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PubMed2004

Inhibitory effect of cadmium and tobacco alkaloids on expansion of porcine oocyte-cumulus complexes.

Studies aimed at the influence of smoking on reproductive functions have found out fertility disorders in smokers occurring at any stage of reproductive processes. In our experiments the role of cadmium, nicotine and anabasine was investigated in the expansion of oocyte-cumulus complexes (OCC) isolated from large antral porcine follicles. Suppression of FSH-induced cumulus expansion and significant inhibition of synthesis and accumulation of hyaluronic acid in the cell/matrix compartment of the OCC was observed in the presence of different concentrations of tested compounds. The suppressive effect of cadmium and tobacco alkaloids on the cumulus expansion was accompanied by decreased progesterone production by cumulus cells during 42 h incubation of the OCC with FSH.

Alkaloids↗
PubMed2006

Cadmium induced mitochondrial injury and apoptosis in vero cells: protective effect of diallyl tetrasufide from garlic.

Oxidative stress and mitochondrial injury has been implicated in cadmium-induced apoptosis. In this study, we examined the protective effect of diallyl tetrasulfide from garlic on cadmium induced oxidative stress and apoptosis in vero cells. Exposure of vero cells to cadmium (10 microM) for 18 h showed the apoptotic events such as loss of cell viability, alterations in nuclear morphology and decreased mitochondrial membrane potential with significantly increased levels of reactive oxygen species (super oxide anion and hydrogen peroxide). Treatment of vero cells with cadmium (10 microM) and diallyl tetrasulfide (5-50 microg/ml) showed that diallyl tetrasulfide attenuated the cadmium-induced suppression of cell viability in a dose dependent manner and highly significant effect was observed at 40 microg/ml. The nuclei morphological analysis with 4',6-diamidino-2-phenylindole staining confirmed that diallyl tetrasulfide at 40 microg/ml prevented the Cd (10 microM) induced apoptosis. Flow cytometric analysis with 2',7'-dichlorofluorencein diacetate showed that the inhibitory effect of diallyl tetrasulfide (10-40 microg/ml) on reactive oxygen species generation parallel with its effect on cell viability. In addition, diallyl tetrasulfide (40 microg/ml) remarkably reduced the cadmium-induced accumulation of superoxide radical and hydrogen peroxide with in cells. Further, diallyl tetrasulfide significantly protected the cadmium-induced decrease in mitochondrial membrane potential, an indicator of mitochondrial function. Our study suggest that diallyl tetrasulfide affect the reactive oxygen species generation induced by cadmium, and possesses a novel protective effect on the cytolethality associated with mitochondrial injury, which contributes to the antiapoptotic effect of diallyl tetrasulfide against cadmium.

Allyl Compounds↗
PubMed1991

A comparative study of the influence of vicinal dithiols and a dithiocarbamate on the biliary excretion of cadmium in rat.

The effect of two vicinal dithiols, 2,3-dimercaptopropan-1-ol (BAL) and N-(2,3-dimercaptopropyl)phthalamidic acid (DMPA), and a dithiocarbamate, sodium N-(4-methoxybenzyl)-D-glucamine dithiocarbamate (MeOBGDTC), on the biliary excretion of cadmium was examined in rats. Tissue cadmium levels were also determined following the measurements of biliary excretion of cadmium. At 30 min after the injection of CdCl2.2.5H2O (1 mg/kg, iv) each rat was given 400 mumol/kg ip of one of the compounds, BAL, DMPA or MeOBGDTC. While all the compounds increased the biliary excretion of cadmium, the most effective was MeOBGDTC, whose administration resulted in a 580% increase in biliary cadmium content. The effectiveness of the MeOBGDTC may be due to the presence of both nonpolar and nonionizing polar groups attached to nitrogen. MeOBGDTC was able to mobilize cadmium to the bile even after the occurrence of the synthesis of metallothionein and the incorporation of the cadmium into it. An attempt was also made to determine the chemical nature of the Cd-MeOBGDTC complex present in the bile by comparing a newly synthesized authentic sample of Cd(MeOBGDTC)2 complex with the hot dioxane extract of the freeze-dried bile samples using thin-layer chromatography and proton NMR. The results suggested that cadmium excreted in the bile in part, is complexed to MeOBGDTC and glutathione.

