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PubMed1991

Studies on focal alveolar bone healing with technetium (Tc)-99m labeled methylene diphosphonate and gold-collimated cadmium telluride probe.

The benefit of using a collimator for a miniaturized cadmium telluride probe was evaluated by monitoring the bone-healing processes for 13 weeks after the induction of small iatrogenic alveolar bone lesions in one side of the mandible in beagles. Technetium (Tc)-99m labeled methylene diphosphonate (200 to 300 MBq, 5.1 to 8.1 mCi, in a solution of 0.5 to 1 ml, intravenously) was used as a bone-seeking radiopharmaceutical. The radioactivity over the bone lesion (L) and the contralateral normal site (C) in the mandible were measured between 1.5 and 2 hours after injection of the tracer, and the activity ratio L/C served as an index of relative bone uptake. A study of six dogs revealed that the healing response to a hemispheric bone defect of 2 mm diameter in the cortical bone could not be detected by an uncollimated probe, and in a repeated study in two dogs the use of a gold collimator (5 mm in diameter, 5 mm in length) did not increase the L/C ratio significantly. A second study in six dogs with 5 mm lesions showed that although systematic trends in the time courses of the L/C ratio obtained both with and without the collimator could be demonstrated, the L/C ratio of collimated versus uncollimated measurements was significantly (p less than 0.005) increased. In three of the latter six dogs, abscesses developed after 9 weeks, leading to a second increase (p less than 0.05) of the L/C ratio with collimation compared with the noninflammation group; without collimation no significant (p greater than 0.15) difference between the two groups could be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolar Process↗
PubMed1986

Toxicity of cadmium chloride in vitro: indices of cytotoxicity with the pulmonary alveolar macrophage.

Pulmonary alveolar macrophages were isolated from adult, male New Zealand white rabbits by bronchial lavage and exposed to cadmium chloride in vitro. The observed cell sensitivity to this metal was highly dependent upon the incubation conditions used as well as the cytotoxic index selected. An LC50 value, as measured by dye exclusion (erythrosin B), was determined to be 390 microM when these cells were exposed to cadmium in Ham's F12 culture medium for 8 hr at 35 degrees C. The presence of fetal calf serum in the medium (10%; v/v) enhanced this toxicity slightly, LC50 = 235 microM, as did raising the incubation temperature to 37 degrees C, LC50 = 201 microM. No effect on cadmium toxicity was observed when the culture medium was made deficient in Cu, Zn, and Fe, nor was there any effect observed when Hepes buffer was substituted for the bicarbonate/carbon dioxide buffering system. Measurements of cadmium-109 uptake by pulmonary alveolar macrophages were consistent with and could explain, at least in part, the above observations of cytotoxicity. In the standard culture system (an 8-hr exposure period at 35 degrees C in Ham's F12 culture medium plus serum), the appearance in the culture medium of two lysosomal enzyme activities, acid phosphatase and cathepsin D, paralleled cell death. In addition, an EC50 value of 102 microM was found for cadmium when cell respiration (O2 uptake) was measured; an EC50 value of 31 microM was found for cadmium when cell function (engulfment of killed yeast particles) was followed; and scanning electron microscopic studies showed cell membrane changes (loss of fine structure and blebbing) at cadmium concentrations as low as 30 microM. These findings suggest that loss of cell function and/or changes in cell morphology are more sensitive measurements of macrophage exposure to cadmium than is either cell death, lysosomal enzyme release, or cell respiration.

Adenosine Triphosphate↗
PubMed1982

Opposite effects of inhaled cadmium microparticles on mouse susceptibility to an airborne bacterial and an airborne viral infection.

An experimental study on 489 mice is reported. The test animals were submitted to a single 15-mn exposure to atmosphere containing about 10 mg of cadmium microparticles (CdO) per m3 of air and the controls to an equivalent amount of aluminium microparticles (Al2o3). At the 48th hour after exposures, the test and control mice were submitted to a bacterial (Pasteurella multocida) or to a viral (Orthomyxovirus influenzae A) challenge, via the respiratory route. The exposure to cadmium significantly increased the death-rate of mice submitted to the bacterial challenge, but it significantly decreased the death-rate following the viral challenge.

Air Pollutants↗
PubMed1985

Adsorption and desorption of polydimethylsiloxane, PCBs, cadmium nitrate, copper sulfate, nickel sulfate and zinc nitrate by river surface sediments.

