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PubMedDate not supplied

Optimization of chelating agent structure for the mobilization of aged renal and hepatic cadmium deposits: sodium N-benzyl-4-O-(beta-D-galactopyranosyl)-D-glucamine-N-carbodithioate.

An examination of the structure-activity relationships for the mobilization of intracellular cadmium by previously synthesized dithiocarbamates indicates that superior compounds can be prepared by increasing the molecular weight by using bulky polar but nonionic substituents. This suggested the synthesis and characterization of sodium N-benzyl-4-O-(beta-D-galactopyranosyl)-D-glucamine-N-carbodithioate++ +. The preparation of this compound and its characterization as an agent for the mobilization of aged renal and hepatic cadmium deposits in mice show it to be superior to the compounds reported earlier which have been used for this purpose. Five ip injections at 0.40 mmol/kg reduced hepatic cadmium levels to 35% of their initial level and renal cadmium levels to 37%. The nature of the structural factors responsible for the efficacy of such agents is outlined as well as the relationship of these to the toxicity of the compounds and their cadmium complexes. These factors indicate clearly the differences in the molecular requirements for the mobilization of extracellular and intracellular toxic metal ions. The requirement that intracellular toxic metals be mobilized places several constraints on the structures of potentially efficacious compounds in addition to the thermodynamic and kinetic restrictions imposed by the requirements for extracellular efficacy.

Animals↗

PubMed2004

Functional characterization of mouse alpha4beta2 nicotinic acetylcholine receptors stably expressed in HEK293T cells.

Mouse alpha4beta2 nicotinic acetylcholine receptors (nAchRs) were stably expressed in HEK293T cells. The function of this stable cell line, termed mmalpha4beta2, was assessed using an aequorin-based luminescence method that measures agonist-evoked changes in intracellular calcium. Agonist-elicited changes in intracellular calcium were due primarily to direct entry of calcium through the alpha4beta2 channel, although release of calcium from intracellular stores contributed approximately 28% of the agonist-evoked response. Agonist pharmacologies were very similar between the mmalpha4beta2 cells and most cell lines that stably express human alpha4beta2 nAchRs. Based on agonist profiles and sensitivity to the antagonist dihydro-beta-erythroidine (DHbetaE), the predominant alpha4beta2 nAchR expressed in the mmalpha4beta2 cells exhibits a pharmacology that most resembles the DHbetaE-sensitive component of 86Rb+ efflux from mouse brain synaptosomes. However, when evaluated with the aequorin assay, the mmalpha4beta2 nAchR was found to be atypically sensitive to blockade by the presumed alpha7-selective antagonist methyllycaconitine (MLA), exhibiting an IC50 value of 31 +/- 0.1 nm. Similar IC50 values have been reported for the MLA inhibition of nicotine-stimulated dopamine release, a response that is mediated by beta2-subunit-containing nAchRs and not alpha7-subunit-containing nAchRs. Consequently, at low nanomolar concentrations, MLA may not be as selective for alpha7-containing nAchRs as previously thought.

Acetylcholine↗

PubMed1986

Effects of dithiocarbamates on cadmium distribution and excretion in chronically exposed rats.

One month after termination of a 3-mo exposure of rats to cadmium (Cd in drinking water at a concentration of 50 mg/l), the effects of dithiocarbamate analogs on the excretion and distribution of the cadmium were determined. Sodium salts of three dithiocarbamates [sodium bis(hydroxyethyl) dithiocarbamate, DEDTC; sodium N-methyl-D-glucamine dithiocarbamate, MGDTC; and sodium 4-carboxamidopiperidine dithiocarbamate, INADTC] were given to rats ip 2 times at 2.46 mmol/kg. In the following administration of the first injection of DEDTC, cadmium excretion via the urine amounted to 15.8 micrograms and via bile amounted to 124.4 micrograms Cd. Following administration of MGDTC, the urinary and biliary excretions of cadmium were 14.5 and 47 micrograms, respectively, while in the case of INADTC the corresponding values were 23.6 and 7.9 micrograms cadmium. In control animals the urinary and biliary excretion per 12 h reached 0.09 and 0.12 micrograms Cd. Gel permeation chromatography (GPC) analysis of bile revealed differences in the distribution of Cd in the elution fractions after the first injections of the individual dithiocarbamates. For all three dithiocarbamates, significant decreases of the concentrations of cadmium in the liver and kidney were found. DEDTC (but neither of the other compounds) increased the concentration of cadmium in the brain from control levels of 49 +/- 5 ppb to 105 +/- 16 ppb.

