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PubMed2003

Toxicity of a mancozeb containing formulation and Cd-sulphate to chicken embryos after administration as single compounds or in combination.

Environmental pollution of metal modelled by cadmium-sulphate and a 80% mancozeb containing fungicide formulation (Dithane M-45) were studied on chicken embryos after administration as a single compounds or in combination. The test materials were injected into the air-chamber in a volume of 0.1 ml/egg on day 0 of incubation. The concentration of cadmium-sulphate was 0.01%. The applied concentration of Dithane M-45 fungicide was 0.2%. Evaluation was done on day 19 of the hatching period. The individual administration of cadmium-sulphate and the 80% mancozeb containing fungicide formulation did not cause a significant reduction in body weight as compared to the control data. Embryonic mortality increased at all individual treated groups and reached almost a 35% rate. After the individual administration of pesticide, the number of chicken embryos with developmental anomalies did not differ markedly from the control. After the combined administration of cadmium-sulphate and the 80% mancozeb containing fungicide formulation (Dithane M-45) on day 0 of the hatching period embryonic mortality markedly increased. 88% of the treated embryos were dead. Results from the combined administration of cadmium-sulphate and an 80% mancozeb containing fungicide formulation (Dithane M-45) caused higher embryomortality with respect to individual toxicity test of cadmium-sulphate and fungicide in our study.

Animals↗
PubMed2005

Urinary cadmium and serum levels of estrogens and androgens in postmenopausal Japanese women.

BACKGROUND: Recent laboratory studies have suggested that cadmium is an estrogenic compound and may be a potential risk factor for breast cancer. METHODS: We investigated the relationship between urinary cadmium concentrations and serum concentrations of estrone, testosterone, and dehydroepiandrosterone sulfate in 164 postmenopausal Japanese women. RESULTS: There was a significant positive association between the urinary cadmium and serum testosterone levels after controlling for age and body mass index. The mean testosterone level was 28% higher in women with high urinary cadmium (> or = 3.00 microg/g creatinine) than in those with low urinary cadmium (< 2.00 microg/g creatinine). Urinary cadmium was not significantly associated with serum estrone and dehydroepiandrosterone sulfate levels. Additional adjustment for smoking, alcohol and reproductive factors including known risk factors for breast cancer did not substantially alter the results. CONCLUSION: Data suggested that cadmium exposure is associated with increased testosterone levels. As high testosterone levels have been associated with the risk of breast cancer, the involvement of cadmium exposure in breast cancer risk should be evaluated in future studies.

Aged↗
PubMed1987

Characterization of metal binding peptides from cadmium resistant plant cells.

The majority of the cellular cadmium (less than 80%) in cadmium resistant Datura innoxia cells is bound to a small, metal induced peptide which is not metallothionein. This peptide consists of glutamate, cysteine and glycine in a ratio between 2:2:1 and 3:3:1 and has an apparent molecular weight of 776, under denaturing conditions. It is heat stable and complexes with cadmium to produce multimeric forms which are separable by gel filtration. Chemical analyses suggest that some amino acids are not joined by classical peptide linkages. This indicates that the synthesis of the peptide may not be directed by mRNA and that induction of its synthesis may not involve increased transcription from a putative gene corresponding directly to this peptide. A smaller proportion (greater than 15%) of the cellular cadmium is bound to a larger compound which is also heat stable and binds copper more readily than cadmium in vivo. This larger compound has an amino acid composition similar, in some respects, to metallothioneins.

Amino Acids↗
PubMed1985

Selenium deficiency and detoxication functions in the rat: effect of chronic dietary cadmium.

