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 919 records · Page 51Linked to original sources
PubMedDate not supplied

A review of the carcinogenicity of chemicals most frequently found at National Priorities List sites.

Several studies have shown that numerous National Priorities List (NPL) sites have been contaminated with arsenic (747), cadmium (791), chloroform (596), or nickel (664). The National Toxicology Program (NTP, 1991) has classified these substances as known human carcinogens (arsenic and certain arsenic compounds) or as substances that may reasonably be anticipated to be carcinogens (cadmium and certain cadmium compounds, chloroform, and nickel and certain nickel compounds). The general population is probably exposed to low levels of these hazardous substances through drinking water, eating food, or inhaling contaminated air. People working or living near industries and facilities that manufacture and use chloroform, nickel, arsenic, or cadmium may be exposed to higher than background levels of these hazardous substances. Multiple pathways of exposure may exist for populations near hazardous waste sites. For example, high levels of chloroform (1,890 ppb) were found in well water near a waste site; high levels of cadmium exposure may exist for individuals living near cadmium-contaminated waste sites.

Animals↗
PubMed1994

Cadmium mobilization by monoaralkyl- and monoalkyl esters of meso-2,3-dimercaptosuccinic acid and by a dithiocarbamate.

Syntheses and relative cadmium mobilizing properties are described for three new monoaralkyl esters (HOOCCH(SH)CH(SH)COOR, where R = phenylethyl ((CH2)2C6H5), MPhEDMS; R = 3-phenylpropyl ((CH2)3C6H5), MPhPDMS; and R = 2-phenoxyethyl ((CH2)2OC6H5). MPhOEDMS) of meso-2,3-dimercaptusuccinic acid. These were prepared by the reaction of the corresponding alcohol with meso-2,3-dimercaptosuccinic acid (DMSA) in aqueous HCl. When administered intraperitoneally to cadmium-loaded mice at 0.50 mmol/kg/day for four consecutive days, all induced significant reductions in the whole body cadmium levels. MPhEDMS, 60%; MPhPDMS, 66%; and MPhOEDMS, 58% in comparison with control levels. At the same dosage monoisoamyl meso-2,3-dimercaptosuccinate (Mi-ADMS) and a dithiocarbamate, sodium N-benzyl-4-O-(beta-D-galactopyranosyl)-D-glucamine-N-carbodithioate++ + (BLDTC) induced reductions of 65% and 57%, respectively. Hepatic and renal cadmium were also depleted significantly, while brain cadmium levels were unchanged. These compounds induced a significant reduction in the cadmium levels of the spleen, and one, MPhOEDMS, produced a 10% decrease in pancreatic cadmium. The manner in which the later injections removed smaller fractions of the total body cadmium is consistent with a bodily distribution of these compounds by which they are concentrated primarily in the kidneys and the liver, with much smaller amounts reaching other organs. It is proposed that these compounds enter renal and hepatic cells through an anion transport system.

Animals↗
PubMed1997

Effects of cadmium and nisoldipine on the delayed rectifier potassium current in guinea pig ventricular myocytes.

Block of the slow inward calcium current (Isi) during assessment of the delayed rectifier potassium current (IK) of cardiac ventricular myocytes is commonly achieved by use of either inorganic compounds such as cadmium or dihydropyridine derivatives such as nisoldipine. Effects of these two Isi blockers on IK characteristics of guinea pig ventricular myocytes were compared in this study. Currents were measured in the whole cell configuration of the patch-clamp technique and IK tail amplitudes were measured at -40 mV after depolarizations to various test potentials (voltage steps, -20 to +50 mV) for either 250 (IK250), 450 (IK450) or 5000 (IK5000) msec. Activating and tail currents measured in the presence of cadmium were of greater amplitudes when voltage steps were more positive than 0 mV but were of smaller amplitudes at Vtest < or = 0 mV compared to currents measured in the presence of nisoldipine or Tyrode solution. In the presence of the rapid component of the delayed rectifier E-4031, a blocker of cadmium increased IKs amplitude during high voltage tests and caused a positive shift in the voltage dependence of IKs activation at low depolarizing potentials. In contrast, no effect on IK was observed when nisoldipine was added to Tyrode solution. In conclusion, results obtained in this study suggest that cadmium depresses and/or shifts the activation curve of the rapid component and increases and positively shifts the slow component of IK in guinea pig ventricular myocytes. These observations lead us to propose that nisoldipine may be a better tool to inhibit long lasting inward calcium current during assessment of IK.

