Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cadmium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1996

Toxicity of cadmium species on luminescent bacteria.

The toxicity of cadmium compounds against luminescent bacteria has been measured using the Microtox(R) toxicity bioassay and has been related to the cadmium species. Since the Microtox(R) test is carried out in NaCl (2%) and cadmium forms stable chloro complexes, NaNO(3) and NaClO(4) have been tested successfully as alternative to sodium chloride to provide the adequate osmotic protection of the bacteria. The influence of medium and ionic strength as well as different exposure times on EC(50) values has been evaluated.

Journal Article↗
PubMed1977

Photodynamic aspects of some metal complexes.

The potential phototoxic capacity of some metal compounds of clinical significance in dermatology has been investigated by means of the photohemolysis technique. No photosensitized hemolysis of erythrocytes was observed with the chromium, nickel, copper and cobalt compounds studied. On the contrary, nickel and cobalt compounds proved to be efficient in quenching singlet oxygen mediated photo-oxidative membrane damage of red blood cells. Cadmium compounds showed a pronounced photohemolytic activity and the reaction was oxygen dependent. The deuterium test for singlet oxygen showed a significant increase in photohemolytic efficiency. The addition of histidine, a known quencher of singlet oxygen, resulted in a significant inhibition of the photohemolysis. Pronounced photo-oxidative damage to plasma membranes was also observed in vitro cultivated cells by means of scanning electron microscopy.

Chromium↗
PubMed1993

Effect of cadmium on enzymatic digestion and sugar transport in the small intestine of rabbit.

Cadmium compounds are found widely in our environment: for example, in food, water, soil, and ambient air. The most important exposure route of animals to cadmium in the general environment is via oral exposure. In oral cadmium intoxication, the immediate target organ is the gastrointestinal tract. The aim of the present work was to determine how cadmium acts on the intestinal absorption of sugars and on the sucrase activity through rabbit jejunum, after in vitro administration and/or oral administration of CdCl2 in drinking water. Results obtained show that cadmium decreases D-galactose accumulation in the jejunum tissue. This effect seems to be the results of an action mainly located on Na(+)-dependent sugar transport of the mucosal border of the intestinal epithelium, because cadmium seems not to modify the sugar diffusion across the intestinal epithelium. Cadmium has also been shown to inhibit the (Na(+)-K+)-ATPase activity of the enterocyte, which might explain the inhibition of the D-galactose Na(+)-dependent transport. Nevertheless, a direct action of the cadmium molecule on the Na(+)-dependent carrier cannot be discarded. Cadmium altered the sucrose activity when it was administered in the drinking water for 4 d.

Adenosine Triphosphatases↗
PubMed1993

Effect of cadmium on D-galactose transport across the small intestine of rabbits.

Cadmium compounds are found widely in the environment: for example, in food, water, soil and ambient air. The most important exposure route of animals to cadmium in the general environment is oral. The aim of the present work was to determine how cadmium acts on the intestinal absorption of sugars by rabbits. Results obtained show that cadmium decreases both D-galactose accumulation in the jejunum tissue, and mucosal to serosal transepithelial fluxes of this sugar, in a dose-dependent way. Furthermore, cadmium seems not to modify the sugar diffusion across the intestinal epithelium. This inhibitory mechanism is non-competitive and it is partly reversed with dithioerythritol (thiol groups protector). Therefore, these results suggest that cadmium decreases carrier-mediated intestinal absorption of sugar in rabbits.

Animals↗
PubMed1992

Validity and limitations of animal experiments in assessing lung carcinogenicity of cadmium.

Several cadmium compounds have been observed to induce in rats, but in rats only, a dose-dependent increase in lung cancer. A similar sensitivity to lung cancer induction in both humans and rats can be deduced from a comparison of the histogenesis of tumours and the dose response to radiation, since similar numbers of DNA lesions are produced. Since the carcinogenic action of cadmium is limited to the site of deposition, the toxicokinetics of inhaled particles in human and rodents are discussed in relation to the exposure of the respective target cells in both species. It is stressed that the rat may be much more sensitive to the induction of cancer following the retention of poorly soluble compounds. A comparison of the possible dose-effect response in humans and the dose response in rats showed that the shape of the "dose" response cannot be extrapolated. Finally, clonogenicity and DNA repair of tracheal cells sublethally exposed in vitro to cadmium differ significantly in rats and hamsters. This may explain why hamsters exposed in vivo do not develop tumours.

