• Environmental Analysis Health and Toxicology
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• v.19 no.1
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• pp.65-72
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• 2004

Environmental risk assessment of cadmium compounds was conducted using national monitoring data of aquatic and terrestrial compartments of local area. Aquatic and terrestrial toxicities of cadmium compounds on algae, daphnid, fish, earthworm, springtails and other species were evaluated. The toxicity data evaluated in this study were mainly from ECOTOX database provided by US EPA. Assessment factors were determined according to the EU technical guidance document and/or OECD proposal. Predicted no effect concentration (PNEC) values of aquatic and terrestrial toxicity were 25$\mu\textrm{g}$/L and 0.2 mg/kg, respectively and they were compared with cadmium exposure data of several local areas, which were used as Predicted exposure concentration(PEC) values. Most of the local area were found to be not risky. However, the risk values (PEC/NEC) of some metropolitan areas were greater than 1 when the most conservative PNEC value was applied.

• 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.

• Proceedings of the PSK Conference
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• 2003.10a
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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)

• Nutrition Research and Practice
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• v.3 no.1
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• pp.15-22
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• 2009

This study was performed to investigate the effect of chlorella on cadmium (Cd) toxicity in Cd-administered rats. Sixty male Sprague-Dawley rats (14 week-old) were blocked into 6 groups. Cadmium chloride was given at levels of 0 or 325 mg (Cd: 0, 160 ppm), and chlorella powder at levels of 0, 3 and 5%. Cadmium was accumulated in blood and tissues (liver, kidney and small intestine) in the Cd-exposed groups, while the accumulation of Cd was decreased in the Cd-exposed chlorella groups. Fecal and urinary Cd excretions were remarkably increased in Cd-exposed chlorella groups. Thus, cadmium retention ratio and absorption rate were decreased in the Cd exposed chlorella groups. Urinary and serum creatinine, and creatinine clearance were not changed in experimental animals. In addition, metallothionein (MT) synthesis in tissues was increased by Cd administration. The Cd-exposed chlorella groups indicated lower MT concentration compared to the Cd-exposed groups. Moreover, glomerular filtration rate (GFR) was not changed by dietary chI orella and Cd administration. According to the results above, this study could suggest that Cd toxicity can be alleviated by increasing Cd excretion through feces. Therefore, when exposed to Cd, chlorella is an appropriate source which counteracts heavy metal poisoning, to decrease the damage of tissues by decreasing cadmium absorption.

• Korean Journal of Clinical Laboratory Science
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• v.41 no.3
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• pp.111-122
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• 2009

Cadmium (Cd) is known to exert gonadotoxic and spermiotoxic effects. The present study was performed to investigate the morphological effects and metallothionein (MT) expression by zinc pretreatment in the course of time of cadmium-induced testicular injury in rat. Fifty male Spraque-Dawley rats weighing 160~180 g were divided into two groups : saline-pretreated cadmium group and zinc-pretreated cadmium group. Rats of two groups received subcutaneous injection of saline and 100 mg/kg $ZnSO_4$ at 0, 2, 5 and 8 hrs intervals respectively. Cadmium chloride (4.5 mg/kg $CdCl_2$) was administrated intraperitoneally at 2 hrs after zinc injection and rats were killed 0, 12, 24, 48 and 72 hrs later. Testicular tissue damages, interstitial (Leydig) cells status and MT expression were determined using hematoxylin-eosin stained sections and a computerized image analysis system on sections immunostained with a mouse anti-metallothionein respectively. Zinc pretreatment was significantly reduced testicular damages in five pathological categories after cadmium administation. The number of surviving interstitial cells was significantly higher in the zinc-pretreated group than in the saline-preatreated group at 48 and 72 hrs after cadmium administration. Non-damaged testis showed the positivity of MT staining in spermatogenic cells, Sertoli cells and endothelium of blood vessel, but not in the Leydig cells. The positivity of MT staining in saline-pretreated group was significantly reduced at 24 hrs after cadmium administration, whereas zinc-pretreated group showed strong MT positive staining similar to the 0 hr by 42 hrs after cadmium administration. In damaged testis, MT positive staining was also observed in the Leydig cells of both groups. These results suggest that a major preventive effect of zinc against cadmium-induced testicular toxicity may be due to its ability to reduce the cytotoxicity of cadmium in spermatogenic cells and Leydig cells by inhibiting the susceptibility of the testis to cadmium but not MT production by cadmium.