Administration, Oral↗

PubMedDate not supplied

An international literature survey of "IARC Group I carcinogens" reported in mainstream cigarette smoke.

The International Agency for Research on Cancer (IARC) currently lists 44 individual chemical agents, 12 groups or mixtures of chemicals and 13 exposure circumstances as "Group 1 human carcinogens". A comprehensive search of the published literature revealed that nine of the 44 chemical agents classified as "Group I carcinogens" by IARC have been reported to occur in mainstream cigarette smoke. The other 35 have never been reported to occur in cigarette smoke. The nine agents reported are benzene, cadmium, arsenic, nickel, chromium, 2-naphthyl-amine, vinyl chloride, 4-aminobiphenyl and beryllium. The reported yields of each of these nine agents in mainstream smoke varies widely. The range of yields reported for a given compound is influenced by the type of cigarette tested and when the analysis was conducted. In micrograms/cigarette, the ranges that have been reported for each of the nine compounds are: benzene (0.05-104), cadmium (0-6.67), arsenic (0-1.4), nickel (0-0.51), chromium (0.0002-0.5), 2-naphthylamine (0.0002-0.022), vinyl chloride (0.0013-0.0158), 4-aminobiphenyl (0.00019-0.005) and beryllium (0-0.0005). Although some of the variation in reported yields may be due to differences in analytical methodology, several correlations between the yield of a particular chemical in mainstream smoke and certain cigarette characteristics were observed. For example, charcoal filtration was associated with reduced vinyl chloride, and the concentration of sodium nitrate in the tobacco was positively correlated with the mainstream yield of both 2-naphthylamine and 4-aminobiphenyl. Benzene yield in mainstream cigarette smoke was correlated with the amount of tobacco burned and with the 'tar' level. Agronomic factors such as production practices and soil characteristics, and environmental conditions such as rainfall, reportedly influence the accumulation of metals, for example, cadmium, beryllium, chromium, nickel and arsenic, in the leaf. The use of fertilizers low in nitrate and heavy metals would be expected to substantially reduce the yields of most of the "IARC Group 1 carcinogens" reported to occur in mainstream cigarette smoke. Additionally, modifications in cigarette design, for instance, the use of enhanced charcoal filters or heated instead of burned tobacco, would also be expected to reduce the yields of several of these agents.

2-Naphthylamine↗

PubMed1988

Temperature regulation in laboratory mammals following acute toxic insult.

The purpose of this paper is to provide a concise review of the effects of acute chemical toxicity on thermoregulation in mammals, with particular emphasis on the effects of xenobiotic compounds in laboratory rodents. It has been shown that acute administration of compounds such as nickel, cadmium, lead, and some pesticides causes a reduction in the body temperature of mice when tested at normal room temperatures. When provided with the option of selecting their preferred ambient temperature, the toxic-treated animals generally select cool temperatures which augment the hypothermic effect of the toxic compounds. It would appear that many of the xenobiotic compounds have central as well as peripheral effects on the control of body temperature. That is, the hypothermic animals select cool temperatures, a condition indicative of a centrally mediated decrease in the set-point. This decrease in set-point, or regulated hypothermia, may be beneficial to survival since the lethality of most xenobiotic compounds increases with rising body temperature. The observation that acute doses of various compounds leads to behaviorally and autonomically mediated changes in body temperature may have significant implications for the measurement of other biological effects of these chemical agents (e.g., CNS dysfunction, bradycardia, immunosuppression).

