• Journal of Microbiology and Biotechnology
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• v.4 no.1
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• pp.20-23
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• 1994

The polymerase chain reaction was used to study the genes inducible under stress from the heavy metal cadmium. Schizosaccharomyces pombe, grown in the presence or absence of sublethal concentration of cadmium, was isolated to purify the total RNAs. The Induced RNA Random Fishing (IRRF) method in which random oligonucleotides were used as primers was applied to the identification of cadmium-induced gene expressions. A PCR-DNA product of 400-bp was cloned and sequenced. Computer analysis showed that this DNA has no homology with any known DNA sequences in GenBank or EMBL databases. The induction of this gene was confirmed by Northern blot analysis of total RNAs isolated from both cadmium-treated and untreated yeast cells.

• Biomedical Science Letters
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• v.12 no.4
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• pp.371-374
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• 2006

This study was carried out to investigate the relationship of the cadmium and lead levels in blood by age, gender and smoking status among 181 students in Gyeongnam province from June 2005 to July 2006. The cadmium and lead levels in blood was analyzed by atomic absorption spectrophotometer. Subjects were classified for the investigation according to smoking status as smokers and nonsmokers, age and gender. Mean blood cadmium level in male and female was $1.65{\mu}g/dl,\;1.10{\mu}g/dl$ respectively. Male was significantly higher than that of female. Blood cadmium levels in heavy smokers ($11{\sim}20\;ea/day$) and light smokers ($1{\sim}10\;ea/day$) were $2.34{\mu}g/dl,\;1.10{\mu}g/dl$ respectively. Heavy smokers were significantly higher than those of light smokers. In the comparison of age, gender and smoking status in blood Lead levels were no significant differences. In conclusion, heavy smoking was the most significant risk factor to increase blood cadmium levels. The further study will need analysis of the other factors related to the elevation of the cadmium and lead levels.

• Environmental Analysis Health and Toxicology
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• v.19 no.4
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• pp.389-399
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• 2004

Metallothionein (MT), a small protein molecule which can bind or release metal ions, is involved in the regulation of cellular metal homeostasis. This study was investigated the accumulation of cadmium in blood, tissue (liver, kidney and brain), and the effect of cadmium on several key genes (MT-I, MT-II, ZnT-1) in zinc metabolism in the mouse. Mouses weighing 20∼25 g were randomly assigned to control and cadmium treated group (Cd group). Cd group was intraperitoneally injected with cadmium 2, 4, 8 mg/kg and control group was administerd with saline. Mouses of each group were sacrificed by decapitation 4 hours after the administration of cadmium. Cadmium contents in blood, liver, kidney and brain were increased by a dose-dependent manner. Accumulation of cadmium was mainly occurred in liver and kidney. Induction of MT-I and MT-II protein was increased, but ZnT-1 expression was decreased in a dose-dependent manner by the treatment of 2∼8 mg/kg cadmium. These results suggested that cadmium can be transported to brain and alter the expression of several key genes in zinc homeostasis.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2003.05a
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• pp.107-107
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• 2003

The heavy metal cadmium is a xenobiotic toxicant of environmental and occupational concern and it has been classified as a human carcinogen. Inhalation of cadmium has been implicated in the development of emphysema and pulmonary fibrosis, but, the detailed mechanism by which cadmium induces adverse biological effects is not yet known. Therefore, we undertook the investigation of genes that are induced after cadmium exposure to illustrate the mechanism of cadmium toxicity For this purpose, we employed the polymerase chain reaction-based suppression subtractive hybridization technique. We identified 29 different cadmium-inducible genes in human peripheral mononuclear cells, such as macrophage migration inhibitory factor, lysophosphatidic acid acyltransferase-${\alpha}$, enolase-1${\alpha}$, VEGF, Bax, neuron-derived orphan receptor-1, and Nur77, which are known to be associated with inflammation, cell survival, and apoptosis. Induction of these genes by cadmium treatment was further confirmed by semi-quantitative reverse-transcription polymerase chain reaction. Further, we found that these genes were also induced after cadmium exposure in normal human lung fibroblast cell line, WI-38, suggesting potential use of this induction profile to monitor cadmium toxicity in the lung. Next, Nur77, one of cadmium-inducible genes, was further studied since the products of Nur77 are known to be involved in the apoptotic process of lung cells. Following cadmium treatment, Nur77 gene expression was increased at protein-level in A549 cells. Consistently, the reporter containing Nur77 binding sequence was activated by 2.5-fold after exposure to cadmium in reporter gene analysis by transient transfection experiments. When the plasmid encoding dominant negative Nur77 that represses the transcriptional function of wild-type Nur77 was transfected into A549 cells, the expression of Bax was significantly reduced, suggesting that induction of Nur77 was an important process in cadmium-induced apoptosis in the cells. Cadmium induced the expression of Nur77 in vivo, confirming the relevance of the data obtained in viro. Together our results suggest that Nur77 gene expression in exposure to cadmium leads apoptosis of lung cells which may cause pathological changes in lung.