Animals↗
PubMed1993

Presentation of a general algorithm to include effect assessment on secondary poisoning in the derivation of environmental quality criteria. Part 1. Aquatic food chains.

Effect assessment on secondary poisoning can be an asset to effect assessments on direct poisoning in setting quality criteria for the environment. This study presents an algorithm for effect assessment on secondary poisoning. The water-fish-fish-eating bird or mammal pathway was analyzed as an example of a secondary poisoning pathway. Parameters used in this algorithm are the bioconcentration factor for fish (BCF) and the no-observed-effect concentration for the group of fish-eating birds and mammals (NOECfish-eater). For the derivation of reliable BCFs preference is given to the use of experimentally derived BCFs over QSAR estimates. NOECs for fish eaters are derived by extrapolating toxicity data on single species. Because data on fish-eating species are seldom available, toxicity data on all birds and mammalian species were used. The proposed algorithm (MAR = NOECfish-eater/BCF) was used to calculate MARS (maximum acceptable risk levels) for the compounds lindane, dieldrin, cadmium, mercury, PCB153, and PCB118. By subsequently, comparing these MARs to MARs derived by effect assessment for aquatic organisms, it was concluded that for methyl mercury and PCB153 secondary poisoning of fish-eating birds and mammals could be a critical pathway. For these compounds, effects on populations of fish-eating birds and mammals can occur at levels in surface water below the MAR calculated for aquatic ecosystems. Secondary poisoning of fish-eating birds and mammals is not likely to occur for cadmium at levels in water below the MAR calculated for aquatic ecosystems.

Algorithms↗
PubMedDate not supplied

In vivo screening of potential antidotes for chronic cadmium intoxication.

Nineteen chelating agents have been screened under identical conditions of metal loading in an attempt to establish their relative ability to mobilize cadmium from the liver and kidney in mice with chronic cadmium intoxication. The compounds investigated were divided into five groups: polyaminocarboxylic acids, monothiols, dithiols, macrocycles, and a miscellaneous category. Only 2,3-dimercaptopropanol (BAL) and sodium diethyldithiocarbamate (NaDDTC) were able to produce a statistically significant (at the 95% level) reduction in the cadmium content of the kidney. The closely related dithiols sodium 2,3-dimercaptopropane-1-sulfonate and 2,3-dimercaptosuccinic acid produced statistically significant increases in the liver cadmium contents, as did N-(2-mercaptopropionyl)-glycine. The reduction in kidney cadmium levels produced by both BAL and NaDDTC was just under 40%.

Animals↗
PubMed1993

Presentation of a general algorithm to include secondary poisoning in effect assessment.

A general algorithm for effect assessment on secondary poisoning for birds and mammals is presented. This algorithm (Maximum Permissible Concentration = NOECbird/mammal/BCF) was drawn up by analysing an aquatic food chain (water--fish--bird or mammal) and a terrestrial food chain (soil--worm--bird or mammal). NOECs and bioconcentration factors (BCFs) were collected for a set of selected compounds: lindane, dieldrin, cadmium and mercury in both water and soil, PCB153 only in water and DDT and PCP only in soil. BCFs for the terrestrial pathway are frequently < 1 and rarely above 10, though for the aquatic pathway BCFs up to 10(4) were found for the same compounds. By calculating MPCs for fish-eaters and comparing these to MPCs calculated for aquatic organisms, secondary poisoning could be a critical pathway for methyl-mercury and PCB153. For lindane the conclusion depends on whether a separate or combined data set is chosen for birds and mammals. By calculating MPCs for a standard soil situation and comparing these to MPCs for terrestrial organisms, secondary poisoning could be a critical pathway for cadmium and methyl-mercury.