Male rats from moderately selenium-deficient dams were fed a Torula yeast-based, selenium-deficient diet for 7 weeks, with or without added supplements of sodium selenite (0.2 ppm selenium) and cadmium chloride (50 ppm cadmium) in the drinking water. Cadmium caused about 10% body-weight loss in selenium-deficient, as well as in supplemented rats. Glutathione peroxidase activity in liver 105,000 g supernatant and in erythrocyte hemolysate from selenium-deficient rats was about 1% and 3%, respectively, of that in supplemented rats. A cadmium-induced decrease of glutathione peroxidase activity was found in erythrocyte and liver preparations from selenium-supplemented rats, while cadmium caused an increase of the liver activity in selenium deficiency. Selenium deficiency per se caused a significant decrease of cytochrome P-450 content, while cadmium treatment did not modify further the content of this enzyme. NADPH-cytochrome c reductase was not changed by selenium regimen or cadmium treatment, while cytochrome b5 was increased on cadmium treatment of the supplemented rat. The microsomal metabolism of N,N-dimethylaniline showed a decrease of the cytochrome P-450-dependent C-oxygenation in selenium-deficient groups. Cadmium treatment had no further significant effect. The flavin-containing monooxygenase, which performs N-oxygenation of N,N-dimethylaniline, was decreased significantly by cadmium treatment in selenium deficiency. Selenium deficiency seems thus to be connected with higher susceptibility to cadmium-induced impairments of liver detoxication functions, although progressive accumulation of cadmium in the liver appears to produce only modest effects.

Aniline Compounds↗
PubMed1989

[Activity of certain salivary enzymes in school children exposed to excessive concentrations of lead and cadmium].

The purpose of the study was assessment of the effect of an environment contaminated with heavy metals on the activity of certain enzymes of mixed saliva. The activity was determined of total acid phosphatase and phosphatase resistant to tartrate and formaldehyde, alkaline phosphatase, alanine and aspartate aminotransferase, and alpha-amylase. The studied material comprised 110 saliva samples obtained from three groups of children aged 8 years. Group I of 21 children lived in Szopienice, group II of 30 children lived in Miasteczko Slaskie. In both these localities the children were exposed to mean daily concentrations, above the permitted ones, mainly of lead compounds, in lower degree to cadmium and zinc compounds. Environment contamination in Szopienice was greater than in Miasteczko Slaskie. Group III of 59 children living in Lubowice served as controls. In that town the permissible concentrations of these compounds were not exceeded. Statistical analysis of these results showed that the activity of total acid phosphatase in groups I and II, that is in the contaminated areas, was highly significantly greater than in the control group. The activity of alkaline phosphatase was raised only in the saliva in group I. No differences were found in the activity of alpha-amylase and aminotransferases.

Acid Phosphatase↗
PubMed2006

Phenotypic anchoring of arsenic and cadmium toxicity in three hepatic-related cell systems reveals compound- and cell-specific selective up-regulation of stress protein expression: implications for fingerprint profiling of cytotoxicity.

Exposure of cells to toxic chemicals is known to up-regulate the expression of a number of stress proteins (SPs), including metallothionein (MT) and members of the heat shock protein (HSP) family, and this response may allow the development of a fingerprint profile to identify mechanisms of toxicity in an in vitro toxicology setting. To test this hypothesis, three hepatic-derived cell culture systems (rat hepatoma FGC4 cell line, rat hepatocytes, human hepatoma HepG2 cell line) were exposed to cadmium (as CdCl2) and arsenic (as NaAsO2), two compounds believed to exert their toxicity through an oxidative stress mechanism, under conditions of phenotypic anchoring defined as minimal and mild toxicity (approximately 5 and 25% reduction in neutral red uptake, respectively). The expression of six SPs--MT, HSP25/27, HSP40, HSP60, HSP70, and HSP90--was then determined by ELISA. Expression of four of these SPs--MT, HSP25/27, HSP40 and HSP70--was up-regulated in at least one experimental condition. However, the patterns of expression of these four SPs varied across the experimental conditions, according to differences in toxicant concentration and/or level of toxicity, cell-type and toxicant itself. This lack of uniformity in response of a focussed set of mechanistically defensible targets suggests that similar problems may emerge when using more global approaches based on genomics and proteomics, in which problems of redundancy in targets and uncertain mechanistic relevance will be greater.

Animals↗
PubMed1978

Long-term effectiveness of dietary iron and ascorbic acid in the prevention and cure of cadmium toxicity in rats.