Animals↗
PubMed2000

The importance of performing in vitro cytotoxicity testing before immunomodulation evaluation.

This study uses the well known sensitive and reproducible human peripheral blood lymphocyte (PBL) assay as a model for the possible discrimination between cytotoxic and/or immunomodulative properties of 5 reference compounds: cadmium chloride (CdCl2): didodecyl-dimethyl ammonium bromide (DDAB); cyclosporin (CsA); dexamethasone (DEXA); and theophylline. Two colorimetric cytotoxicity assays were employed, the thiazolyl blue tetrazolium bromide and neutral red, and the H-thymidine DNA incorporation assay on phytohemagglutinin stimulated or non-stimulated PBL was used, as a parameter of cell mediated immunity. This study demonstrated the importance of performing colorimetric or other cytotoxicity assays before any investigation of mechanisms of action of different substances on immunomodulation and relative human risk assessment. This study showed that CdCl2 and DDAB have a cytotoxic rather than immunomodulative effect on PBL and that CsA, DEXA and to a lesser extent theophylline have immunomodulative rather than cytotoxic effects on PBL within the range of the concentrations studied.

Antineoplastic Agents, Hormonal↗
PubMed2006

Physiological modes of action of toxic chemicals in the nematode Acrobeloides nanus.

To gain a better understanding of the mechanisms through which a chemical exerts toxicity, a deeper insight is needed regarding the physiological processes that take place during a toxic stress. This issue can have important benefits for risk assessment, because it can contribute to a better interpretation of toxicity data. Here, we study the physiological mode of action of three different compounds (cadmium, carbendazim, and pentachlorobenzene) with an experimental data-based approach using whole life-cycle toxicity data from the nematode Acrobeloides nanus. We use a process-based model, based on the dynamic energy budget theory, to study the fluxes of energy related to physiological processes and their variation throughout the life cycle. With this approach, we unravel the physiological modes of action based on resource allocation, and we model the effects of the different modes of action at the population level. The mode of action of carbendazim was through a decrease in assimilation, with an additional effect on the production of reactive oxygen species (ROS). Cadmium increased the costs of growth, with an extra effect on ROS production, and pentachlorobenzene decreased assimilation. We compared the present results with those of previous studies using the nematode Caenorhabditis elegans, and we found that the modes of action for the three compounds differed from those found in A. nanus, showing that the life-history characteristics of each organism have a clear influence on the resulting modes of action. This highlights the importance of the interactions between a chemical and the biological characteristics of the organism in determination of the resulting physiological modes of action.

Animals↗
PubMed1992

Metal carcinogenesis: mechanistic implications.

Cancer epidemiology has identified several metal compounds as human carcinogens. Recent evidence suggests that carcinogenic metals induce genotoxicity in a multiplicity of ways, either alone or by enhancing the effects of other agents. This review summarizes current information on the genotoxicity of arsenic, chromium, nickel, beryllium and cadmium compounds and their possible roles in carcinogenesis. Each of these metals is distinct in its primary modes of action; yet there are several mechanisms induced by more than one metal, including: the induction of cellular immunity and oxidative stress, the inhibition of DNA metabolism and repair and the formation of DNA- and/or protein-crosslinks.

Animals↗
PubMed2004

Cadmium and cancer of prostate and testis.

Cancer of the prostate is an important and potentially fatal disease in humans but the etiology is yet undefined. Cadmium and cadmium compounds are known to be human carcinogens based on findings of increased risk to lung cancer among exposed workers, but a relationship between cancer of the prostate and/or testis in humans is unclear in spite of suggestive results in rats. Parenteral administration or oral exposure to cadmium can result in proliferate lesions and tumors of the prostate in rats. The ability of cadmium to produce neoplasms in the prostate of rats is atypically dose-related and only occurs in rats at doses below the threshold for significant testicular toxicity. Testicular androgen production is essential for the maintenance of the prostate and prostate tumors. The rat testis may also develop tumors if cadmium is given parenterally at high doses. Subsequent to testicular hemorrhagic necrosis, there will be loss of testosterone production and hyperplasia and neoplasia of testicular interstitial cells, thought to be a response to trophic hormone release from the pituitary. The pathogenesis of prostatic cadmium carcinogenesis might include aberrant gene expression resulting in stimulation of cell proliferation or blockage of apoptosis. Activation of transcription factors such as the metallothionein gene and activation of some protooncogenes may enhance cell proliferation with damaged DNA. Suppression of DNA repair would add to the population of cells with damaged DNA. Chemically induced apoptosis can be blocked by cadmium, facilitating aberrant cell accumulation.