Algorithms↗
PubMed2000

Bis(&mgr;-hexamethylenetetramine)bis(aquadibromocadmium)diaquadibromo cadmium dihydrate

The title compound, poly[[diaquadibromocadmium-&mgr;-(1,3,5, 7-tetraazatricyclo[3.3.1.1(3, 7)]decane-N(1):N(5))-aquacadmium-di-&mgr;-bromo-aquacadmium-&mgr;-(1, 3,5,7-tetraazatricyclo[3.3.1.1(3, 7)]decane-N(1):N(5))-di-&mgr;-bromo] dihydrate], [Cd(3)Br(6)(C(6)H(12)N(4))(2)(H(2)O)(4)].2H(2)O, is made up of two-dimensional neutral rectangular coordination layers. Each rectangular subunit is enclosed by a pair of Cd(3)(&mgr;(2)-Br)(6)(H(2)O)(3) fragments and a pair of (&mgr;(2)-hmt)Cd(H(2)O)(2)Br(2)(&mgr;(2)-hmt) fragments as sides (hmt is hexamethylenetetramine). The unique Cd(II) atom in the Cd(2)Br(2) ring in the Cd(3)(&mgr;(2)-Br)(6)(H(2)O)(3) fragment is in a slightly distorted octahedral CdNOBr(4) geometry, surrounded by one hmt ligand [2.433 (5) A], one aqua ligand [2.273 (4) A] and four Br atoms [2.6409 (11)-3.0270 (14) A]. The Cd(II) atom in the (&mgr;(2)-hmt)Cd(H(2)O)(2)Br(2)(&mgr;(2)-hmt) fragment lies on an inversion center and is in a highly distorted octahedral CdN(2)O(2)Br(2) geometry, surrounded by two trans-related N atoms of two hmt ligands [2.479 (5) A], two trans-related aqua ligands [2.294 (4) A] and two trans-related Br atoms [2.6755 (12) A]. Adjacent two-dimensional coordination sheets are connected into a three-dimensional network by hydrogen bonds involving lattice water molecules, and the aqua, bromo and hmt ligands belonging to different layers.

Journal Article↗
PubMedDate not supplied

Toxicokinetics and biochemistry of cadmium with special emphasis on the role of metallothionein.

Cadmium is a toxic metal with extremely long biological half-time of 15-20 years in humans. It has for decades been known that cadmium exposure can cause a variety of adverse health effects, among which kidney dysfunction, lung diseases, disturbed calcium metabolism and bone effects are most prominent. Following long term exposure the kidney is the critical organ. Cadmium and its compounds give rise to lung cancer after inhalation and have been classified as human carcinogens. Metallothionein (MT) is a low-molecular -weight protein, 6500Da with high cysteine content and high metal affinity, which plays a major role in the kinetics and metabolism of cadmium. The balance between CdMT and non-bound Cd in renal tissue has been shown to be of crucial importance for expression of toxicity. The most well studied metallothioneins are metallothioneins I and II with their isoforms which are expressed in almost all mammalian tissues. Metallothionein III is expressed in brain and is rich in zinc. Since the blood-brain barrier keeps Cd outside the CNS, reported neurotoxic effects of Cd during development are likely to be secondary to an interference of Cd with Zn-metabolism and not a direct effect of Cd on brain cells. It is therefore of importance to investigate whether neurotoxicity induced by cadmium is related to mechanisms involving MT III in brain.

Animals↗
PubMed2006

Comparative investigations of sodium arsenite, arsenic trioxide and cadmium sulphate in combination with gamma-radiation on apoptosis, micronuclei induction and DNA damage in a human lymphoblastoid cell line.

