Search PubMed⌕ Search

Biomedical subjects

J Chmielnicka

Publications and source records attributed to J Chmielnicka.

At least 73 records · Page 4Linked to original sources
PubMed1979

Evaluation of methods for the estimation of 5-aminolevulinate dehydratase for a broad range of lead concentrations in the blood of exposed workers.

5-aminolevulinate dehydratase activity was estimated in the blood of 30 lead-exposed workers and 15 control persons, using (I) the method of Tomokuni ((1974) Arch. Environm. Health 29, 274--281) and (II) the European standard method (Berlin & Schaller (1974) Z. Klin. Chem. Klin. Biochem. 12, 389--390). The lead level in the blood was in the range 0--11.6 mumol/l. It was found that the correlation between the activity of 5-aminolevulinate dehydratase and the lead level in blood (up to 4.35 mumol/l) are higher for method I than method II. These two methods only give similar results for the units of 5-aminolevulinate dehydratase activity when the lead concentrations in the blood are low. For higher concentrations of this metal (up to 11.6 mumol/l), a high correlation was obtained (r = -- 0.80) between the 5-aminolevulinate dehydratase activity ratio (enzyme measured at pH 6.8/enzyme measured at pH 6.0; method I) and lead concentrations in the blood.

Humans↗
PubMed1978

Whole-body retention of mercury and selenium and histopathological and morphological studies of kidneys and liver of rats exposed repeatedly to mercuric chloride and sodium selenite.

Distribution and retention of mercury and selenium was studied in rats exposed repeatedly to HgCl2 injections (0.5 mg Hg/kg to the tail vein every other day) and intragastrically to Na2SeO3 (0.5 mg Se/kg every day), applying combined and separate administration of these metals for 2 weeks. Whole-body retention of mercury in the presence of selenium was augmented by 20% and that of selenium in the presence of mercury by 4% with respect to the administered dose. Combined administration of mercuric chloride and sodium selenite brought about damage to the epithelial cells of renal proximal convolutions and formation of protein casts in their lumen. These changes had the same pattern as those induced by administration of mercuric chloride alone, but the intensity was lower. Submicroscopic studies revealed that repeated combined administration of sodium selenite and mercuric chloride did not completely abolish the mercury-induced mitochondrial swelling and contributed to chromatin destruction in the hepatocyte nuclei.

Animals↗
PubMed1978

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↗
PubMed1978

Activity of glutamate and malate dehydrogenases in liver and kidneys of rats subjected to multiple exposures of mercuric chloride and sodium selenite.

Rats were subjected for 2 weeks to separate and combined exposures to mercuric chloride and sodium selenite at doses of 0.5 mg Hg/kg and 0.5 mg Se/kg. The content of mercury, selenium and protein as well as the activities of glutamate dehydrogenase (GLDH) and malate dehydrogenase (MDH) were determined in homogenates, mitochondria and intramitochondrial structures of the exposed animals. It was found that both separate and combined exposures of rats to mercuric chloride and sodium selenite inhibited GLDH activity and did not affect MDH activity in the examined organs. Mercury-selenium interaction brought about a decrease in the content of mercury in the intramitochondrial structures of kidneys and an increased accumulation of both elements in the outer and inner membranes of liver mitochondria. The biochemical mechanism of mercury-selenium interaction is discussed.

Animals↗
PubMed1977

Binding of mercury and selenium in subcellular fractions of rat liver and kidneys following separate and joint administration.

The distribution of mercury and selenium has been examined in subcellular fractions of rat liver and kidneys in prolonged exposure to HgCl2 and Na2SeO3 administered separately and simultaneously. The molar ratio of mercury and selenium concentrations in subcellular fractions of the organs examined varied considerably. Selenium displaced mercury from the soluble kidney fraction bound mainly with metallothionein to the nonhistone protein fraction of liver nuclei. The Hg-stimulated biosynthesis of metallothionein has been eliminated under the influence of selenium.

Animals↗
PubMed1977

Changes in activity of malate dehydrogenase and glucosephosphate isomerase in serum of rats exposed chronically to inorganic mercury and its aryl and alkyl compounds.