Animals↗
PubMed1992

On the carcinogenicity of cadmium by the oral route.

Cadmium and cadmium compounds are carcinogenic both by inhalation and by injection. For purposes of risk assessment, a prudent public health approach has been that, if a chemical has been demonstrated to be carcinogenic by one route, it should be considered carcinogenic by all routes. This policy has been questioned for several toxic metals including cadmium. After reviewing the literature on cadmium carcinogenicity and genotoxicity, we think that cadmium should be considered noncarcinogenic by the oral route. The bases for this decision included: (1) a database for genotoxicity of cadmium with more negative test results than positive results and with most positive results in in vitro tests, indicating that cadmium has limited genotoxicity; (2) some epidemiologic evidence of respiratory tract cancer and prostatic cancer in people occupationally exposed to airborne cadmium but no reliable evidence of gastrointestinal tract cancers in workers; and (3) a large dietary oncogenicity study in rats of cadmium chloride at several dose levels, including a maximally tolerated dose (50 ppm) in males, which showed no increase of tumors due to cadmium ingestion in all of the 19 tissues examined. The conclusion that an agent, which has been shown to be carcinogenic by one route of exposure, is not carcinogenic by a second route should be made only in the presence of robust data which indicate the lack of effect via the second route of exposure.

Administration, Oral↗
PubMed2001

Is the capacity of lead acetate and cadmium chloride to induce genotoxic damage due to direct DNA-metal interaction?

Even though the toxic effects of lead and cadmium compounds have been studied over many years, inconsistent results have been obtained about their mutagenic, clastogenic and carcinogenic properties. However, these metals are considered to be potential human carcinogens. The mechanism of metal-induced carcinogenesis is still unknown, but one possible pathway may involve the interaction of metals with DNA, either directly or indirectly. In this work we explore the capacity of lead, cadmium or a mixture of both metals to interact with acellular DNA, by employing a variant of the comet assay. Our results, using low non-cytotoxic metal concentrations (0.01, 0.1 and 1.0 microM) with the standard protocol for the acellular assay, showed an induction of DNA damage in cells of all organs studied; however, basal DNA damage was different in each organ. To confirm that we were working with pure DNA, proteinase K was added to the lysis solution. With this enriched-lysis solution we found a negative response in the induction of DNA damage in cells derived from the liver, kidney and lung of CD-1 male mice. To support the results obtained by the enriched-acellular assay, we studied the capacity of lead and cadmium (0.1 microM) to induce breaks in pooled genomic DNA in cells of the same organs, with negative results. Consistent with these findings, these metals do not induce DNA breaks in the plasmid pUSE amp+. On the whole, we did not detect direct induction of DNA strand breaks by lead acetate, cadmium chloride or a mixture of both metals, all at low non-cytotoxic concentrations. However, we found an induction of lipid peroxidation and an increase in free radical levels in the different organs of CD-1 male mice after inhalation of lead acetate (0.0068 microg/cc) or cadmium chloride (0.08 microg/cc) for 1 h, suggesting the induction of genotoxicity and carcinogenicity by indirect interactions, such as oxidative stress.

Animals↗
PubMed2003

Magnetometric evaluation of cadmium oxide-induced toxicity to pulmonary alveolar macrophages of Syrian golden hamsters.