Animals↗
PubMed1988

Acute toxicity of cadmium and zinc in the earthworm (Lumbricus terrestris).

Studies are continuing to explore the use of the earthworm (Lumbricus terrestris) for the determination of the acute toxicity of metal compounds. Worms were injected intraperitoneally with cadmium and zinc chlorides, and also zinc chloride followed by cadmium chloride to see if zinc could protect against the toxicity of cadmium. The 48 h acute toxicity (LD50) values were 22 and 23 mg/kg for Cd and Zn respectively and 30 mg/kg for Cd after the worms were pretreated with Zn. It appears that the earthworm can be a useful test subject for obtaining preliminary information on metal toxicity.

Animals↗
PubMed1992

Inhibition by germanium oxide of the mutagenicity of cadmium chloride in various genotoxicity assays.

The effects of germanium oxide on the genotoxicity of cadmium chloride were investigated. The incorporation of [3H]thymidine into testicular DNA was inhibited in mice injected ip with 1.35, 1.80 or 2.70 mg cadmium chloride/kg body weight. Germanium oxide (0.05 or 0.1 mg/kg body weight, sc) alone did not affect [3H]thymidine incorporation into testicular DNA but 0.05 mg germanium oxide/kg antagonized the inhibitory effect of 1.35 mg cadmium chloride/kg. However, combinations of the other doses of the two compounds did not show statistically significant antagonistic effects. Cadmium chloride significantly increased the frequencies of micronucleus formation in polychromatic erythrocytes, and of chromosome aberrations in the bone marrow of mice treated with 0.7, 1.4 or 2.7 mg/kg body weight, in a dose-related manner. These effects were inhibited by germanium oxide at doses of 0.1 or 0.5 mg/kg body weight, although germanium oxide alone did not affect micronucleus formation or the chromosome aberration rate. Cadmium chloride produced a dose-related increase in the frequency of sister chromatid exchanges in cultured human lymphocytes at concentrations of 5, 10 or 50 mumol. This effect was also inhibited by germanium oxide (0.05 or 0.1 mumol), although germanium oxide alone had no effect. There was a dose-related increase in the frequency of sperms with abnormal head morphologies from mice treated with 0.6, 1.1 or 2.2 mg cadmium chloride/kg body weight and this too was antagonized by the injection of germanium oxide (0.1 or 0.5 mg/kg body weight). Germanium oxide alone did not affect the frequency of sperm-head abnormalities.

Animals↗
PubMed1992

Evaluation of Drosophila melanogaster as an alternative animal for studying the neurotoxicity of heavy metals.

Heavy metals cause irreversible neurobehavioral damage in many developing mammals, but the mechanisms of this damage are unknown. The influence of three heavy metal compounds, triethyllead chloride, lead acetate and cadmium chloride, on lethality, development, behavior and learning was studied using the fruit fly, Drosophila melanogaster. This animal was used because it allows hundreds of subjects to be assayed very easily in individual experiments and because it is a system in which toxicological questions might be answered by using the techniques of modern molecular genetics. When triethyllead chloride, lead acetate or cadmium chloride was placed in the medium, the larval LC50 (+/- standard error) was found to be 0.090 +/- 0.004, 6.60 +/- 0.64 and 0.42 +/- 0.04 mM, respectively. Each of the tested compounds produced a dose-related delay in development. In particular, they caused a delay in the development of larvae to pupae. When larvae were reared on medium containing triethyllead chloride (0.06 mM), lead acetate (3.07 mM) or cadmium chloride (0.11 mM), phototaxis, locomotion and learning were not inhibited. Since significant neurobehavioral effects were not observed under the experimental conditions used, Drosophila does not appear to be an appropriate animal for the genetic dissection of such effects of heavy metals during development.

Animals↗
PubMed2006

Correlation between induction of DNA fragmentation in lung cells from rats and humans and carcinogenic activity.