An investigation into the adsorption and desorption of polydimethylsiloxane, PCBs, cadmium nitrate, copper sulfate, nickel nitrate and zinc nitrate by river sediments was carried out using either a flow-through system or a semi-static system. The material balance in the sediment compartment could be explained by the equation, dCs/dT= K1Cw-K2Cs. The adsorption rate constants (K1), desorption rate constants (K2) and concentration factors (K1/K2) were calculated. For hydrophobic chemicals, the K1's were independent of water solubility, but the K2's were relatively related to water solubility. For both hydrophobic chemicals and heavy metals, the concentration factors per fraction organic carbon were similar to the soil sorption coefficients (Koc), expressed on a organic carbon basis.

Adsorption↗
PubMed1992

Cadmium in blood and urine after cessation of exposure.

A plant for the synthesis and packaging of cadmium oxide was operated for 32 months (1982-84) in a small chemical factory producing zinc and copper oxide. The cumulative exposure of 6 workers was from 12 to 190 days. Five years after cessation of exposure the blood cadmium levels in the exposed were, on average, 4-10 times higher than those of a reference group and the urinary cadmium levels were 1-6-times higher. In view of the long half-life of cadmium in the human body, the choice of normal reference values requires particular care since brief and sometimes forgotten exposures to cadmium may be a confounding factor to set reference values.

Cadmium↗
PubMed1987

On coordination modes of adenine in cadmium(II) complexes.

Complexes of cadmium(II) derivatives with adenine from water or by simulation of physiological conditions are obtained. The complexes have been studied by spectroscopic, conductometric, 1H-NMR, and by TG and DSC measurements. Possible coordination modes of the ligand are proposed.

Adenine↗
PubMed1992

Conversion in the peptides coating cadmium:sulfide crystallites in Candida glabrata.

Cultures of Candida glabrata treated with CdCl2 form intracellular Cd(II) complexes that evolve with the time of culturing. Initially, glutathione (gamma ECG) appears to be the major buffering component. One type of Cd(II)-glutathione complex exists as a cadmium:sulfide (CdS) crystallite coated with glutathione. A time dependent change in the coating of the CdS particles occurs with a decrease in the (gamma ECG) content and a corresponding increase in the abundance of (gamma EC)nG peptides with (gamma EC)2G becoming the predominant peptide. The des-Gly variant (gamma EC)2 appears in significant concentration only in late cultures. The evolution in isopeptide coating appears to be dependent on the sulfide content of the CdS particles. Cellular conditions that enhance the generation of sulfide ions facilitate the conversion from gamma ECG to (gamma EC)2G.

Buffers↗
PubMed1994

Metal-induced genotoxic adaptation in barley (Hordeum vulgare L.) to maleic hydrazide and methyl mercuric chloride.

Presoaked seeds of barley, Hordeum vulgare L., were exposed for 2 h to maleic hydrazide (MH), 5 x 10(-2) M or methyl mercuric chloride (MMCl), 10(-4) M with or without a prior conditioning with MH, 5 x 10(-3) M; MMCl, 10(-5) M; cadmium sulfate (CdSO4), 10(-4) M or zinc sulfate (ZnSO4), 10(-1) M; the interexposure time was 2 h. Subsequently as the seeds germinated a number of endpoints were measured that included mitotic index, mitotic chromosome aberrations and micronuclei (MNC) in embryonic shoot cells fixed at 32, 36, 40, 44, 48 and 52 h of recovery, and seedling height on day 7. The results demonstrated that prior conditioning exposure to MH or metals induced genotoxic adaptation to the subsequent challenge exposure to MH and MMCl. Cadmium-induced genotoxic adaptation against either MH or MMCl challenge exposure was, however, significantly prevented when the presoaked seeds were pre-exposed to buthionine sulfoximine, 10(-3) M for 2 h, thereby providing evidence that the underlying mechanism of genotoxic adaptation possibly involved phytochelatins.

Adaptation, Physiological↗
PubMed1996

Stabilization of adhesion plaques by the expression of drebrin A in fibroblasts.