Animals↗

PubMed2001

A study of the coordination environment in aqueous cadmium-thiol complexes by EXAFS spectroscopy: experimental vs. theoretical standards.

Using EXAFS, we investigated the changes in the local structure of Cd(II) complexes formed with a series of low-molecular-weight thiols at different thiol/cadmium stoichiometries. For dilute solutions, a comparison of theoretical and experimental standards proved the latter approach superior. The number of bound oxygen atoms decreased while the number of sulfur atoms increased as the thiol/cadmium ratios increased, indicating that up to four thiol compounds can bind to cadmium in aqueous solutions. The computer code FEFFIT was modified to employ experimental and theoretical standards with equal facility.

Journal Article↗

PubMed1986

Selenium deficiency and detoxication functions in the rat: short-term effects of cadmium.

Weanling rats were fed a Torula yeast-based selenium-deficient diet with or without supplementation of sodium selenite (0.2 ppm selenium) in the drinking water. After 5-6 weeks on the diet regimens, the liver glutathione peroxidase activity of the selenium-deficient groups had decreased to about 1% of the supplemented groups, and the rats were then used in experiments. Cadmium-induced effects on the drug-metabolizing system of the liver were measured as the microsomal capacity to perform N- and C-oxygenation of N, N-dimethylaniline. Cadmium in vitro caused a decrease of the cytochrome P-450-dependent C-oxygenation. This effect tended to be more prominent in the selenium-deficient groups. On the other hand, N-oxygenation was increased when cadmium was added in vitro, and no significant difference was found between selenium-deficient and -supplemented groups. However, as was found for the capacity to perform C-oxygenation, there was a tendency for lower N-oxygenation in the selenium-deficient rat. Lipid peroxidation, measured as thiobarbituric acid reactive substances in liver homogenates, was higher in selenium-deficient groups after in vivo treatment or in vitro addition of cadmium, and preincubation or phenobarbital induction enhanced this selenium-dependent difference. Although, the selenium-deficient rat seems more susceptible to cadmium-induced disturbances, 5-6 weeks of selenium deficiency was not enough to cause prominent impairment on the drug-metabolizing system as measured here and with the doses used in the present study.

Aniline Compounds↗

PubMed1991

[Experimental study of toxic properties of dimethylcadmium].

The article presents the results of research into the physical, chemical and toxicological properties of metallo-organic compound dimethylcadmium. Through functional, morphologic and biochemical technique, in acute, pre-acute and chronic experiments on animals, established were the major toxicometric parametres, the substance's action on the blood system, respiration, functioning of the kidney, the liver, the CNS and the gonads. The data showed that, if inhaled, dimethylcadmium was more toxic than the other cadmium non-organic compounds, being a polythropic poisonous substance with particular damaging effects on the kidney, the liver, the CNS and the respiratory organs. The MAC for dimethylcadmium concentrations in the working zone air was proposed at 0.001/0.005 mg/m3.

Acute Disease↗

PubMed1995

Relationships between metal ions and oxygen free radicals in ethanol-induced damage to cultured rat gastric mucosal cells.

The current study investigated whether metal ions were cytoprotective against ethanol-induced injury to cultured rat gastric mucosal cells in vitro. Secondly, the relationships between oxygen free radicals and cytoprotection by metal ions were examined. Cultured cells exposed to ethanol produced superoxide anion, as assessed by reduction of cytochrome c, in a time-related fashion, and the production of superoxide anion increased dose-dependently as the concentration of ethanol increased. Cellular damage increased proportionately to the production of superoxide anion. ZnCl2, AlCl3, CoCl2, CuCl2, and CdCl2 significantly diminished ethanol-induced injury dose-dependently. All of the agents studied decreased the reduction of cytochrome c in ethanol-induced damage dose-dependently. These results led to the conclusions that: (1) cultured rat gastric mucosal cells exposed to ethanol generate oxygen free radicals; (2) the production of oxygen free radicals is closely linked with ethanol-induced damage to the cells; and (3) metal ions decrease ethanol-induced gastric mucosal cell damage in vitro. Metal ions protect cultured rat gastric mucosal cells from ethanol-induced damage in which oxygen free radicals participate.