Six chemicals, known to induce lung tumors in rats, were examined for their ability to induce DNA fragmentation in primary cultures of rat and human lung cells, and in the lung of intact rats. Significant dose-dependent increases in the frequency of DNA single-strand breaks and alkali-labile sites, as measured by the single-cell gel electrophoresis (Comet) assay, were obtained in primary lung cells from male rats with the following, minimally toxic, concentrations of the six test compounds: N-nitrosodimethylamine (NDMA; 2.5-10 mM), hydrazine (HZ; 0.5-4 mM), cadmium sulfate (CD; 31.2 and 62.5 μM), 4,4'-methylene bis (2-chloroaniline) (MOCA; 31.2-125 μM), isobutyl nitrite (IBN; 7.8-31.2 μM) and tetranitromethane (TNM; 1.9-15.6 μM). Similar degrees of DNA fragmentation were obtained in primary human lung cells; however, due to inter-donor differences, the minimum effective concentrations were in some donors lower and in others higher than in rats, and IBN induced DNA damage only in one of three donors. The DNA-damaging potency of HZ was higher in rats than in humans, and the opposite was true for MOCA. In agreement with these findings, statistically significant increases in the average frequency of DNA breaks were obtained in the lung of rats given a single oral dose (1/2 LD50) of the six test compounds. These findings give evidence that genotoxic lung carcinogens may be identified by use of the DNA fragmentation/Comet assay on rat lung cells as targets cells, and show that the six compounds tested produce in primary cultures of lung cells from human donors DNA-damaging effects substantially similar to those observed in rats.

Adenocarcinoma↗
PubMed1978

[Effect of cadmium on serum level of total protein and glycoprotein carbohydrate components in rats].

In experimental cadmium intoxication 100 rats were intraperitoneally injected with single doses of 0; 5 1,0, 2,0 5,0 mg Cd++/kg body weight as well as with 14 doses of 0,25 mg Cd++/kg. In the serum of animals the level of total protein and of glycoprotein carbohydrate components was determined. After doses in the range of cadmium concentration from 0,5 to 2,0 mg Cd++/kg body weight, a statistically and significant increase of the serum level of the protein-bound hexose hexoamine and sialic acids was stated. On the other hand the dose of 5,0 mg Cd++/kg caused only the increase of hexose in comparison with values of these constituents recorded in the control group. In animals receiving multiple doses of cadmium and also in those after a single administration of 1,0 mg Cd++/kg, a significant increase of the total protein level was started. The last group revealed the highest concentrations of protein and glycoprotein carbohydrate constituents on the third day after injection of cadmium while after 14 days, amouunts of these compounds approximated the levels estimated in the control group. A univocal evaluation of the obtained results is difficult, however in the mechanism of the quantitative alterations within the glycoprotein components of rats serum, the possibility of cadmium--induced biosynthesis of these compounds should be taken into consideration.

Animals↗
PubMed2006

Localization of S-nitrosoglutathione and expression of S-nitrosoglutathione reductase in pea plants under cadmium stress.

S-nitrosoglutathione (GSNO) is considered a natural nitric oxide (NO.) reservoir and a reactive nitrogen intermediate in animal cells, but little is known about this molecule and its metabolism in plant systems. In this work, using pea plants as a model system, the presence of GSNO in collenchyma cells was demonstrated by an immunohistochemical method. When pea plants were grown with a toxic Cd concentration (50 microM) the content of GSNO in collenchyma cells was drastically reduced. Determination of the nitric oxide (NO.) and gluthathione contents in leaves by confocal laser scanning microscopy and HPLC, respectively, showed a marked decrease of both compounds in plants treated with cadmium. The analysis of the S-nitrosoglutathione reductase (GSNOR) activity and its transcript expression in leaves showed a reduction of 31% by cadmium. These results indicate that GSNO is associated with a specific plant cell type, and this metabolite and its related catabolic activity, GSNOR, are both down-regulated under Cd stress.

Cadmium↗
PubMed1991

Regulation of cadmium induced porphyria by ascorbic acid in chick embryos.

Sublethal doses of cadmium chloride (2.5, 5.0 and 10.0 mu mole/kg egg weight) were found to significantly alter the first two rate limiting enzymes of heme biosynthesis in chick embryos. Delta-aminolevulinic acid synthase activity was elevated by 2.05 and 2.11 fold with 5.0 and 10.0 mu moles of cadmium treatment respectively. However, this was reduced to 1.25 and 1.3 fold by the simultaneous administration of ascorbic acid. Blood delta-aminolevulinic acid dehydratase (ALA-D) activity was decreased by 48.4 and 55.0 per cent with 5.0 and 10.0 mu moles cadmium treatment respectively; in the presence of ascorbic acid only 18 and 24 per cent inhibition of ALA-D activity was observed. Further 1.39 and 2.08 fold accumulation of delta-aminolevulinic acid and 4.17 and 4.62 fold increase of blood porphyrins was observed in chick embryos treated with 5.0 and 10.0 mu moles cadmium respectively. This elevation of intermediate compounds of heme biosynthesis was effectively checked by the administration of ascorbic acid. Depletion of hepatic heme and free sulfhydryl level by cadmium were countered by the treatment of ascorbic acid. Hence, the present findings suggest the protective role of ascorbic acid against cadmium induced chemical porphyria in chick embryos.