The protective and curative effects of dietary iron and ascorbic acid on chronic (180 days) cadmium toxicity in rats were examined. Growth retardation and anemia were observed in rats fed a diet containing 50 ppm of cadmium for 180 days; during this period the contents of iron in the liver, kidney, spleen, testis, intestine, and tibia decreased and the zinc contents of the liver and kidney increased, but the calcium content of bone did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the cadmium-containing diet overcame the growth retardation and anemia due to cadmium toxicity and reduced the tissue levels of cadmium; however, it did not restore the zinc contents in the liver, kidney, and bone to normal. Similar effects were observed when these compounds were added to cadmium containing diet for 90 days after feeding the cadmium diet alone for 90 days. The glutamic-pyruvic transminase and glutamic-oxaloacetic transminase activities in the plasma of rats fed the cadmium diet increased significantly and these increases were prevented by supplementing the diet with iron and ascorbic acid. Glucose, urea, and alkaline phosphatase in the plasma and glycogen in the liver were not changed by feeding the cadmium diet for 180 days. These results indicate the long-term effectiveness of supplementing the diet with iron and ascorbic-acid for preventing and curing dietary cadmium toxicity in rats.

Animals↗
PubMed2003

Metal-1,4-dithio-2,3-dihydroxybutane chelates: novel inhibitors of the Rho transcription termination factor.

Rho is an enzyme that is essential for the growth and survival of Escherichia coli, and bicyclomycin (1) is its only known selective inhibitor. We show that metal (Cd(2+), Ni(2+), and Zn(2+)) complexes of 1,4-dithio-2,3-dihydroxybutanes (2) serve as effective and potent rho inhibitors with I(50) values that can exceed that of 1. Maximal inhibition for ZnCl(2) and L-dithiothreitol (2a) corresponded to Zn(2):L-DTT stoichiometry. The I(50) value for the 2:1 Zn-L-DTT solution was 20 microM, which made it 3 times more potent than 1 (I(50) = 60 microM). Kinetic studies showed that a Zn-L-DTT solution functioned as a noncompetitive inhibitor with respect to ATP in the rho poly(C)-dependent ATPase assay and as a competitive inhibitor with respect to ribo(C)(10) in the poly(dC).ribo(C)(10)-stimulated ATPase assay. These findings demonstrated that both 1 and a Zn-L-DTT solution disrupted rho-mediated ATP hydrolysis but that they inhibit using different mechanisms. Substitution of L-DTT with 1,2-ethanedithiol in ZnCl(2) solutions led to a comparable loss of rho poly(C)-dependent ATPase activity, indicating that other metal chelates can serve as efficient inhibitors. The site and pathway of rho inhibition by the putative metal-1,4-dithio-2,3-dihydroxybutane chelates are discussed in light of the current data.

Adenosine Triphosphatases↗
PubMed1975

Metabolism and toxicity of cadmium, mercury, and lead in animals: a review.

Cadmium, mercury, and lead are toxic to humans and animals. Although cadmium and inorganic mercury toxicities occur in humans, they have not been observed in domestic livestock under practical conditions. In contrast, cattle, especially young calves, are extremely susceptible to lead toxicity. Apparently, cattle are more tolerant of cadmium than are other animal species. Due partially to higher absorption and longer retention times in the body, the alkyl mercuries, especially methyl mercury, are more toxic than inorganic mercury compounds. Inorganic forms of cadmium, mercury, and lead are poorly absorbed from the intestine. However, due to lack of effective homeostasis, after absorption retention time is long. Injected cadmium, mercury, and lead are metabolized differently from that naturally absorbed. Most cadmium and mercury are in kidney and liver (50 and 23% of total body in goats); but highest total load of methyl mercury is in muscle (72% in cows). With low to moderate body burden, most lead is retained in the skeleton. However, beyond a certain point, the kidney accumulates large quantities. Only minute amounts of cadmium and mercury are secreted into milk, but milk is only moderately well protected from dietary lead. Likewise, little cadmium and inorganic mercury pass the placental barrier whereas lead and methyl mercury pass more readily.

Animals↗
PubMed2004

cis-Bis[1,3-bis(2-fluorophenyl)triazenido-kappa2N1,N3]bis(pyridine-kappaN)cadmium(II).