• Analytical Science and Technology
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• v.20 no.4
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• pp.355-360
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• 2007

The title complex, $(C_3H_{12}N_2)[\{Cd(H_2O)(C_6H_5O_7)\}_2]{\cdot}6H_2O$, I, has been prepared and its structure characterized by FT-IR, EDS, elemental analysis, ICP-AES, and X-ray single crystallography. It is triclinic system, $P{\bar{1}}$ space group with a = 10.236(2), b = 11.318(2), c = $13.198(2){\AA}$, ${\alpha}=77.95(1)^{\circ}$, ${\beta}=68.10(1)^{\circ}$, ${\gamma}=78.12(1)^{\circ}$, V = $1373.5(3){\AA}^3$, Z = 2. Complex I has constituted by protonated 1,3-diaminopropane cations, citrate coordinated cadmium(II) anions, and free water molecules. The central cadmium atoms have a capped trigonal prism geometry by seven coordination with six oxygen atoms of three different citrate ligands and one water molecule. Citrate ligands are bridged to three different cadmium atoms. Each cadmium atom is linked by carboxylate and hydroxyl groups of citrate ligand to construct an one-dimensional ladder-type assembly structure. The polymeric crystal structure is stabilized by three-dimensional networks of the intermolecular O-H${\cdots}$O and N-H${\cdots}$O hydrogen-bonding interaction.

• Analytical Science and Technology
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• v.20 no.1
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• pp.41-48
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• 2007

The determination method for the trace lead and cadmium in glass materials was developed by ICP-AES. The lead- and cadmium-DDTC chelates were formed by adding Na-DDTC (sodium diethyldithiocarbamate) as a chelating agent and extracted into MIBK (methyl-isobutyl ketone). Direct measuring of the trace lead and cadmium in glass was not possible because of the interferences of matrix elements as Na, Si, Mg and Ca of glasses unless solvent extraction of lead and cadmium was applied. This procedure was confirmed to be valid quantitative method of Pb and Cd analysis in glass did not influence of sample matrix, by applying it procedure to artifact sample and NIST SRM 1412.

• Journal of Ginseng Research
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• v.37 no.1
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• pp.37-44
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• 2013

Korean red ginseng is known to regulate the immune system and help the body struggle infection and disease. Cadmium is widely distributed in the environment due to its use in industry. Exposure to cadmium is problematic causing organ dysfunction. This study was conducted to evaluate the protective effect of Korean red ginseng extract (RGE) against cadmium-induced hepatotoxicity in rats. In experiments, animals were orally administrated with RGE (25, 50 mg/kg) for 7 d and then intravenously injected with cadmium ($CdCl_2$, 4 mg/kg) to induce acute hepatotoxicity. Cadmium caused the elevated levels of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase in serum. In contrast, pretreatment with RGE significantly reduced those serum indexes related with liver damage. In histopathological analysis, RGE decreased the centrilobular necrosis around central veins and the peripheral hemorrhage around portal triads. Moreover, RGE restored the deficit in hepatic glutathione level resulting from cadmium treatment. RGE also inhibited the increase in the expression of Bad, a representative apoptosis marker protein, induced by cadmium treatment. Collectively, these results demonstrate that RGE can reduce the cadmium-induced hepatic toxicity, partly via anti-oxidative and anti-apoptotic process.

• Environmental Analysis Health and Toxicology
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• v.3 no.1_2
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• pp.43-54
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• 1988

Experiment was performed to investigate the immunotoxicity of cadmium administered orally and the effect of ginseng petroleum ether fraction on it. Mice were given 3, 30, or 300 ppm cadmium as cadmium chloride orally in the drinking water and injection of ginseng petroleum ether fraction intraperitoneally for 4 weeks. Mice were sensitized and challenged with sheep red blood cells (S-RBC). Humoral immune response was evaluated by antibody production and Arthus reaction. Body weight gain, spleen weight, thymus weight, and liver weight were also measured. In the present study, cadmium generally suppressed the humoral immunity. There was decrease in the rate of body weight gain and liver weight to body weight by cadmium-administration. Ginseng petroleum ether fraction showed restoring effect, to some extent, on the decrease in PFC and in the rate of liver weight to body weight by cadmium-administration. But it more suppressed Arthus reaction.

• Journal of Environmental Health Sciences
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• v.17 no.1
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• pp.110-119
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• 1991

This study was performed to investigate the applicability of 9 chromosome aberration and sister chromatid exchange analysis for the assessment of cytotoxicity and cytogenetic effects of cadmium. Induction of chromosome aberration and sister chromatid exchange in CHO-K1 cells and human peripheral lymphocytes by 2 hour-treatment of CdCl$_{2}$ with various concentrations was observed in relation to their frequencies and types of aberration. The frequency of chromosome aberration in CHO cells treated with CdCl$+{2}$ at G$_{1}$ was increased with dose-dependent manner. When human peripheral lymphocytes were treated with cadmium at G0 and harvested at 72 hours there after, the response was dose-dependent and all the aberrations were also chromatid types. There was no significant increase in frequencies of sister chromatid exchange in both CHO cells and human lymphocytes treated with different concentrations of cadmium. It was suggested that SCE analysis was not a good assessment method for cadmium toxicity.

• Proceedings of the KSME Conference
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• 2008.11a
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• pp.244-249
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• 2008

It happened a failure on special bolt which supported main landing gear actuator up-lock rod of 00 aircraft. Fracture was occurred at end of center drilled hole and thread machined on bolt. Metallographic, fractographic, and other characteristics of embrittlement analysis and experiments carried out on the failed bolt to find out the reason. Bolt surface was cadmium electroplated(EP) to give lubrication and provide excellent corrosion resistance. Resultly, Bolt was failed due to cadmium embrittlement occurred during baking treatment as well as center drilled hole. for the failure that are relevant to failure analysis and prevention. For their successful functional application, cadmium EP bolts require proper and adequate baking treatment after electroplating, and is complete with no center drilled hole