• Environmental Mutagens and Carcinogens
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• v.24 no.3
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• pp.137-142
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• 2004

Dioxin-like compounds are ubiquitous environmental polltants that could be accumulated in biological system and toxic to human and wildlife. Given this issue, it is important to develop a reliable dioxin detection methods for a rational risk assesment of dioxin-like compounds. In this study, we tried to set up and validate a sensitive, reliable risk assessment of dioxin-like compounds. In this study, we tried to set up and validate a sensitive, reliable and rapid bioassay model, CALUX bioassay as a screening tool for routine measurement of dioxin-like conpounds in environmental matrices. For the valisation of CALUX bioassay, firstly, we performed dose-response assay for 2,3,7,8-TCDD, most potent dioxin-like compound, using two different methods CALUX and EROD assay. Induction of luciferase activity and CYPIA catalyzed EROD activity were dose-dependently induced by 2,3,7,8-TCDD, with initial induction at 0.1 pM and maximal induction at 1 nM. In order t determine whether the CALUX bioassay could predict the effects of dioxin-like compounds, 2,3,7,8-TCDD dose-response from CALUX was compared with that from EROD assay. The correlation coefficient ($r^2$) was found to be 0.89, indicating a good correlation between two different methods and the possibility of CALUX bioassay as a useful dioxin detecting method.

• Journal of Food Hygiene and Safety
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• v.18 no.3
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• pp.166-170
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• 2003

This study was carried out to investigate the inhibitive effect of Saururus chinenesis Baill (SCB) on lipid peroxidation in Sprague-Dawely rat (SD-rat) accutely exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Saururus chinenesis Baill (200 mg/kg) was administered into rats intraperitoneally for four weeks, seven days after the injection of TCDD (1 ${\mu}$g/kg). we examined th lipid parameters by measuring the levels of Total Cholestero, Triglyceride(TG), HDL-Cholestero, and LDL-Cholesterol in serum and Malone Dialdehyde (MDA) in liver tissue of rats. Cholesterol was siginificantly elevated in TCDD-treated abnormal group (TTA). The higher level of HDL-Cholesterol was found in Saururus chinenesis Baill and TCDD administered group (STT), which showed the lower levels of Total-Cholesterol and LDL-Cholesterol. TG content in the TTA was 34.84% increased compared to Non TCDD-treated group (NTT). That of STT was inhibited by 18.90% compared to TTA. MDA content in the TTA was 44.72% increased compared to NTT. That of STT was inhibited by 17.14% compared to TTA.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.129-129
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• 2002

2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD) a prototype of many halogenated aromatic hydrocarbons, is a ubiquitous, persistent environmental contaminant and the most powerful carcinogen categorized by IARC. Despite extensive research, the mechanisms of TCDD-induced carcinogenesis are poorly understood.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.178-178
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• 2003

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototype of many halogenated aromatic hydrocarbons, is a ubiquitous, persistent environmental contaminant and the most powerful carcinogen categorized by IARC. It is display high toxicity in animals and is associated with several cancers in human. Although the mechanism of carcinogenesis by TCDD is unclear, it is considered to be a non-genotoxic and rumor promoter.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.190-191
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• 2003

We investigated the effects of gestational and lactational exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the differential induction of CYP1A1 in the levels of protein and gene expression in the liver and brain regions of offspring rats. For this study, pregnant Sprague Dawley rats were orally exposed to TCDD (1 or 10 ng/kg body weight/day) starting at Day 1 of gestation up to Day 20 of postpartum. (omitted)

• Molecules and Cells
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• v.21 no.2
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• pp.276-283
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• 2006

The potent environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), induces thymus atrophy in experimental animals. However, its mechanism of action is not fully understood. To gain insight into its immunosuppressive effect, Balb/c mice were intraperitoneally injected with TCDD ($30{\mu}g/kg$ body weight) and genes regulated by TCDD were identified using cDNA arrays [Park and Lee (2002)]. One of the regulated genes was that for plasma glutathione peroxidase (pGPx). Upon TCDD injection, pGPx mRNA levels in the thymus increased, in parallel with increases in GPx activity and the frequency of anti-human pGPx antibody-reactive cells. pGPX mRNA levels were also moderately up-regulated in the testis and spleen. This is the first report that a particular isotype of the glutathione peroxidase family is regulated by TCDD at both mRNA and protein levels. pGPx is expressed in various tissues in contact with body fluids, and detoxifies hydrogen peroxides and lipid hydroperoxides. It will be of interest to assess the role of pGPx in TCDD-induced thymic atrophy.

