• 동의생리병리학회지
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• 제16권6호
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• pp.1243-1252
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• 2002

To experiment the effects between cadmium inhalation toxicity and extracts of Folium Mori, rat inhalation exposure groups were exposed to cadmium aerosol in air by whole-body inhalation exposure for 6 hours/day, 5 days/week, and 4 weeks. Cadmium concentration in the air of cadmium aerosol was 1.02㎎/㎥ and mass median diameter(MMD) was 1.40μm. Intraperitoneal injection of extracts of Folium Mori to inhalation exposure groups was done for 4 weeks and the results were as follows: The highest body weight gain for 4 weeks and food intake per day were 126.39g/4 weeks and 19.18g/day from inhalation exposure group III, respectively. The highest lung and liver weight were 1.27g and 8.19g from inhalation exposure group II, respectively. The highest kidney weight was 1.805g from inhalation exposure control. The lowest cadmium content in lung was 86.39μg/g from inhalation exposure group III. The lowest cadmium concentration in blood was 7.12㎍/㎗ from inhalation exposure group III. Cadmium concentrations of 40.02㎍/g in liver and 69.18㎍/g in kidney were the lowest from inhalation exposure group I and III, respectively. For weekly cadmium concentration in urine, the value of the fourth week from inhalation exposure group III was the highest, 3.12㎍/㎖. For weekly cadmium concentration in feces, the value of the fourth week from inhalation exposure group III was the highest, 2.67 ㎍/g. The highest metallothionein concentration in lung was 74.65㎍/g from inhalation exposure group III and the highest metallothionein concentration in liver was 386.84㎍/g from inhalation exposure group II. The highest metallothionein concentration in kidney was 236.17 ㎍/g from inhalation exposure group II.

• Environmental Analysis Health and Toxicology
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• 제17권1호
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• pp.53-61
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• 2002

Histopathological changes and cadmium accumulations in the gills were investigated in crucian carp (Carassius auratus) exposed to 0, 0.01, 0.1, 0.5 mg/1 cadmium (Cd) concentrations for 25 days. After 25 days of exposure. cadmium accumulations increased in each of the different exposure concentrations. Histopathological changes in the gills of curcian carp exposed to cadmium included the acidification of mucous cell, the terminal clubbing of lamellae, the hyperplasia of epitherial cell and the curved of secondary lamellae. The similar histopathological changes were observed once the accumulations of cadmium reached the similar levels found in the present study with the different exposure schemes. Also the acidification of mucous cell in gills appeared when cadmium accumulations reached 5 $\mu\textrm{g}$/g and more. These results suggested that histopathological changes in the gills, an appearance of mucous cell acidification. be used to estimate the relation between toxic effect and cadmium accumulations in the gills.

• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2003년도 춘계학술대회
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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.

• 한국환경보건학회지
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• 제22권4호
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• pp.91-101
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• 1996

Exposure indices are important tools which enable scientists to reliably predict and detect exposures to xenobiotics and resultant cell injury. Since the de novo synthesis of stress proteins can be detected early after exposure to some agents, analysis of toxicant-induced changes in gene expression, i.e. alterations in patterns of protein synthesis, may be useful to develop as biomarkers of exposure and toxicity. The acute and chronic effects of cadmium(Cd, $CdCl_2$ 20 mg/kg) on Wistar male rats were evaluated concerning cadmium contents, tissues enzyme activity, HSP expression. The results of the study were as follows: 1. Less cadmium was absorbed through the digestive tracts, but the ratio of contents in renal to hepatic cadmium was higher at 8 weeks after treatment. 2. ALT(alanine aminotransferase), AST(aspartate aminotransferase), glucose, BUN(blood urea nitrogen), creatinine, the key indices of the clinical changes in hepatic and renal function were significantly changed by the cadmium treatment after 1 week in liver, after 4 weeks in kidney. 3. Enhanced synthesis of 70 KDa relative molecular mass proteins were detected in 2 hours after cadmium exposure, with maximum activity occurring at 8~48 hours. Induction of $HSP_{70}$ was evident at proximal tubules and glomeruli in kidney. Testicular cells produced enough HSP to be detected normally. From the above results, it could be concluded that $HSP_{70}$ induction by the cadmium treatment was a rapid reaction to indicate the exposure of xenobiotics.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.167.1-167.1
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• 2003

The human exposure level of cadmium can be varied by environmental level of cadmium and individual life style. This study was conducted to estimate current exposure of cadmium using up-to date in Korea. The exposure estimates were intended to representative of the general adult group with 60kg. This study quantified human exposure level of cadmium through food, air and soil except water because domestic all data was not detected. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-1
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• pp.73-73
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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. (omitted)

• Safety and Health at Work
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• 제11권2호
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• pp.235-240
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• 2020

Background: Cadmium exposure may induce chronic intoxication with renal damage. Silver soldering may be a source of cadmium exposure. Methods: We analyzed working environment measurement data and periodic health screening data from a small-scale silver soldering company with ten workers. Concentrations of cadmium in air from working environment measurement data were obtained. Concentrations of blood and urinary cadmium, urine protein, and urine β2-microglobulin (β2M) were obtained. The generalized linear model was used to identify the association between blood and urine cadmium and urine β2M concentrations. Clinical features of chronic cadmium intoxication focused with toxicological renal effects were described. Results: The mean duration of work was 8.5 years (standard deviation [SD] = 6.9, range = 3-20 years). Cadmium concentrations in air were ranged from 0.006 to 0.015 mg/㎥. Blood cadmium concentration was elevated in all ten workers, with a highest level of 34.6 ㎍/L (mean = 21.288 ㎍/L, SD = 11.304, range = 9.641-34.630 ㎍/L). Urinary cadmium concentration was elevated in nine workers, with a highest level of 62.9 ㎍/g Cr (mean = 22.151 ㎍/g creatinine, SD = 19.889, range = 3.228-62.971 ㎍/g creatinine). Urine β2M concentration was elevated in three workers. Urinary cadmium concentration was positively associated with urine protein concentration (beta coefficient = 10.27, 95% confidence interval = [4.36, 16.18]). Other clinical parameters were compatible with renal tubular damage. Conclusion: Cadmium intoxication may occur at quite low air concentrations. Exposure limit may be needed to be lowered.