In the title compound, [Cd(C12H8F2N3)2(C5H5N)2], the Cd atom lies on a crystallographic twofold axis in space group Iba2. The coordination geometry about the Cd(II) ion corresponds to a rhombically distorted octahedron, with two deprotonated 1,3-bis(2-fluorophenyl)triazenide ions, viz. FC6H4NNNC6H4F-, acting as bidentate ligands (four-electron donors). Two neutral pyridine (py) molecules complete the coordination sphere in positions cis with respect to one another. The triazenide ligand is not planar (r.m.s. deviation = 0.204 A), the dihedral angle between the phenyl rings of the terminal 2-fluorophenyl substituents being 24.6 (1) degrees. The triazenide and pyridine Cd-N distances are 2.3757 (18)/2.3800 (19) and 2.3461 (19) A, respectively. Intermolecular C-H.F interactions generate sheets of molecules in the (010) plane.

Journal Article↗
PubMed2006

Di-mu2-sulfito-kappa8O,O':O',O''-bis[(2,4,6-tri-2-pyridyl-1,3,5-triazine-kappa3N2,N1,N6)cadmium(II)] octahydrate.

The title compound, [Cd2(SO3)2(C18H12N6)2].8H2O, is a dimer built up around a symmetry center, where the sulfite anion displays a so far unreported coordination mode in metal-organic complexes; the anion binds as a mu2-sulfite-kappa4O,O':O',O'' ligand to two symmetry-related seven-coordinate Cd(II) cations, binding through its three O atoms by way of two chelate bites with an O atom in common, which acts as a bridge. The cation coordination is completed by a 2,4,6-tri-2-pyridyl-1,3,5-triazine ligand acting in its usual tridentate mode.

Journal Article↗
PubMed2005

Natural analcime zeolite modified with 5-Br-PADAP for the preconcentration and anodic stripping voltammetric determination of trace amount of cadmium.

A procedure for separation and preconcentration of trace amounts of cadmium has been proposed. A column of analcime zeolite modified with benzyldimethyltetradecylammonium chloride and loaded with 2-(5-bromo-2-pyridylazo)-5-diethylaminophenol (5-Br-PADAP) was used for retention of cadmium. The cadmium was quantitatively retained on the column at pH approximately 9 and was recovered from column with 5 ml of 2 M nitric acid with a preconcentration factor of 140. Anodic stripping differential pulse voltammetry was used for determination of cadmium. A 0.05 ng/ml detection limit for the preconcentration of aqueous solution of cadmium was obtained. The relative standard deviation (RSD) for eight replicate determinations at the 1 microg/ml cadmium levels was 0.31% (calculated with the peak height obtained). The calibration graph using the preconcentration system was linear from 0.01 to 150 microg/ml in final solution with a correlation coefficient of 0.9997. For optimization of conditions, various parameters such as the effect of pH, flow rate, instrumental conditions and interference of number of ions, were studied in detail. This method was successfully applied for determination of cadmium in various complex samples.

Alloys↗
PubMed2002

Cadmium detoxification processes in the digestive gland of cephalopods in relation to accumulated cadmium concentrations.

The high concentrations of cadmium recorded in the digestive gland of cephalopods from various temperate and subpolar waters suggest that these molluscs have developed efficient cadmium detoxification mechanisms. The subcellular distribution of cadmium in the digestive gland cells was investigated in seven cephalopod species from the Bay of Biscay (France) and the Faroe Islands. In most species, cadmium was mainly found in the cytosolic fraction of the digestive gland cells, reaching up to 86% of the total cadmium for the squid Loligo vulgaris from the Bay of Biscay. But species with the highest total level of cadmium showed a higher percentage of cadmium associated to insoluble compounds. The quantification of metallothioneins (MTs) by the polarographic method was performed in order to evaluate the involvement of these proteins in the detoxification of the high amounts of bioaccumulated cadmium. Metallothionein levels in cephalopods ranged form 742 +/- 270 to 3478 +/- 1572 microg/g wet weight. No relationship could be established between total cadmium, cytosolic cadmium and MT levels suggesting the occurrence of other Cd-binding ligands. Although these proteins have not been characterised, as cadmium in the digestive gland of cephalopods is mainly associated with soluble ligands, a high potential transfer to predators can be predicted.