In course of prolonged exposure [14 weeks] to various mercury compounds [MetHg - a fluid seed-dressing preparation 0,8. Phenyl and Ethyl chlorides and HgC1(2) in doses corresponding to 5% of DL(50)[3 times weekly], enhanced levels of activity of malate dehydrogenase [MDH] and glucosephosphate isomerase [PHI] in blood serum were observed. After 7 weeks of exposure about fourfold increase of MDH and 2-3-fold enhancement of PHI activities were found relative to controls. After 14 weeks of exposure in livers of rats, given MetHg and EtHg, organic mercury was found at concentrations of 28.8 and 4 microng/g tissue, respectively. Inorganic mercury in liver was found in animals given all coumpounds and concentrations were in the range of 1,2 - 4,7 microng/g tissue.

Animals↗
PubMed1976

Binding of inorganic mercury by subcellllar fractions and proteins of rat kidneys.

Inorganic mercury, administered to rats in a single dose of 0.5 mg Hg/kg is accumulated in the kidneys mainly in the soluble (54%) and nuclear (30%) fractions, showing decreasing tendency with time. Mitochondrial and microsomal fractions, initially accumulating approx. 11 and 6% of total Hg, show a tendency to increase the absolute level of Hg for the first week after administration. In the soluble fraction low-molecular weight, metallothioneinlike proteins are mainly responsible for the accumulation of mercury, in other fractions proteins of higher molecular weight prevail.

Animals↗
PubMedDate not supplied

Effects of interaction between 65Zn, cadmium, and copper in rats.

Distribution and retention of zinc in the presence of cadmium and copper was studied in rats exposed repeatedly to these metals. The experiment was performed on white rats of the Wistar strain. The animals were divided into four groups/five rats each: 1) 65ZnCl2; 2) 65ZnCl2 + CdCl2; 3) 65ZnCl2 + CuCl2; and 4) control group. Rats were administered sc every other day for two weeks: 65ZnCl2-5 mg Zn/kg; CdCl2-0,3 Cd/kg; and CuCl2-2 mg Cu/kg. The zinc content was measured in rat tissues by gamma-counting. Effect of Cd and Cu on subcellular distribution of zinc in the kidney and liver and on the level of metallothionein were also examined. Whole body retention of zinc under the influence of cadmium was lower than that observed in animals treated with zinc alone. However, copper increased twofold the whole body retention of zinc. Cadmium elevated the accumulation of zinc only in the kidneys nuclear fraction and liver soluble fraction. In the kidneys and liver, copper elevated the accumulation of zinc, in the nuclear, mitochondrial, and soluble fractions. The level of metallothionein-like proteins (MT) in the kidneys after a combined supply of zinc and copper was significantly increased with respect to the group of animals treated with zinc alone. These results indicated complex interactions between cadmium, copper, and zinc that can affect the metabolism of each of the metals.

Animals↗
PubMedDate not supplied

New aspects on the distribution and metabolism of essential trace elements after dietary exposure to toxic metals.

Under present environmental conditions, an increase in pollution owing to metals such as cadmium (Cd), lead (Pb), and methylmercury (MeHg) must be expected. The resulting effects would be seen particularly in the food chain. The daily intake of toxic metals in various parts of the world is different and depends on both the dietary habits and the concentration in foodstuffs. Oral ingestion of these toxic metals perturbs the metabolism of essential elements, especially zinc (Zn), copper (Cu), iron (Fe), and selenium (Se). The elemental composition of body tissues and fluids is an indicator of the nutritional and pathological status of humans. This review will describe the dietary intake and gut absorption of essential and toxic elements. Furthermore, it will discuss threshold values, toxic effects in relation to body burden of toxic metals, the biological indices of exposure, and the interaction between toxic and essential elements. The overall ratio of Cu, Zn, Fe, and Se concentration to Cd in the human kidney is the lowest in comparison to Hg and Pb. Increased kidney copper and urinary losses may be common denominators in the manifestation of renal toxicity induced by heavy metals. Factors affecting availability and loss of copper should be identified and measured. The critical kidney concentration for Cd, Pb, and MeHg should be revised in relation to essential elements.

Animals↗