• Korean Journal of Clinical Laboratory Science
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• v.42 no.3
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• pp.136-148
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• 2010

Cadmium (Cd) is known to exert gonadotoxic and spermiotoxic effects. The present study was performed to investigate the morphological effects and metallothionein (MT) expression by zinc pretreatment in the course of time of cadmium-induced testicular injury in rat. Fifty male Spraque-Dawley rats weighing 160-180 g were divided into two groups: saline-pretreated cadmium group and zinc-pretreated cadmium group. Rats of two groups received subcutaneous injection of saline and 100 mg/kg $ZnSO_4$ at 0, 2, 5 and 8 hrs intervals respectively. Cadmium chloride (4.5 mg/kg $CdCl_2$) was administrated intraperitoneally at 2 hr after zinc injection and rats were killed 0, 12, 24, 48 and 72 hrs later. Testicular tissue damages, Interstitial (Leydig) cells status and MT expression were determined using hematoxylin-eosin stained sections and a computerized image analysis system on sections immunostained with a mouse anti-metallothionein respectively. Zinc pretreatment was significantly reduced testicular damages in five pathological categories after cadmium administation. The number of surviving interstitial cells was significantly higher in the zinc-pretreated group than in the saline-preatreated group at 48 and 72 hrs after cadmium administration. Non-damaged testis showed the positivity of MT staining in spermatogenic cells, Sertoli cells and endothelium of blood vessel, but not in the Leydig cells. The potitivity of MT staining in saline-pretreated group was significantly reduced at 24 hrs after cadmium administration, whereas zinc-pretreated group showed strong MT positive staining similar to the 0 hr by 42 hrs after cadmium administration. In damaged testis, MT positive staining was also observed in the Leydig cells of both groups. These results suggest a major preventive effect of zinc against cadmium-induced testiculat toxicity may be due to its ability to reduce the cytotoxicity of cadmium in spermatogenic cells and Leydig cells by inhibiting the susceptibility of the testis to cadmium but not MT production by cadmium.

• Journal of Environmental Health Sciences
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• v.21 no.3
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• pp.1-15
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• 1995

Tolerance to toxic effects of cadmium(Cd), including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicity and renal toxicity. Three groups of rats(A, B, C), each consisting of 52 rats, were studied and each group was divided into three subgroups(1,2,3), 28 rats for each subgroup. Rats were subcutaneously pretreated with saline(A), $CdCl_2$(0.5 mg/kg, B), and $ZnCl_2$(13.0 mg/kg, C) during time periods of 5 days. At the end of the period, rats were challenged with $CdCl_2$(3.0 and 6.0 mg/kg) by intraperitoneal injection. As for the cadmium levels in rat tissues after 1,3,5,6 days of pretreatments, it was highest in the liver. Then kidney, heart, blood and muscle followed it in that order. After 24, 48 and 96 hours of intraperitoneal injection by challenge doses the concentration of cadmium in liver and kidney increased proportionally to the increase of challenge dosage. However metallothioneins in liver and kidney were increased by the pretreatment of cadmium and zinc. These data indicate the liver is a major target-organ of acute Cd poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to short-term exposure to cadmium. This result suggest that increasing cadmium concentrations, gradually accumulating in liver and kidney as the result of the pretreatment, served to induce the synthesis of metallothionein, thus making them resistant to the challenge from cadmium.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.29-30
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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 cadmiumhas 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.(omitted)

• Journal of environmental and Sanitary engineering
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• v.9 no.2
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• pp.101-109
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• 1994

Acute toxicity of heavy metals( mercury, cadmium lead, chromium and copper ), organophosphours insecticides( EPN, 2, 4- D, and parathion ), and other chemicals( arsenic, cyanide, and phenol ) to Daphnia magna was analyzed. Acute toxicity of heavy metals, organophosphours insecticides and other chemicals on Daphnia magna, LC$_{50}$ was showed 0.07-0.73mg/1, 0.22-1.94mg/t and 1.73-39.92mg/1 respectively. Daphnia magna to most of toxic chemicals was sensitive and then it seems to be useful except phenol in toxic test of water. Toxic chemicals were classified as Group 1 which had a high LC$_{50}$ value and the low increase rate of toxicity according to the increase of concentration, Group 2 which had a high LC$_{50}$ value and the high increase rate of toxicity, Group 3 which had a low LC$_{50}$ value and the low increase rate of toxicity. To Daphnia magna, lead, chromium, EPN, and parathion were included in Group 1; Mercury and copper in Group 2; Arsenic and cadmium in Group 3; Cyanide 2,4- D, and phenol in Group 4.

• Applied Microscopy
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• v.19 no.2
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• pp.59-73
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• 1989

To investigate the effect of cadmium and cadmium binding protein on the electron transport system and conformational changes of rat kidney mitochondria, various cadmium concentration were treated in vitro and respiration rate, NADH-CoQ reductase activity were measured. Ultrastructural changes at state IV respiration were also observed. CdBP was isolated from the rat liver by Sephadex G-75 column fractionation and treated in vitro with cadmium. Also mitochondrial state IV respiration rate was measured. When cadmium was treated in vitro, state IV respiration and enzyme activity were decreased and ultrastructural transformation of mitochondria from a condensed to an orthodox conformation was inhibited under state IV respiration. In case cadmium and CdBP were treated together, oxygen consumption was more increased than cadmium only. Conformational changes of mitochondria from a condensed to orthodox conformation were also observed. This indicates that CdBP have a protective effect against cadmium toxicity.