• 한국식품위생안전성학회지
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• 제18권3호
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• pp.166-170
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• 2003

삼백초가 TCDD 투여로 유발된 rat의 지질대사에 미치는 효과를 알아보기 위해 NTT, TTA, STT군으로 각각 10마리씩 나누어 TCDD를 투여하고 4주 동안 물질을 투여하였다. 4주 후 희생시켜서 혈청과 간의 지질대사를 관찰한 결과는 다음과 같다. 1. Total Cholesterol에서 삼백초를 투여한 STT군은 NTT군 비교해서 14.46% 증가하였으며, 혈청 중의 HDL-Cholesterol은 SST군이 TTA군과 비교하여 21.29% 증가하였고 94.98%로 엑제되었다. LDL-Cholesterol에서는 STT군이 TTA군 보다 12.86% 감소하였으며, 48.34%로 억제되었다. 2. 혈청중의 TG의 함량은 TTA군이 NTT군에 비해 34.84% 증가하였다. TTA 군에 비해 STT군은 7.06% 감소하였으며, 18.9% 억제시킨다 3. 간조직 중의 MDA량은 STT군이 TTA군에 비해 17.14% 감소하였고, 32.72%의 억제율을 보였다.

• 한국식품위생안전성학회지
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• 제18권3호
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• pp.161-165
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• 2003

삼백초가 TCDD 투여로 유발된 rat의 간손상에 미치는 효과를 알아보기 위해 NTT, TTA, STT군의 3군으로 각각 10마리씩 나누어 TCDD를 투여하고 4주 동안 물질을 투여하였다. 4주 후 희생시켜서 생체 내 간 조직 활성 효과 및 항산화 효과를 관찰한 결과 1. AST 활성도는 STT군이 TTA군과 비교해서 70.05%,의 억제 효과를 보였다. 반면에, ALT활성도는 STT군이 TTA군에 비해 24.00% 감소하였으며 64.80%의 억제 효과를 보였다. 2. SOD는 TTA군이 NTT군보다 137.78% 감소하였으며 , STT군은 TTA군에 비해 81.94%로 상승되었다. Catalase는 TTA군은 NTT군 보다 199.13% 감소하였으며, STT군의 catalase 활성도는 TTA 군과 비교하여 52.48% 증가하였고 55.45%의 회복율을 보였다. 3. TTA군의 GSH함량은 NTT군 보다 291.29% 감소하고 STT군은 TTA군보다 비교하여 74.20% 증가하였으며, 98.72%로 회복하였다. TTA군은 GSSG함량은 NTT군 보다 46.80% 증가하였고 STT군의 간조직중의 GSSG 함량은 TTA군과 비교하여 61.08% 감소하였으며, 81.01%로 억제되었다.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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• pp.89-89
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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). Constitutive androstane receptor (CAR) also regulates the transcription of gene. In this study, we have examined how RAR, RXR and CAR regulated CYP1A1 in rainbow trout hepatoma cell (RTH 149) using luciferase reporter gene assay system. We did transient transfection with CYP1A1 luciferase reporter gene and treated with TCDD, all-trans RA, 9-cis RA and phenobarbital. Treatment of all-trans RA, 9-cis RA or phenobarbital decreased the TCDD induced transcription of CYP1Al. When we did transient cotransfection with CYP1A1 luciferase reporter gene and RXR, as increase of RXR concentration, the TCDD induced transcription of CYP1A1 was decreased. Transfection with CAR also decreased the TCDD induced transcription of CYP1A1 in RTH 149 cells.

• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2003년도 추계국제학술대회
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• pp.179-179
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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). Constitutive androstane receptor (CAR) also regulates the transcription of gene. In this study, we have examined how RAR, RXR and CAR regulated CYP1A1 in rainbow trout hepatoma cell (RTH 149) using luciferase reporter gene assay system. We did transient transfection with CYP1A1 luciferase reporter gene and treated with TCDD, all-trans RA, 9-cis RA and phenobarbital. Treatment of all-trans RA, 9-cis RA or phenobarbital decreased the TCDD induced transcription of CYP1A1. When we did transient cotransfection with CYP1A1 luciferase reporter gene and RXR, as increase of RXR concentration, the TCDD induced transcription of CYP1A1 was decreased. Transfection with CAR also decreased the TCDD induced transcription of CYP1A1 in RTH 149 cells.