The expression of drebrin A was induced in mouse fibroblasts (L cells) after transformation of cells with a vector that carried cDNA for rat drebrin A (developmentally regulated brain protein A) under the control of the promoter of the gene for metallothionein-I. When drebrin was expressed in the transformed cells (MTI-5 cells), the organization of actin filaments changed such that stress fibers were converted to a mesh-like structure. After subsequent treatment with 5 micrograms/ml cytochalasin D (a reagent that depolymerizes actin filaments), MTI-5 cells maintained their shape, while cells of a drebrin-negative cell line, MTI-11, formed retraction processes. Simultaneously, actin filaments changed into patchy dot-like aggregates in the cytoplasm of both MTI-5 and MTI-11 cells. These aggregates are known as cytoplasmic pools. In MTI-5 cells, adhesion plaques that were resistant to treatment with cytochalasin D appeared upon expression of drebrin. These adhesion plaques were immunostained with vinculin-specific antibodies, while those in MTI-11 cells were hardly immunostained. The amount of vinculin in MTI-5 cells increased in parallel with increase in the level of drebrin. These results suggest that expression of drebrin A induces changes in the assembly of actin filaments and adhesion plaques, with resultant modulation of cellular adhesion to the substratum.

Blotting, Western↗
PubMed1993

Inhibition of protein synthesis by cycloheximide does not prevent adaptive responses triggered by heavy metal salts in Vicia faba.

Copper sulfate, lead nitrate, and cadmium nitrate conditioning treatments of Vicia faba root tip meristem cells result in adaptive responses to triethylenemelamine (TEM)- and maleic hydrazide (MH)-induced genotoxic effects, i.e., they significantly reduce the yield of metaphases with chromatid aberrations. Contrary to adaptive responses triggered by low clastogen concentrations or heat shock, protective effects induced by heavy metals cannot be prevented by inhibition of protein synthesis and last for a much longer time span (up to at least 48 h). These and other data support the conclusion that the cells can react to the impact of external factors by various inducible functions which eventually protect their DNA from damage.

Adaptation, Physiological↗
PubMed1995

Cycloheximide and buthionine sulfoximine prevent induction of genotoxic adaptation by cadmium salt against methyl mercuric chloride in embryonic shoot cells of Hordum vulgare L.

Presoaked seeds of barley Hordeum vulgare L. pretreated with cycloheximide (CH), 10(-6) M or bythionine sulfoximine (BSO), 10(-4) M, were exposed to methyl mercuric chloride (MMCl), 10(-4) M, with or without prior conditioning with cadmium sulfate (CdSO4), 10(-4) M. Subsequently as the seeds germinated the endpoints measured were mitotic index, cells with mitotic aberrations and micronuclei (MNC) in embryonic shoot cells fixed at 40, 44, 48 and 52 h of recovery. Indicated by the significant reduction (p < or = 0.05) of the yield of cells with aberrations or MNC, the results confirmed that CdSO4-conditioning triggered an adaptive response to MMCl-challenge. Pretreatments of CH and BSO, whereas they potentiated the genotoxicity of MMCl, significantly prevented (p < or = 0.05) the Cd-induced genotoxic adaptation. That underscores a possible involvement of proteins in addition to phytochelatins in the underlaying mechanisms.

Adaptation, Physiological↗
PubMed1983

Selective crystallization of horse isoferritins.

Various precipitating agents were examined in order to crystallize horse heart and spleen ferritins. Cadmium sulfate induced the crystallization of the spleen ferritin, while 2-methyl-2,4-pentanediol and poly(ethylene glycol) only induced that of the heart ferritin. Isoelectric focusing analysis showed that the crystals grown from cadmium sulfate contained only the more acidic isoferritins, and those grown from methyl pentanediol only the less acidic isoferritins. Heart ferritin crystallizes in a cubic space group, as previously reported for spleen ferritin crystals grown from cadmium sulfate.

Animals↗
PubMed1996

Production of cadmium sulphide microcrystallites in batch cultivation by Schizosaccharomyces pombe.

Cadmium sulphate was added to separate batch cultures of Schizosaccharomyces pombe during different growth phases to determine the effect on cadmium sulphide microcrystallite production. Exit gas analysis was used to determine the impact on metabolism. Addition during the early-exponential growth phase resulted in an immediate intracellular uptake of cadmium, followed by rapid efflux from the cells, permanent reduction in cell metabolism and a lower intracellular inorganic sulphide content. This response was not suitable for cadmium sulphide microcrystallite production. Stationary phase cultures did not induce cadmium sulphide microcrystallite production. However, the addition of cadmium sulphate to a culture during the mid-exponential growth phase increased the intracellular cadmium and inorganic sulphide concentrations for approximately 8 h before reaching a saturation level for the cell. This resulted in a significant level of cadmium sulphide microcrystallite production.