In the field of radiation protection the combined exposure to radiation and other toxic agents is recognised as an important research area. To elucidate the basic mechanisms of simultaneous exposure, the interaction of the carcinogens and environmental toxicants cadmium and two arsenic compounds, arsenite and arsenic trioxide, in combination with gamma-radiation in human lymphoblastoid cells (TK6) were investigated. Gamma-radiation induced significant genotoxic effects such as micronuclei formation, DNA damage and apoptosis, whereas arsenic and cadmium had no significant effect on these indicators of cellular damage at non-toxic concentrations. However, in combination with gamma-radiation arsenic trioxide induced a more than additive apoptotic rate compared to the sum of the single effects. Here, the level of apoptotic cells was increased, in a dose-dependent way, up to two-fold compared to the irradiated control cells. Arsenite did not induce a significant additive effect at any of the concentrations or radiation doses tested. On the other hand, arsenic trioxide was less effective than arsenite in the induction of DNA protein cross-links. These data indicate that the two arsenic compounds interact through different pathways in the cell. Cadmium sulphate, like arsenite, had no significant effect on apoptosis in combination with gamma-radiation at low concentrations and, at high concentrations, even reduced the radiation-induced apoptosis. An additive effect on micronuclei induction was observed with 1muM cadmium sulphate with an increase of up to 80% compared to the irradiated control cells. Toxic concentrations of cadmium and arsenic trioxide seemed to reduce micronuclei induction. The results presented here indicate that relatively low concentrations of arsenic and cadmium, close to those occuring in nature, may interfere with radiation effects. Differences in action of the two arsenic compounds were identified.

Apoptosis↗
PubMed1991

Selenium antagonizes the induction of human heme oxygenase by arsenite and cadmium ions.

Effects of selenium compounds on the induction of heme oxygenase in human cells exposed to sodium arsenite or cadmium chloride have been investigated by an immunoblotting technique. Exposure of HeLa cells to arsenite or cadmium ions caused a marked increase in the synthesis of heme oxygenase, and the presence of sodium selenite suppressed the induction. DL-Selenocystine was an effective suppressor, and sodium selenate was less effective. DL-Selenomethionine had no effect. Northern blot analysis showed that selenite abolished the induction of heme oxygenase mRNA in the cells exposed to arsenite or cadmium ions. These results indicated that selenium antagonizes the induction of heme oxygenase by heavy metals ions.

Arsenic↗
PubMed2001

Postimplantation whole embryo culture assay for hamsters: an alternative to rat and mouse.

Postimplantation whole embryo culture (WEC) assay for rats and mice has been well established and introduced to many laboratories. Recently WEC technique for rabbits has been developed; however, information on culture of other species is very limited. Knowing the usefulness of hamsters in classical embryotoxicology, we reasoned that hamster WEC could be an alternative model for the most frequently used rat and mouse WEC. Previously we have optimized culture conditions for postimplantation hamster embryos. The aim of this study was to test the susceptibility of hamster embryos cultured in vitro to embryotoxic compounds and to compare our results with those reported by others on rat or mouse embryo culture. For that purpose we choose three known embryotoxic compounds--valproic acid, cadmium chloride, and diethylstilbestrol--and tested them using a postimplantation hamster whole embryo culture assay. Hamster embryos were cultured from 7.5 days gestation for 24 h in a medium consisting of 35% hamster serum and 65% synthetic culture medium (Iscove's or McCoy 5A). At the end of the culture period, the embryos were examined morphologically, measured with the aid of a computer image analysis system, and total protein content was assessed. All three compounds exhibited dose-related embryotoxic and teratogenic effects in hamster embryos. The malformations observed were similar to those reported on rat and mouse embryos. Comparison of the results with data reported by other authors indicates that hamster embryos cultured in vitro might be more susceptible to embryotoxic stimuli than rat and mouse embryos.

Abnormalities, Drug-Induced↗
PubMed1995

Acute pulmonary toxicity of copper gallium diselenide, copper indium diselenide, and cadmium telluride intratracheally instilled into rats.