Aluminum Chloride↗

PubMed1991

Choroid plexus protects cerebrospinal fluid against toxic metals.

Although heavy metal ions are known to be toxic to the central nervous system (CNS), the mechanisms by which the CNS may protect itself from initial challenges of such toxic ions is unknown. The choroid plexus is the principal site of formation of the cerebrospinal fluid (CSF) which bathes the brain. We have determined in rats and rabbits that after intraperitoneal administration of lead, cadmium, mercury, and arsenic compounds, these toxic metal ions accumulated in the lateral choroid plexus at concentrations of Pb, Hg, and As that were 70-, 95-, and 40-fold higher, respectively, than those found in the CSF. Cd was not detected in the CSF. In addition, concentrations of these heavy metal ions were found to be many fold greater in the choroid plexus than in the brain or blood. The accumulation of Pb in the choroid plexus was dose-dependent and time-related. When the choroid plexus was preincubated, in vitro, with ouabain (1.5 mM), the uptake of Cd from the CSF side of the choroid plexus was inhibited 57%. Cadmium metallothionein was not found in the choroid plexus. Whereas the concentration of reduced glutathione in the choroid plexus was less than that in the brain cortex, the concentration of cystine was fourfold greater. The lateral choroid plexus sequesters Pb, Cd, As, and Hg. It appears to be one of the important mechanisms that protects the CSF and the brain from the fluxes of toxic heavy metals in the blood.

Animals↗

PubMed2001

Syntheses of semiconductor nanoparticles using single-molecular precursors.

Methods for the preparation of II-VI, III-V, and II-V as well as other compound semiconductor nanoparticles using main group single-molecular precursors have been developed. The work involves the design and synthesis of compounds containing all the elements required within the desired nanoparticulate material. Precursors are tailored to give reproducible, clean decomposition at moderate temperatures, leading to high quality, defect free, mono-dispersed nanoparticles. In this article we cover key aspects of precursor and nanoparticle synthesis. One of the more successful and reproducible series of single-source precursors used, and the one on which we have concentrated our research efforts, is the bis(dialkyldithio-/diseleno-carbamato)cadmium(II)/zinc(II) compounds, M(E(2)CNR(2))(2) (M = Zn or Cd, E = S or Se, and R = alkyl) for the preparation of chalcogenide nanoparticulate materials. Preliminary mechanistic studies suggest that the precursor to nanoparticle deposition route is strongly influenced by the alkyl substituent groups present, and may well determine the phase and quality of the final metal chalcogenide nanoparticles produced. Herein we discuss the synthesis of semiconductor nanoparticles using such single-molecular precursors.

Journal Article↗

PubMed1994

[Evaluation of the toxic effects of cadmium on the body in light of research on the behavior of lipid compounds in aortic walls of animals].

The goal of this project was to observe certain paths of lipid metabolism in the aorta under the influence of chronic cadmium poisoning. A statistically very significant concentration of cadmium was found in the aortic walls of poisoned rats. However, the concentration of cadmium was not changed in the blood serum, where only a slight tendency towards increase was observed. Among the lipid compounds traced in the blood serum, a considerable increase in triglycerides was observed. The increase in the concentration of total cholesterol in the aortic wall was slight but statistically significant. The concentration of other analyzed lipids--i.e. free fatty acids, triglycerides and phospholipids--did not change. The above observations suggest the hypothesis of the possible development of atherosclerotic changes resulting from chronic cadmium poisoning.