Biological Transport, Active↗
PubMed1989

Toxicity of cadmium oxide instilled into the rat lung. I. Metabolism of cadmium oxide in the lung and its effects on essential elements.

The metabolism of cadmium oxide (CdO, insoluble form) and cadmium chloride (CdCl2, soluble form) instilled intratracheally into the rat lung was investigated. CdO might be solubilized rapidly in the lung and consequently pulmonary clearance rate of CdO was not so different from that of CdCl2. At a dose of 5 micrograms Cd/rat about 20% of the dose was translocated to the liver within 12 h, whereas gradual and consistent accumulation of Cd was observed in the kidney up to 7 days. Both pulmonary clearance and translocation of Cd to the liver were accelerated with the dose of instilled CdO, however, Cd accumulated in the kidney was proportional to the dose. Lung weight was increased by the instillation of CdO. Lung essential elements such as S, P, Mg, Zn and Mn were not affected in the inflammatory-reparative proliferative process, but Cu content of unit lung weight was slightly decreased.

Animals↗
PubMed1989

Toxicity of cadmium oxide instilled into the rat lung. II. Inflammatory responses in broncho-alveolar lavage fluid.

Biochemical and cytological responses in the broncho-alveolar lavage fluid were investigated after instillation of cadmium oxide (CdO) or cadmium chloride (CdCl2) into the rat lung. Although biochemical responses of the lung to CdO were similar to the CdCl2-exposed lung, cytological response was more sensitive to CdO than CdCl2. Increases of lactate dehydrogenase, protein content and number of cells in the lavage fluid were proportional to the dose over the range of 0.5-10 micrograms Cd/rat. beta-Glucuronidase activity in the fluid increased with dose at low doses of Cd, but the activity did not continue to increase above 2 micrograms Cd/rat. A dose-response profile of phosphorus content in the lavage fluid, which might indicate amount of surfactant produced by Type II cells was similar to that observed for beta-glucuronidase in CdO-treated rats. Thus, tolerable level of instilled CdO for the rat lung was about 2 micrograms Cd/rat.

Animals↗
PubMed1989

Cadmium-binding protein in a cadmium-resistant strain of Saccharomyces cerevisiae.

A Cd-binding protein in the Cd2+-resistant strain 301N of Saccharomyces cerevisiae was induced by administration to 0.5 mM CdSO4. The protein was purified by a gel-permeation and subsequent ion-exchange column chromatographies. The purified Cd-binding protein had the characteristics of metallothioneins: (1) low molecular weight (9.0 kDa), (2) high Cd content (63 micrograms/mg protein), (3) amino-acid composition rich in cysteine (18%), basic and acidic amino acids and free from aromatic amino acids, and (4) an absorption shoulder at near 250 nm. Acid pH or EDTA treatments abolished 250 nm absorption of the Cd-binding protein, and the formed apoprotein was capable of binding Cd2+, Cu2+ and Zn2+, respectively. Heat treatment (75 degrees C) little affected the ultraviolet absorption or sodium dodecyl sulfate-polyacrylamide gel electrophoresis profiles of Cd-binding protein. These results suggest that metallothionein generally found in animals also occurs in Cd-adapted yeast cells and thus has a role in its Cd-resistance.

Amino Acids↗
PubMed1988

Preparation of metallothionein from rat liver and studies of its properties with respect to use as a standard in gel permeation chromatography, polyacrylamide gel systems, autoradiography and Western blotting.

1. A simple method for preparation of metallothionein (Mt) I and II has been developed for the purpose of making standards for use in various biochemical systems and in antibody production. 2. The theoretical content of SH groups in a Mt protein; assuming the mol. wt to be 10,000 and each molecule to contain 20 SH groups was found to be 7.1 and 7.7 times higher than for our purified Mt I and II, respectively. 3. In our native polyacrylamide gel system Mt I ran ahead of Mt II, while the two Mt forms were not separated in the Laemmli SDS system in which it behaved as a protein with mol. wt 10,000. In both gel systems, however, Mt I stained as a very faint band in comparison to Mt II, despite equal absorbance at 254 nm and Cd binding capacity. 4. Compared to staining of polyacrylamide gels with Coomassie Brilliant Blue less than 1/50 parts (1 ng) of the protein could be easily seen after silver staining. 5. It was found that Mt may undergo spontaneous modification, polymerization and loss of metal binding properties. 6. Spontaneous modification and polymerization reduced the antigenic properties of our purified Mt. Only Mt II appeared to be immunologically active.

Animals↗