• Environmental Mutagens and Carcinogens
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• v.22 no.2
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• pp.112-124
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• 2002

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been reported to exert detrimental toxicities on various organ systems including reproductive, cardiovascular, nervous, or dermal system. Immunomodulatory effects of TCDD is thymic atrophy, downregulation of cytotoxic T or B lymphocyte differentiation and activation, which were demonstrated using experimental animals, whereas immunotoxicity in human has not been investigated well. This study was proceeded to evaluate general immunologic spectrum of the Korean Vietnam War veterans exposed to TCDD during their operation, and compare with that of the non-exposed control subjects with similar age. Regarding composition and quantity, immune cells in peripheral blood collected from the TCDD-exposed was not much different from those of the control except decreased red blood cell, hemoglobin and hematocrit level. Furthermore, plasma IgG2, G3, and G4 isotype distribution was similar between two groups, but IgG1 level was significantly lowered in the TCDD-exposed, indicating a TCDD-mediated functional alteration of B cells. Significantly enhanced level of IgE in plasma, a hallmark of dermal or respiratory allergic response, was also observed in the TCDD-exposed compared with that of the control. Elevated generation of IL-4 and IL-10 was resulted from in vitro stimulation of T cells with PMA plus ionomycin or PHA, respectively, from the TCDD-exposed in comparison to those of the control, suggesting a skewed type-2 response. In addition, the level of IFN${\gamma}$, a multifunctional cytokine for T cell-mediated immunity, was lowered in the TCDD-exposed with upregulation of tumor necrosis factor $\alpha$. The present study suggests that TCDD exposure disturbs immunohomeostasis in humans observed as an aberrant plasma IgE and IgG1 levels and dysregulation of T cell activities.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.9
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• pp.1178-1184
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• 2006

This study was carried out to investigate the effect of ethanol extract of antler velvet (EAV) on common serum chemistry panels and histopathological change in rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Administration of TCDD ($50{\mu}g/kg$ body weight) induced significant decrease in platelet count (p<0.01), creatine phosphokinase (CPK, p<0.01), lactatate dehydrogenase (LDH, p<0.05) and glucose (p<0.05) levels and increase in hemoglobin (p<0.05), aspartate aminotransferase (AST, p<0.01), alanine amino transferase (ALT, p<0.05) and lipase activities (p<0.05), and blood urea nitrogen (BUN, p<0.05), triglyceride (p<0.01) and low density lipoptotein cholesterol (LDL-C, p<0.05) levels. However, pretreatment of EAV at daily dose of 20 mg/kg b.w. from 1 wk before TCDD exposure for 5 wks attenuated the abnormality of the overall serum chemistry panels but statistical difference between TE and TA groups was observed only in testicular weight (p<0.01), LDH activity (p<0.05), glucose (p<0.05) and lipase activity (p<0.01). In addition, TCDD induced significant histopathological changes including swelling, fatty metamorphosis, and vacuolar degeneration in liver; edema in proximal and distal convoluted tubules, and glomerulus in kidney; severe atrophy of red purple and appearance of significant number of macrophage in spleen; prominent atrophy and decrease in immune cells in thymus. On the other hand, administration of EAV attenuated histopathological damage induced by TCDD. These results further suggest that administration of EAV attenuates TCDD induced testicular, liver, pancreatic, hematopoietic and nephrotic toxicities in rats.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.149-150
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• 2002

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent halogenated aromatic hydrocarbon congener that induces expression of several genes including CYP1A. Exposure to TCDD results in many toxic actions such as carcinogenesis, hepatotoxicity, immune suppression, reproductive toxicity and developmental toxicity.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.179-179
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• 2003

2,3,7,8-Tetrachlorodibenzo-$\rho$-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanisms of TCDD-induced carcinogenesis are poorly understood, it considered to be non-genotoxic and tumor promoter. In this study, we investigated the tumor promotion effect of TCDD on the two-stage skin chemical carcinogenesis using hairless mouse (SKH1).(omitted)