Animals↗
PubMed1995

Effect of chelators, monoisoamyl meso-2,3-dimercaptosuccinate and N-(4-methylbenzyl)-4-O-(beta-D-galactopyranosyl)-D-glucamine-N-carbodit hioate, on cadmium and essential element levels in mice.

In experiments performed on male mice (ICR) the mobilizing effect of monoisoamyl meso-2,3-dimercaptosuccinate (Mi-ADMS) and a dithiocarbamate analogue, N-(4-methylbenzyl)-4-O-(beta-D-galactopyranosyl)-D-glucamine-N-carbod ithioate (MeBLDTC) on the cadmium deposits was studied. The influence of these compounds on the changes in the level of essential elements caused by cadmium was explored. CdCl2.H2O was injected intravenously. The chelators were administered every 48 h over 12 d. Both compounds are effective in mobilizing cadmium from the body in animal experiments. On an equimolar basis MeBLDTC was superior to Mi-ADMS. Mi-ADMS can, however, be administered orally. Both compounds were able to correct, at least partly, the changes in the level of essential elements caused by cadmium.

Animals↗
PubMed2000

Dynamics of dendritic calcium transients evoked by quantal release at excitatory hippocampal synapses.

Synaptic N-methyl-D-aspartate (NMDA) receptors detect coincident pre- and postsynaptic activity and play a critical role in triggering changes in synaptic strength at central synapses. Despite intensive study of synaptic plasticity, relatively little is known about the magnitude and duration of calcium accumulation caused by unitary events at individual synapses. We used fluorescence imaging to detect NMDA receptor-mediated miniature synaptic calcium transients (MSCTs) caused by spontaneous release of synaptic vesicles in dendrites of cultured hippocampal neurons. MSCTs originated focally in dendritic regions <1 microm in length and decayed with a time constant of 0.35 +/- 0.03 s. Multiple occurrences of MSCTs recorded at single sites had fluctuating amplitudes, with a coefficient of variation of 0.34. From the reduction in the spatial spread of MSCTs with decreasing concentration of indicator dye, we estimated that the dominant endogenous calcium buffer in dendrites is relatively immobile (diffusion coefficient between 10 and 50 microm(2)/s). We conclude that calcium rise caused by spontaneous quantal synaptic NMDA receptor activation (i) is variable, (ii) lasts for a time period briefer than previous measurements indicate, and (iii) is confined by endogenous calcium buffers to local dendritic regions even when synapses are not on spines.

Aniline Compounds↗
PubMed2001

Examination of cadmium(II) complexation by the Suwannee River fulvic acid using 113Cd NMR relaxation measurements.

Aquatic and terrestrial fulvic acids are environmentally important because they affect the bioavailability and transport of metal ions. Prior studies demonstrated that Cd(ll) binds to the oxygen containing functional groups of fulvic acids. The complexation of Cd(II) is further investigated in this study using 113Cd NMR relaxation measurements for solutions of the Suwannee River fulvic acid (SRFA). Spin-lattice (T1) and spin-spin (T2) relaxation times are measured over a range of Cd(II):SRFA ratios. The results clearly indicate two types of Cd(II) binding sites for the SRFA. A series of model ligands was also examined to gain further understanding of the two types of binding motifs present in the fulvic acid. The results for a model compound containing several carboxylate functionalities in near proximity correspond very closely to the results obtained for the strong binding sites of the Cd(II)-SRFA complexes.

Algorithms↗
PubMed1986

Structural effects in the dithiocarbamate-enhanced biliary excretion of cadmium.

The dithiocarbamate enhancement of the biliary excretion of cadmium in rats loaded with cadmium (by either the oral or sc route) was found to be strongly dependent on the structure of the groups attached to the nitrogen atom of the dithiocarbamate moiety. Those dithiocarbamates containing hydroxyl-bearing attached groups were found to be capable of causing the greatest enhancement of the cadmium content of the bile. For the compounds of this type that were examined, this enhancement of biliary cadmium content varied from 30-fold to over 2000-fold. No enhancement of the biliary excretion of cadmium was found subsequent to the administration of sodium diethyldithiocarbamate, though this compound is known to cause a significant increase in the fecal excretion of cadmium.

Administration, Oral↗