Acute toxicity studies were conducted on copper gallium diselenide (CGS), copper indium diselenide (CIS), and cadmium telluride (CT), three novel compounds used in the photovoltaic and semiconductor industries. Female Sprague-Dawley rats (six rats/dose) were administered 0, 12, 25, 50, or 100 mg/kg body wt of CGS, CIS, or CT by intratracheal instillation. At 72 hr after treatment, body weight gain was significantly decreased in the 100 mg/kg CIS group and in all CT dose groups. Lung weights were increased in most chemical-treated rats, with CT causing the greatest increase. Total numbers of cells in bronchoalveolar lavage fluid (BALF) were significantly increased in treated rats and were greatest in the 100 mg/kg CIS group. Differential cell counts of BALF demonstrated a marked decrease in the percentage of alveolar macrophages and an increase in the percentage of polymorphonuclear leukocytes in all dose groups of all three chemicals. Slight to moderate increases in lactate dehydrogenase activity were observed in BALF from CGS- and CIS-treated rats; marked increases were observed in CT-treated rats. BALF protein was significantly increased in rats treated with CIS and CT. Microscopic examination revealed lymphoid hyperplasia in lungs of rats treated with all three chemicals. CT caused necrosis of the terminal bronchiolar epithelium and epithelium of the alveolar duct region with inflammation, prominent fibrin exudates, and type II cell hyperplasia. CGS and CIS also caused intraalveolar inflammation and type II cell hyperplasia, but did not cause the necrosis and fibrin exudate observed in lungs of CT-treated rats. Based on changes in lung weight, BALF indices, and histopathology, CT was the most toxic for the lung; CIS had intermediate toxicity and CGS was the least toxic. The solubilities of CGS and CIS were relatively low and similar at both pH levels and do not readily explain the observed differences in pulmonary toxicity. The solubility of CdTe was considerably greater than that of CGS and CIS and likely contributed to the greater toxicity of this compound.

Animals↗
PubMed1977

Air pollution and COPD.

Air pollution referable to increased ambient levels of sulfur dioxide and suspended particulates is associated with increased episodes of acute bronchitis and is also causally related to some cases of chronic bronchitis. Oxidant air pollution is associated with abnormalities of pulmonary function in children and is a major contributory factor in COP, especially bronchitis, in some areas of the United States. The relationship of nitrogen dioxide atmospheric contamination to COPD is still controversial. In our opinion, the epidemiologic studies conducted to date have been inadequate and further elucidation is indicated. Cadmium fumes and compounds have been found to be instrumental in the development of some cases of chronic bronchitis and emphysema in Sweden. This association is unproved in the United States and warrants a thorough clinical and epidemiologic evaluation.

Air Pollutants↗
PubMed1984

[Heavy metals--toxicity at low doses in the environment and in the work place].

Ecotoxicity of heavy metals is related to their persistence, accumulation and dispersion tendency. Sources, pathways of exposure and adverse health effects of low doses are reviewed. Environmental and occupational toxicity of lead, cadmium and mercury compounds are discussed and the carcinogenic and sensitizing effects of chromium compounds as an example of a heavy metal which is essential in low doses. High risk groups, most susceptible target organs, early symptoms, signs of subclinical poisoning, numbers of diseases from heavy metals accepted in Austria as occupational diseases and environmental hazards are summarized.

Air Pollution↗
PubMed1988

Current concepts in the assessment of effects of metals in chronic low-level exposures--considerations of experimental and epidemiological evidence.

Human exposure to metals and their compounds may give rise to a number of adverse effects. Of particular interest are such effects that can be elicitated by chronic low-level exposure, since such exposures may occur in human populations both in the general environment and occupationally. The adverse effect that occurs at the lowest exposure has been termed the "critical effect" since it is critical in relation to preventive action aiming at limiting exposures to a safe level. When reviewing the present evidence on the toxicology of metals it becomes evident that "critical effects" may be related to various organ systems, disease categories and biochemical mechanisms of damage. A category of effects, which is of particular interest in relation to critical effects, is hypersensitivity (e.g. with dermal or respiratory manifestations). However conceptual recognition of this category of effects is as yet incomplete. Other important considerations are whether effects display threshold- or non-threshold type dose-response relationships, the latter category obviously being more likely to display a low incidence response at low dose exposure. In this context mutagenic, carcinogenic, developmental and reproductive toxicity of metals are of particular interest. Information on these types of effects compiled during previous meetings of the scientific committee on the toxicilogy of metals and recently updated, indicates that some compounds of arsenic, beryllium, cadmium, chromium and nickel may be regarded as carcinogenic for humans. Available evidence in experimental systems as well as in humans concerning effects of metallic compounds on male and female reproductive systems, congenital teratogenicity and perinatal toxicity as well as effects on the developing central nervous system indicates that such effects should be considered further in relation to critical effects for arsenic, cadmium, lead, mercury and their compounds.

Animals↗