• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.188-188
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• 2003

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototype of halogenated aromatic hydrocarbons, is a persistent environmental contaminant and one of the most powerful tumor promoters. The molecular mechanism underlying induction of tumor promotion by TCDD has not been elucidated.(omitted)

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.167.1-167.1
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• 2000

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.294.1-294.1
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• 2002

The effects of estradiol and its metabolites on the regulation of CYP1A1 expression. K.E. Joung and Y.Y. Sheen College of Pharmacy, Ewha womans University, Seoul. 120-750, Korea 2, 3.7.8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent halogenated aromatic hydrocarbon congener that induces expression of several genes including CYP1A1. Exposure to TCDD results in many toxic actions such as carcinogenesis, hepatotoxicity. immune suppression. and reproductive and developmental toxicity. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.283.1-283.1
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• 2002

The adverse health effects on humans and domestic and wildlife species by exposing to environmental contaminants. which interact with the endocrine system. have he en treated as an important issue without hesitation throughout the 1990s. The chemicals with practical and/or potential interfering actions with the endocrine system functions are called endocrine disrupting chemicals (EDCs). (omitted)

• Environmental Analysis Health and Toxicology
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• v.24 no.1
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• pp.33-41
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• 2009

Among the toxicants in the environment dioxin-like compounds, including TCDD(2,3,7,8-Tetrachlorodibenzo-p-Dioxin), are well known as carcinogen and teratogen. TCDD the most toxic of these compounds, may result in a wide variety of adverse health effects in humans and environment, including carconogenesis, hepatotoxicity, teratogenesis, and immunotoxicity. Also TCDD increases superoxide, peroxide radicals and induces oxidative stress that leads to breakage of DNA single-strand and mitochondrial dysfunction. Recently, there have been reports that persistent organic pollutants(POPs) may be causing metabolic disease through mitochondrial toxicity. In order to examine if dioxin brings about toxicity on mitochondria directly, we measured the change of the mitochondrial membrane potential after exposure to TCDD using JC-1 dye. After short time exposure of dioxin, mitochondrial depolarization was observed but it recovered to the control level immediately. This TCDD effect on mitochondrial membrane potential was not correlated either to the production of reactive oxygen species(ROS) or extracellular $Ca^{2+}$ by TCDD. Less than 2 hours exposure of TCDD did not show any change in ROS production but 0.25 nM TCDD for 48 hours or 0.5 nM TCDD for 12 hours exposure did increase in ROS production. Under these conditions of ROS production by TCDD, no changes in the mitochondrial membrane potential by TCDD was observed.

• 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.

• Biomedical Science Letters
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• v.9 no.1
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• pp.43-49
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• 2003

This study was carried out to investigate the effect of crude ginseng saponin (CGS) on blood chemical parameters in adult female guinea pigs exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). A total of 80 guinea pigs (800$\pm$20g) were divided into 8 groups: group 1 (normal control group) was given vehicle (corn oil containing small amount of acetone and DMSO) and saline; group 2 (single TCDD-treated) received TCDD (1 $\mu\textrm{g}$/kg, i.p.) and saline (i.p.); groups 3 and 4 were administered CGS at a daily i.p. doses of 10 and 20 mg/kg for 4 weeks, respectively; groups 5 and 6 were administered CGS (10 and 20 mg/kg, respectively) for 5 weeks starting 1 week before TCDD-exposure; groups 7 and 8 were administered CGS (10 and 20 mg/kg, respectively) for 3 weeks from 1 week after TCDD-exposure. CGS was prepared by Diaion HP-20 adsorption chromatography. Body weights of G2 were significantly decreased from the and week after TCDD-exposure (P<0.01). Body weights of the CGS-treated groups were also decreased by TCDD-exposure but the weight loss was greatly retarded compared with that of G2. Increase in blood glucose, amylase, lipase, total cholesterol, triglyceride, AST and LDL-cholesterol levels by TCDD exposure was significantly attenuated by the CCS-treatment (P<0.05). From these results, we found that saponin, the main active ingredient of gineseng, played a protective role in TCDD-induced toxicity and ginseng protected female animals from dioxin-induced toxic manifestation.