Since alveolar macrophages play an important role in the clearance of inhaled dust from air-ways, these cells have been used as a target for various toxic chemicals. Alveolar macrophages obtained from bronchoalveolar lavage of Syrian golden hamsters were concurrently exposed in vitro to Fe(3)O(4), as an indicator for magnetometry, and various concentrations of cadmium oxide (CdO) in this study. A rapid decrease of the remnant magnetic field, called relaxation, was observed after the cessation of an external magnetic field stimulus in macrophages concurrently exposed to phosphate-buffered saline or CdO at 0.1 microg/ml, while relaxation was delayed in those concurrently exposed to 1, 25, or 50 microg/ml CdO. Therefore, the concentration of CdO affecting relaxation in vitro was estimated at between 0.1 and 1 microg/ml. Release of LDH activity from CdO-exposed macrophages into the medium significantly increased at levels of 25 and 50 microg/ml CdO. Apoptosis was not detected in macrophages exposed to CdO by the DNA ladder detection method or morphological observations. Electron-microscopic examination revealed severe membrane damage and vacuolar changes in macrophages exposed to CdO. Since delayed relaxation is thought to occur by (1). disrupted cytoskeleton-driven random rotation of phagosomes containing iron oxide particles, (2). significant lactate dehydrogenase (LDH) activity release, and (3). detachment of cell membranes, CdO is considered to affect macrophage functions.

Animals↗
PubMed1991

The safety of low melting point bismuth/lead alloys: a review.

Low melting temperature bismuth alloys that contain about 20% to 25% lead and 10% cadmium are widely used in radiotherapy to construct shielding blocks. Since 1980, five papers have addressed questions concerning potential metal toxicity, safe shop practices, measurement of airborne vapors and metal particulates, and the results of biological testing of personnel fabricating secondary field shaping blocks. In February, 1990, the Occupational Safety and Health Administration (OSHA), proposed new occupational air concentration safety standards for cadmium and cadmium compounds. This review presents the potential toxicity of the components metals in low melting temperature bismuth lead alloys, reviews the proposed OSHA air concentrations standards, and describes proper practices of shop safety required to minimize the hazards of these metals and other potentially hazardous materials used in the block fabrication process. The review reveals that if proper practices are followed, fabrication of those blocks, including those containing cadmium, should not produce a shop environment that would produce metal toxicity in employees, and radiotherapy mold room personnel are unlikely to generate air concentrations of cadmium that exceed new proposed standards.

Alloys↗
PubMed1980

[Environmental pollution and toxicological assessment of major heavy metal (mercury, lead, cadmium) residues].

Correlations are elucidated between contamination of feedstuffs and animal-based foodstuffs as well as crops, with reference being made to pollution of the environment by and residualisation of mercury, lead, and cadmium compounds. Yet, necessary provisions regarding toxicological indices of residues of relevant metals in feed and food should make allowance also for unavoidable pollution of the environment by the toxic agent concerned. Orientation to what is called "normal" or background values in the ecosystem is absolutely essential to any assessment of metallic residues. The proposed WHO tolerances, in the context of animal-based foodstuffs, are 0.1 ppm maximum for mercury and cadmium and 0.5 ppm for lead. However, possible presence of all three toxic agents in one given food item has been left unconsidered in that tolerance proposal.

Animal Feed↗
PubMed2004

Novel triazole-bridged cadmium coordination polymers varying from zero- to three-dimensionality.

Cadmium salts with different triazole ligands have led to a series of novel triazole-cadmium compounds varying from zero- to three-dimensionality. [Cd(2)(deatrz)(2)(H(2)O)Br(4)] (1) (deatrz = 3,5-diethyl-4-amino-1,2,4-triazole) is a zero-dimensional complex which uses a triazole ligand together with micro-OH(2) as bridges to form a 1D chain via hydrogen-bonding contacts. [[Cd(3)(deatrz)(2)Cl(6)(H(2)O)(2)].2H(2)O](n) (2), [[Cd(dmtrz)Cl(2)].1.5H(2)O](n)(3) (dmtrz = 3,5-dimethyl-1,2,4-triazole), and [[Cd(3)(deatrz)(4)Cl(2)(SCN)(4)].2H(2)O](n)(4) are polymeric 1D chains. 2 and 4 were constructed via trinuclear cadmium units bridged by triazole ligands and chloride atoms, while 3 consists of micro(2)-Cl, micro(3)-Cl, and triazole bridges, cross-linked by hydrogen bonding to give a 3D framework. [[Cd(3)(dmatrz)(4)(SCN)(6)]](n)(5) (dmatrz = 3,5-dimethyl-4-amino-1,2,4-triazole) shows a two-dimensional structure whose fundamental units are trinuclear metal cations bridged via triazole ligands. The complex [[Cd(dmtrz)(SCN)(2)]](n)(6) is the first three-dimensional example in N1,N2-didentate-bridged triazole-metal compounds. Six complexes exhibit six types of bridging modes of N1,N2-triazole in combination with single-atom bridges. 2, 4, and 5 are the unprecedented examples of polymeric chains and planes constructed via trinuclear metal ion clusters, whereas 3 is the first example of the micro(3)-Cl bridging mode in triazole-metal complexes. We have briefly discussed the variety of dimensionalities based on the tuning of different organic ligands and anions.

