tissue) but did not change the mercury concentration in the kidneys of guinea pigs exposed to ethylmercuric chloride.

Animals↗
PubMed1983

Effect of zinc, cadmium or copper on mercury distribution in rat tissues.

Distribution and retention of mercury in the presence of zinc, cadmium or copper was studied in rats exposed repeatedly to these metals. Whole-body retention of mercury under influence of zinc and cadmium was slightly lower than that observed in animals treated with mercury alone; however, copper decreased whole-body retention by over 50%. Combined administration of mercury and various metals changed the distribution of mercury in the subcellar fractions of kidney and liver. Zinc, cadmium and copper decreased incorporation of mercury in metallothionein-like proteins (MT) in the kidney; however, in the liver mercury was bound mainly by MT. It seems very likely that one metal may induce changes in the distribution of another by processes other than a single displacement interaction.

Animals↗
PubMed1981

Distribution of tin in the rat and disturbances in the metabolism of zinc and copper due to repeated exposure to SnCl2.

The effect of stannous chloride on tissue concentrations of zinc and copper was studied in female rats. The animals were subjected to repeated exposure to seven doses given every other day 2 mg Sn/kg, subcutaneously. About 60% of tin 113Sn was retained in the body. Of this amount, about 95% accumulated in the skin and hair. In the remaining organs the tin concentrations corresponded to 2.57 to 0.0001% of the retained dose. In comparison with the control group a 3-fold increase of the content of zinc was found in the liver while a decrease were revealed in the spleen, heart, brain, lungs, and especially in muscle. A statistically significant decrease of the copper content was found in the blood and brain.

Animals↗
PubMed1981

Arginase and kallikrein activities as biochemical indices of occupational exposure to lead.

In a group of 60 workers occupationally exposed to lead the blood and urine lead concentrations, haematocrit, ALA-D and arginase activities, and urinary 5-aminolaevulinic acid (ALA) and coproporphyrin concentrations, and kallikrein activity were determined. Correlation coefficients of -0.78 and 0.77 for Pb-B/ALA and Pb-B/arginase were found respectively for lead concentrations above 40 microgram/dl blood, and 0.83, 0.76, 0.74, and -0.64 for Pb-U/ALA, Pb-U/Cp-U, Pb-U/kallikrein, and Pb.U/kallikrein, respectively. It seems that the increase in serum arginase activity may be indicative of liver damage while the decrease in kallikrein activity may indicate kidney damage in workers exposed to lead.

Aminolevulinic Acid↗
PubMed1981

Interaction of alkylmercuric compounds with sodium selenite. I. Metabolism of ethylmercuric chloride administered alone and in combination with sodium selenite in rats.

The effect of sodium selenite administered intragastrically in repeated doses to rats receiving ethylmercuric chloride po in various repeated doses (0.25 or 2.5 mg Hg/kg) on the excretion, whole-body retention, and organ distribution of mercury was studied. Selenium was found to affect the distribution of ethylmercury among tissues and subcellular fractions of the kidneys and liver as well as its binding to proteins of soluble fractions in these organs. Similarities and differences between the effect of interaction of sodium selenite with ethylmercuric chloride and methylmercury as well as inorganic mercury are also discussed.

Animals↗
PubMed1981

[Toxicity and metabolism of acrylonitrile].

The paper presents the problem of occupational exposure to acrylonitrile vapours and toxic properties of this compound, as well as its metabolism in experimental animals, including its administration route. In addition, it deals with the mechanism of its toxic effects depending on the reactivity of the functional group of acrylonitrile particle. The authors discuss also the latest views on the capacity of acrylonitrile metabolites [S-(2-cyanoethyl)-mercapturic acid and rhodanates], depending on the route of acrylonitrile administration to rats.

Acrylonitrile↗