• Journal of Preventive Medicine and Public Health
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• 제54권6호
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• pp.471-480
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• 2021

Objectives: Cadmium is widely used, leading to extensive environmental and occupational exposure. Unlike other organs, for which the harmful and carcinogenic effects of cadmium have been established, the hepatotoxicity of cadmium remains unclear. Some studies detected correlations between cadmium exposure and hepatotoxicity, but others concluded that they were not associated. Thus, we investigated the relationship between cadmium and liver damage in the general population. Methods: In total, 11 838 adult participants from National Health and Nutrition Examination Survey 1999-2015 were included. Urinary cadmium levels and the following liver function parameters were measured: alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), total bilirubin (TB), and alkaline phosphatase (ALP). Linear and logistic regression analyses were performed to assess the associations between urinary cadmium concentrations and each liver function parameter after adjusting for age, sex, race/ethnicity, annual family income, smoking status, alcohol consumption status, physical activity, and body mass index. Results: The covariate-adjusted results of the linear regression analyses showed significant positive relationships between log-transformed urinary cadmium levels and each log-transformed liver function parameter, where beta±standard error of ALT, AST, GGT, TB, and ALP were 0.049±0.008 (p<0.001), 0.030±0.006 (p<0.001), 0.093±0.011 (p<0.001), 0.034±0.009 (p<0.001), and 0.040±0.005 (p<0.001), respectively. Logistic regression also revealed statistically significant results. The odds ratios (95% confidence intervals) of elevated ALT, AST, GGT, TB, and ALP per unit increase in log-transformed urinary cadmium concentration were 1.360 (1.210 to 1.528), 1.307 (1.149 to 1.486), 1.520 (1.357 to 1.704), 1.201 (1.003 to 1.438), and 1.568 (1.277 to 1.926), respectively. Conclusions: Chronic exposure to cadmium showed positive associations with liver damage.

• Toxicological Research
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• 제26권2호
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• pp.131-136
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• 2010

The time-dependent changes in cadmium (Cd) concentration were studied in Female Sprague-Dawley (SD) rats during and after Cd exposure via drinking water (10 and 50 ppm) for 30 days. The cadmium concentration in muscle, liver, kidney, blood plasma, and urine, and the metallothionein concentration in blood plasma were determined every 10 days during exposure and every 7 days after exposure for 3 weeks. The muscle Cd concentration did not change during, and neither after, exposure. The liver Cd concentration increased from 1.4 to 3.3 (at 10 ppm) and from 6.1 to 10.1 folds (at 50 ppm) during exposure and remained higher than those of controls in both groups even during post-exposure period. The kidney Cd concentrations were 2.3 to 5.1 (at 10 ppm) and 4.9-14.0 folds (at 50 ppm) higher than those of controls during exposure and also remained elevated during the post-exposure period. Plasma Cd concentrations were not significantly different from those of controls in both groups. Urine Cd concentrations were more than 2 folds (at 10 ppm) and 6.5 to 12.6 folds (at 50 ppm) higher than those of controls but rapidly decreased over the 7 days of withdrawal. Blood plasma metallothionein concentrations were more than 2.4 folds (at 10 ppm) and 3.1 to 7.4 folds (at 50 ppm), and they remained elevated till 7 days (10 ppm) and 14 days (at 50 ppm) after exposure. Our data support that Cd in urine could be a useful biomarker during Cd exposure period and metallothionein in blood plasma could be as a supportive biological marker for during and post Cd exposure.

• Fisheries and Aquatic Sciences
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• 제23권8호
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• pp.23.1-23.10
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• 2020

This study was conducted to evaluate the acute effects of waterborne cadmium exposure on bioaccumulation and antioxidant enzymes in eels (Anguilla japonica) and to determine the median lethal concentration (LC₅₀). Fish were exposed to different cadmium concentrations (0, 0.15, 0.30, 0.61, 1.83, 3.08, 3.67, 4.29, and 5.51 mg L^-1) for 96 h. The LC₅₀ of A. japonica to cadmium was 3.61 mg L^-1. Cadmium accumulation generally increased in tissues with increasing waterborne cadmium concentrations. At ≥ 1.83 mg L^-1 exposure, all tissues accumulated significant cadmium concentrations compared with the control group, in the order of kidney > liver > gill > spleen > muscle. Measurements of variation in actual cadmium concentrations showed that a reduction of the metal in experimental water was related to cadmium accumulation in tissues. As activity alteration of antioxidant enzymes for reactive oxygen species, superoxide dismutase and catalase activities increased at ≥ 0.61 mg L^-1 significantly, glutathione peroxidase and glutathione S-transferase activities were not significantly changed. The results of this study suggest that acute exposure to waterborne cadmium is potentially fatal to A. japonica due to the metal's major accumulation in various tissues and the effect of antioxidant enzyme activity.