• Journal of Preventive Medicine and Public Health
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• v.46 no.5
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• pp.226-236
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• 2013

Objectives: The aim of this study was to examine the levels of serum 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and evaluate their association with age, body mass index, smoking, military record-based variables, and estimated exposure to Agent Orange in Korean Vietnam veterans. Methods: Serum levels of TCDD were analyzed in 102 Vietnam veterans. Information on age, body mass index, and smoking status were obtained from a self-reported questionnaire. The perceived exposure was assessed by a 6-item questionnaire. Two proximitybased exposures were constructed by division/brigade level and battalion/company level unit information using the Stellman exposure opportunity index model. Results: The mean and median of serum TCDD levels was 1.2 parts per trillion (ppt) and 0.9 ppt, respectively. Only 2 Vietnam veterans had elevated levels of TCDD (>10 ppt). The levels of TCDD did not tend to increase with the likelihood of exposure to Agent Orange, as estimated from either proximity-based exposure or perceived self-reported exposure. The serum TCDD levels were not significantly different according to military unit, year of first deployment, duration of deployment, military rank, age, body mass index, and smoking status. Conclusions: The average serum TCDD levels in the Korean Vietnam veterans were lower than those reported for other occupationally or environmentally exposed groups and US Vietnam veterans, and their use as an objective marker of Agent Orange exposure may have some limitations. The unit of deployment, duration of deployment, year of first deployment, military rank, perceived self-reported exposure, and proximity-based exposure to Agent Orange were not associated with TCDD levels in Korean Vietnam veterans. Age, body mass index and smoking also were not associated with TCDD levels.

• Korean Journal of Veterinary Research
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• v.44 no.3
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• pp.379-387
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• 2004

When an organism is exposed to various toxicants chronically, reactive oxygen species(ROS) are accumulated and eventually result in several biological effects from gene expression to cell death. In the present study we investigated the oxidative damage of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin(TCDD) and/or benzo(a)pyrene (B(a)P) in C100 cells. C100 cells treated with TCDD(30 nM) and B(a)P($3{\mu}M$) underwent diverse oxidative stress as determined through thiobarbituric acid-reactive substances(TBARS) formation, DNA fragmentation, DNA single strand break(SSB) assay, immunohistochemical staining of 8-hydroxy-2'-deoxyguanosine(8-OHdG), and mRNA expressions of antioxidant enzymatic genes such as Cu/Zn-SOD gene, GPx(glutathione peroxidase 5) gene, and catalase gene. Lipid peroxidation in C100 cells was determined through measuing the formation of TBARS. For theat, the cells were pretreated with TCDD(30 nM) and/or B(a)P($3{\mu}M$) for 0.5, 1, 2 and 4 days. TBARS formation was increased in TCDD(30 nM) and B(a)P($3{\mu}M$) and mixture($30nM\;TCDD+3{\mu}M\;B(a)P$) and positive control treatment groups comparing to the controls. Mixture treatment induced more DNA fragmentation than the single treatment group at day 6. Also, SSB in all treatment groups was clearly observed when compared with the negative control group. As with the expression of antioxidant enzyme, GPx 5mRNA, B(a)P alone and mixture($30nM\;TCDD+3{\mu}M\;B(a)P$) treatment were higher comparing to those of the negative control and TCDD treatment groups. Our results suggest that exposure of C100 cells to mixture of TCDD and B(a)P leads to significant oxidative damage comparing to the exposures to the individual chemicals. Mechanisms of action are discussed. Additional studies are needed to elucidate the detailed mechanism of mixture-induced toxicity.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.119.2-119.2
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• 2003

Exposure of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a variety of biological and toxicology effects, most of which are mediated by aryl hydrocarbon receptor (AhR). The ligand-bound AhR as a heterodimer with AhR nuclear translocator (ARNT) binds to its specific DNA recognition site, the dioxin-responsive element (DRE), and it results in increased transcription of CYP1A1 gene. Retinoic acid (RA) regulates the transcription of various genes for several essential functions through binding to two classes of nuclear receptors, the retinoic acid receptor (RAR) and retinoid X receptor (RXR). (omitted)