Animals↗

PubMed1996

Inhibition of acetylcholinesterase activity as effect criterion in acute tests with juvenile Daphnia magna.

In this work we investigated the possibility of using the enzyme acetylcholinesterase (AChE) activity in Daphnia magna homogenates, both in vivo and in vitro conditions, as a specific method for rapid toxicity evaluations. The results from in vivo and in vitro AChE inhibition tests were compared with 48 hours EC50 values obtained in conventional acute bioassays. EC50 values from in vivo AChE inhibition tests were: 2.4 micrograms/l for parathion, 0.2 microgram/l for paraoxon; DCA and cadmium at the concentrations tested had no effects on enzyme activity. I50 values were 764 micrograms/l for parathion, 0.08 micrograms/l for paraoxon and 3367 micrograms/l for cadmium; DCA did not affect AChE activity measured in in vitro conditions. EC50 values from conventional acute tests were: 2.2 micrograms/l for parathion, 0.2 microgram/l for paraoxon, 163 micrograms/l for DCA and 9.5 micrograms/l for cadmium. Our results indicated that the in vivo AChE inhibition test is selective, being very sensitive to detect toxicity of the organophosphates tested. The in vitro AChE inhibition assay is less time consuming, requires less human effort and produces less toxic waste than conventional acute bioassays and the in vivo AChE inhibition test. However, it does not take into account the effect of the metabolization of the toxicants inside live organisms; since the organophosphate metabolism may be activative or degradative, the toxic potential of the parent compound may be under or over evaluated in in vitro conditions.

Aniline Compounds↗

PubMed1982

Histochemical staining of cadmium with benzothiazolylazonaphthol derivatives.

Searching for a chelator with increased sensitivity for use as cadmium stain, a number of benzothiazolylazonaphthol derivatives were synthesized and their staining properties for cadmium and zinc were examined. Benzothiazolylazo-beta-naphthol and -naphthol AS (BTAN-AS) stained cadmium with the highest staining intensity and the most precise localization. Poststaining techniques for differential staining using oxine solution made it possible to distinguish cadmium in the presence of interference by other metals. The observed lowered molar absorptivity of BTAN-AS is believed to be due to the ortho effect of the anilide group of naphthol AS. The solubility of the chelator appears to be a critical factor in the formulation of molecules with higher chelator sensitivities for metal staining.

Animals↗

PubMed2006

[Cd2(Te6O13)][Cd2Cl6] and Cd7Cl8(Te7O17): novel tellurium(IV) oxide slabs and unusual cadmium chloride architectures.

Initial attempts to prepare new Ln-Cd-Te-O-Cl compounds led to the isolation of two novel cadmium tellurium(IV) oxychlorides with two different types of structures, namely, [Cd(2)(Te(6)O(13))][Cd(2)Cl(6)] and Cd(7)Cl(8)(Te(7)O(17)). Both compounds feature novel polymeric tellurium(IV) oxide anions and unusual cadmium chloride substructures. The structure of [Cd(2)(Te(6)O(13))][Cd(2)Cl(6)] is composed of 1D [Cd(2)Cl(6)](2)(-) double chains and (002) [Cd(2)(Te(6)O(13))](2+) layers. The 1D Te(6)O(13)(2)(-) slab of the [Cd(2)(Te(6)O(13))](2+) layer is formed by TeO(3), TeO(4), and TeO(5) groups via corner- and edge-sharing, and it contains six- and seven-membered tellurium(IV) polyhedral rings. The structure of Cd(7)Cl(8)(Te(7)O(17)) features a 3D network with long-narrow tunnels along the b axis. The two types of structural building blocks are 1D [Te(7)O(17)](6)(-) anions and unusual corrugated [Cd(7)Cl(8)](6+) layers based on "cyclohexane-like" Cd(3)Cl(3) rings.

Journal Article↗

PubMed1995

Effect of cadmium on human ovarian cancer cells with acquired cisplatin resistance.