Animals↗
PubMed2004

Rapid determination of mono and dinitrophenols by DPP, in the presence of lead and cadmium and using concentrated CaCl2 electrolyte.

The contamination of drinking water and industrial wastewaters is a critical environmental problem. The nitrophenol, dinitrophenol, cadmium, and lead contaminants are classified as hazardous compounds. Their rapid determination may be obtained using differential pulse polarography with concentrated electrolyte. CaCl2, which is very soluble to levels exceeding 5 mol l(-1), allows separation of coalescent peaks at 0.1 mol l(-1). A systematic study undertaken from 0.1 to 5 mol l(-1) shows good separation of lead and cadmium from the organic compounds, and optimization of the electrolyte concentration according to the objective is described. Preconcentration of real samples is necessary because pollution levels are usually very low.

Cadmium↗
PubMed1989

Induction of SOS response in Escherichia coli strain PQ37 by 16 chemical compounds and human urine extracts.

The SOS Chromotest on Escherichia coli strain PQ37 was used to detect DNA damage induced by 16 chemical compounds and urine samples from smokers and a non-smoking psoriatic patient treated with mineral coal tar. The results confirmed the strong SOS inducing activity of 2-aminoanthracene and benzo[a]pyrene with metabolic activation and N-methyl-N'-nitro-N-nitrosoguanidine, mitomycin C and 4-nitroquinoline-N-oxide without metabolic activation. A weaker response in the absence of microsomal enzymes was observed with hydroxyurea (only at high doses) and the soluble Cr(VI) compounds potassium chromate and potassium dichromate. No effect was observed with ampicillin, cadmium chloride, cyclophosphamide, griseofulvin, the insoluble Cr(VI) compound lead chromate, the soluble Cr(III) compounds chromium nitrate, chromium chloride, chromium potassium sulphate, and the chelating agent sodium nitrilotriacetate. Among the Cr(III) compounds only chromium acetate produced a low but significant increase of SOS inducing activity. Solubilization by nitrilotriacetate of genotoxic Cr(VI) from insoluble lead chromate was observed, whereas no interaction occurred between nitrilotriacetate and the soluble Cr(VI) and Cr(III) compounds. Using urinary XAD-2 extracts, we found the SOS Chromotest poorly sensitive to the mutagens present in urine from tobacco smokers which, on the other hand, were detected by the gene mutation assay in Salmonella typhimurium (Ames test). A urine sample obtained from a psoriatic patient, therapeutically treated with mineral coal tar, had a significant SOS inducing activity with and even without metabolic activation, whereas in the Ames test it was active only in the presence of metabolic activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1987

Marked synergism of dimethylnitrosamine carcinogenesis in rats exposed to cadmium.

The combined carcinogenic effect of cadmium and dimethylnitrosamine (DMN) was examined in male Wistar rats, to test whether the previously observed synergism in mutagenicity between cadmium and 2 N-nitroso compounds would be paralleled by a synergism in carcinogenicity. In experiment 1, 50 five-month old rats received 18 mg DMN/kg i.p. followed by cadmium i.m. in two injections totaling either 1.5 or 3.0 mg Cd2+/kg. In experiment 2, 30 weanling rats received five i.m. doses totaling 6 mg Cd2+/kg followed by 18 mg DMN/kg. After 52 weeks, the incidence of renal tubular neoplasms was significantly increased above additivity in both experiments (P = 0.0005 to 0.017). Experiment 1 also showed a synergistic increase in the incidence of neoplastic (P = 0.024) and preneoplastic (P less than 0.01) microscopic liver lesions, of tumors of organs other than liver and kidney (P less than 0.01), of malignant versus benign tumors (P = 0.038), and of multiple versus single tumors (P = 0.0019). In experiment 2, the incidence of DMN-induced hepatocellular adenomas was significantly lower than additivity, suggesting an antagonistic, protective effect of cadmium pretreatment. The overall incidence of tumors of any type was 17.5 versus 67.7% in control (one agent or none) versus test animals. Malignant tumors included carcinomas, sarcomas, and lymphomas, involving nine different sites. Cadmium appears to enhance the initiation of carcinogenesis induced by DMN. Both cadmium and nitrosamines are known environmental contaminants present in air, food, water supplies, and tobacco smoke.