Journal Article↗
PubMed2000

Occupational exposures and pancreatic cancer: a meta-analysis.

OBJECTIVES: Consolidation of epidemiological data on pancreatic cancer and worksite exposures. METHODS: Publications during 1969-98 were surveyed. Studies without verified exposures were excluded. Meta-analyses were conducted on data from 92 studies covering 161 populations, with results for 23 agents or groups of agents. With a standard format, five epidemiologists extracted risk estimates and variables of the structure and quality of each study. The extracted data were centrally checked. Random meta-models were applied. RESULTS: Based on 20 populations, exposure to chlorinated hydrocarbon (CHC) solvents and related compounds was associated with a meta-risk ratio (MRR) of 1.4 (95% confidence interval (95% CI) 1.0 to 1.8). Nickel and nickel compounds were considered in four populations (1.9; 1.2 to 3.2). Excesses were found also for chromium and chromium compounds (1.4; 0.9 to 2.3), polycyclic aromatic hydrocarbons (PAHs) (1.5; 0.9 to 2.5), organochlorine insecticides (1.5; 0.6 to 3.7), silica dust (1.4; 0.9 to 2.0), and aliphatic and alicyclic hydrocarbon solvents (1.3; 0.8 to 2.8). Evidence on pancreatic carcinogenicity was weak or non-positive for the following agents: acrylonitrile (1.1; 0.0 to 6.2); arsenic (1.0; 0.6 to 1.5); asbestos (1.1; 0.9 to 1.5); diesel engine exhaust (1.0; 0.9 to 1.3); electromagnetic fields (1.1; 0.8 to 1.4); formaldehyde (0. 8; 0.5 to 1.0); flour dust (1.1; 0.3 to 3.2); cadmium and cadmium compounds (0.7; 0.4 to 1.4); gasoline (1.0; 0.8 to 1.2); herbicides (1.0; 0.8 to 1.3); iron and iron compounds (1.3; 0.7 to 2.5); lead and lead compounds (1.1; 0.8 to 1.5); man-made vitreous fibres (1.0; 0.6 to 1.6); oil mist (0.9; 0.8 to 1.0); and wood dust (1.1; 0.9 to 2.5). The occupational aetiological fraction of pancreatic cancer was estimated at 12%. In a subpopulation exposed to CHC solvents and related compounds, it was 29%; to chromium and chromium compounds, 23%; to nickel and nickel compounds, 47%; to insecticides, 33%; and to PAHs, 33%. CONCLUSION: Occupational exposures may increase risk of pancreatic cancer. High quality studies are called for on interactions between occupational, environmental, and lifestyle factors as well as interactions between genes and the environment.

Air Pollutants, Occupational↗
PubMed1992

[The interaction between lead, cadmium and essential trace elements (an experimental study)].

An experimental study is performed on 120 white male Wistar rats with average weight 180-210 g. The animals are distributed in 4 groups. I group--control; II group--animals treated with aqua solution of cadmium sulphate; III group--animals treated with aqua solution of cadmium sulphate and lead acetate simultaneously and IV group--animals treated with aqua solution of lead acetate. The toxic substances are introduced per oral in dose 1/40 of LD50 and for a period of 90 days. The animals are killed by decapitation on the 2, 4, 15, 30 and 90th day from the beginning of treatment. An increased content of cadmium in blood, urine and liver is registered in II and III group of animals, and of lead--in III and IV group animals. The zinc content in liver in group II is increased in comparison with the control group, while in group III and IV remains unchanged. The concentration of zinc in blood in animals from II and III group is increased. There is no deviation in group IV. The copper content in liver is decreased in II, III and IV group. There are no significant deviations in the content of copper in the blood of the examined groups of animals. The level of manganese in liver in II, III and IV group of animals is reduced. No changes in the content of manganese in blood are registered in the examined groups animals.

Animals↗