Cadmium (Cd) dichloride is a compound that has teratogenic, mutagenic, and carcinogenic properties. Recent reports have suggested the possibility that this compound may also have tumor suppressive properties in some settings. For these reasons, we have studied the subcellular pharmacological profile of elemental cadmium in human ovarian cancer cells, when administered as cadmium dichloride. The cell lines A2780 and A2780/CP70 were used, which are well characterized with respect to their cellular response to platinum-based compounds. Cd was measured in all experiments with the use of atomic absorbance spectrometry with Zeeman background correction. In both cell lines, there were direct relationships between; drug dose and cellular accumulation of drug; cellular accumulation of drug and DNA damage levels; and DNA damage levels and cytotoxicity. These cell lines differed in that the cisplatin-resistant A2780/CP70 cell line, was also comparatively resistant to cadmium dichloride. This enhanced cellular resistance appeared to be mediated through decreased drug accumulation, and increased cellular tolerance to higher levels of DNA damage. Total genomic DNA repair and cytosolic inactivation of drug appeared not to differ substantively between these two cell lines.

Cadmium↗

PubMed1989

Cadmium-induced alterations of chlorpropham metabolism in isolated rat hepatocytes.

In order to investigate the various steps of chlorpropham (CIPC) metabolism which could be influenced by cadmium, isolated rat hepatocytes were incubated in the presence of CIPC (0.1 mM) and of increasing Cd concentrations (0-180 microM). The results showed that Cd accumulation in hepatocytes was in good correlation to its concentration in the incubation medium. At 90 microM Cd, hydroxylation of CIPC was only slightly decreased by 30%, while CIPC hydrolysis into 3-chloraniline was unaffected by the presence of Cd. Accordingly, unchanged CIPC increased in hepatocytes. At 27 microM Cd, free 4-hydroxychlorpropham (4-OHCIPC) increased in the intracellular medium as a consequence of a strong suppression of both sulfation and glucuronidation which was related to the strong depletion of the intracellular ATP level under the combined influences of both cadmium and free 4-OHCIPC. Acetylation of 3-chloroaniline, which represents a minor pathway of CIPC metabolism, was already markedly suppressed (43%) with the lowest Cd concentration (27 microM). These in vitro results suggest that Phase II reactions are more sensitive to Cd than Phase I processes and that Cd enhanced the CIPC cytotoxicity as shown by alterations of the membrane integrity.

Acetylation↗

PubMed2006

Effects of cadmium on aneuploidy and hemocyte parameters in the Pacific oyster, Crassostrea gigas.

Pacific oysters, Crassostrea gigas, are commonly reared in estuaries where they are exposed to anthropogenic pollution. Much research has been made on the toxicity of cadmium to aquatic organisms because the compound recurrently contaminates their environment. Our study examined the influence of cadmium on aneuploidy level (lowered chromosome number in a percentage of somatic cells) and hemocyte parameters in C. gigas at different stages of life. Adults and juveniles were exposed to two different concentrations of cadmium. The first concentration applied was equivalent to a peak value found in Marennes-Oléron bay (Charente-Maritime, France; 50 ngL(-1)) and the second was 10 times higher (500 ngL(-1)). Exposure to 50 ngL(-1) cadmium caused a significant decrease in the survival time of C. gigas, but exposure to 500 ngL(-1) surprisingly affected the survival time positively. Significant differences in aneuploidy level were observed between the cadmium treatments and the control in adults but not in juveniles or the offspring of the adult groups. The effects of cadmium on hemocyte parameters were analyzed by flow cytometry. Several hemocyte parameters increased significantly after 21 days of cadmium exposure and subsequently decreased. Phenoloxidase-like activity, evaluated by spectrophotometry, varied over the time of the experiment and increased after 66 days of contact with 500 ngL(-1) cadmium. Taken together, cadmium at environmentally relevant concentrations seems to have only moderate effects on aneuploidy and hemocyte parameters.

Age Factors↗