Animals↗
PubMed2004

Evaluation of immunotoxic and immunodisruptive effects of inorganic arsenite on human monocytes/macrophages.

A trivalent inorganic arsenic, arsenite, has been causing chronic inflammation in humans through the consumption of contaminated well water. The total peripheral blood arsenic concentrations of chronic arsenic-exposed patients, who had inflammatory-like immune responses, are less than 1 microM, thus, nM concentrations may be very important regarding the chronic inflammatory effects by arsenite. However, there are few reports about the biological effects of low concentrations of arsenite in mammalian cells, especially in normal immune effector cells. In this study, we examined whether arsenite has any biological and/or toxicological effects on the differentiation of human peripheral blood monocytes into macrophages using the colony-stimulating factor (CSF) in vitro compared with that of other metallic compounds, and found that arsenite sensitively inhibited the CSF-induced in vitro maturation of monocytes into macrophages at nM levels, and it also induced small, nonadhesive and CD14-positive abnormal macrophage generation from monocytes with granulocyte-macrophage CSF (GM-CSF) at 50-500 nM without cell death. The addition of other metallic compounds, including chromium, selenium, mercury, cadmium, nickel, copper, zinc, cobalt, manganese and other human pentavalent arsenic metabolites, such as inorganic arsenate, monomethylarsonic acid and dimethylarsinic acid, could not induce the same abnormal cell generation from monocytes with CSFs at any concentration and any additional time schedules; they showed only simple cytolethality in monocytes and macrophages at n-mM levels accompanied by cell death. This work may have implications in the arsenic-induced chronic inflammation in humans.

Arsenates↗
PubMed2000

Role of L- and N-type calcium channels in the pathophysiology of traumatic spinal cord white matter injury.

Recent work has suggested a potential role for voltage-gated Ca(2+) channels in the pathophysiology of anoxic central nervous system white matter injury. To examine the relevance of these findings to neurotrauma, we conducted electrophysiological studies with inorganic Ca(2+) channels blockers and L- and N-subtype-specific calcium channel antagonists in an in vitro model of spinal cord injury. Confocal immunohistochemistry was used to examine for localization of L- and N-type calcium channels in spinal cord white matter tracts. A 30-mm length of dorsal column was isolated from the spinal cord of adult rats, pinned in an in vitro recording chamber and injured with a modified clip (2g closing force) for 15s. The functional integrity of the dorsal column was monitored electrophysiologically by quantitatively measuring the compound action potential at two points with glass microelectrodes. The compound action potential decreased to 71.4+/-2.0% of control (P<0. 05) after spinal cord injury. Removal of extracellular Ca(2+) promoted significantly greater recovery of compound action potential amplitude (86.3+/-7.6% of control; P< 0.05) after injury. Partial blockade of voltage-gated Ca(2+) channels with cobalt (20 microM) or cadmium (200 microM) conferred improvement in compound action potential amplitude. Application of the L-type Ca(2+) channel blockers diltiazem (50 microM) or verapamil (90 microM), and the N-type antagonist omega-conotoxin GVIA (1 microM), significantly enhanced the recovery of compound action potential amplitude postinjury. Co-application of the L-type antagonist diltiazem with the N-type blocker omega-conotoxin GVIA showed significantly greater (P<0.05) improvement in compound action potential amplitude than application of either drug alone. Confocal immunohistochemistry with double labelling for glial fibrillary acidic protein, GalC and NF200 demonstrated L- and N-type Ca(2+) channels on astrocytes and oligodendrocytes, but not axons, in spinal cord white matter. In conclusion, the injurious effects of Ca(2+) in traumatic central nervous system white matter injury appear to be partially mediated by voltage-gated Ca(2+) channels. The presence of L- and N-type Ca(2+) channels on periaxonal astrocytes and oligodendrocytes suggests a role for these cells in post-traumatic axonal conduction failure.

Animals↗