• 대한의생명과학회지
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• 제9권1호
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• pp.51-58
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• 2003

This study was carried out to investigate the preventive and therapeutic effect of Panax ginseng water extract (PG-WE) on the toxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), one of the most notorious toxic environmental pollutants belonging to the group of polyhalogenated aromatic hydrocarbons. Normal control (NC) group guinea pigs (180~200 g) received vehicle and saline, and TCDD-treated (TT) group was given TCDD and saline. P100 and P200 group animals received PG-WE for 28 days since 1 week before TCDD exposure at daily doses of 100 mg/kg b.w. and/or 200 mg/kg b.w., respectively. C100 and C200 group received PG-WE for 14 days starting 1 week after TCDD-exposure. Toxicity was induced by a single intraperitoneal injection of TCDD (1 $\mu\textrm{g}$/kg b.w.). Abnormal increase in AST and ALT activities in TT group was significantly improved by the administration of PC-WE. Microscopically, there were mild to moderate swelling of hepatocytes, hyperchromatism of individual cells, acidophilic cytoplasm and cytoplasm vacuolation of some hepatocytes, slight to moderate variations of staining density, occasional single cell necrosis, variable size and shape of some hepatocytes, small groups of degenerating hepatocytes surrounded by mononuclear cells, dilated sinusoids of centrilobular zone and some loss of lobular architecture in TT group liver. From these results, we could find the protective and therapeutic role of PG-WE in TCDD-induced liver toxicity by examining the blood chemical parameters and histopathological observation.

• 한국산업보건학회지
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• 제26권3호
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• pp.277-285
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• 2016

Objectives: This study was performed in order to evaluate whether 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) could be detected among residents living near Camp Caroll in Waegwan and whether serum concentrations of dioxins, including 2,3,7,8-TCDD, and organochlorine pesticides (OCPs) are associated with length of residence. Methods: Study subjects totaled 113 (for dioxins) and 190 (for OCPs) adults who were selected from participants in a medical investigation. Serum concentrations of dioxins and OCPs were measured using HRGC/HRMS. Information on length of residence was obtained through questionnaires. Results: 2,3,7,8-TCDD was not detected in serum among all subjects. When length of residence was classified as a categorical variable, after adjusting for confounding variables, only residents living in Waegwan for 40 years or longer tended to have high total TEQ values and 2,3,4,7,8-PeCDF with marginal significances. There was no dose-response relation between length of residence and serum concentrations of these chemicals. In multiple regression models with continuous values of the length of residence, total TEQ value and 1,2,3,4,6,7,8-HpCDF were positively associated with length of residence. However, they explained about 3-5% of total variations of serum concentrations of these compounds, while age, consumption of fatty fish, body mass index, alcohol drinking, and cigarette smoking were main variables affecting serum concentrations of dioxins or OCPs. Conclusions: In the current study, high concentrations of certain compounds were mainly observed among persons who lived in Waegwan for at least for 40 years without a dose-response relation. Therefore, it seems difficult to conclude that length of residence meaningfully contributed to the current serum concentrations of dioxins or OCPs among residents in Waegwan. However, considering the half-life of 2,3,7,8-TCDD and indirect exposure routes, the limitations of the current study design should be considered in the interpretation of the study findings.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2001년도 추계학술대회 및 정기총회
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• pp.112-112
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• 2001

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxin that activates the aryl hydrocarbon receptor (AhR) and disrupts multiple endocrine signaling pathways by enhancing ligand metabolism, altering hormone synthesis, down regulating receptor levels, and interfering with gene transcription. And TCDD-mediated gene transactivation via the AhR has been shown to be dependent upon estrogen receptor (ER) expression in human breast cancer cells. In the present study, we have examined the effect of natural estrogen, phytoestrognes and environmental estrogens on the regulation of CYP1A1 gene expression in MCF-7 human breast cancer cell line. that ER and AhR are co-expressed. pCYP1A1 -luc reporter gene was transiently transfected into MCF-7 cells. These cells were treated with various chemicals and then luciferase assay was carried out. 17be1a-estradiol significantly inhibited TCDD stimulated luciferase activity dose dependently and this inhibition was partially recovered by concomitant treatment of tamoxifen. 17beta-estradiol metabolites, 2-hydroxyestradiol and 16alpha-estriol resulted in less potent inhibitory effect than estradiol and synthetic estrogen, diethylstilbestrol (DES) showed no effect on CYP1A1 gene expression. This study demonstrated that estrogen down-regulated TCDD stimulated CYP1A1 expression via ER mediation. And we have found out that several flavonoids such as genistein, kaempferol, daidzein, naringenin, and alkylphenols such as nonylphenol, 4-octylphenol and resveratrol also inhibited TCDD induced CYP1A1 expression like estrogen.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Signal transduction in Toxicology
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• pp.154-154
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• 2001

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, and its carcinogenic potential in human is not clear.(omitted)

• Tuberculosis and Respiratory Diseases
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• 제78권2호
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• pp.99-105
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• 2015

Background: Aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor, binds to a wide variety of synthetic and naturally occurring compounds. AhR is involved in the regulation of inflammatory response during acute and chronic respiratory diseases. We investigated whether nuclear receptor coactivator 7 (NCOA7) could regulate transcriptional levels of AhR target genes and inflammatory cytokines in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated human bronchial epithelial cells. This study was based on our previous study that NCOA7 was differentially expressed between normal and chronic obstructive pulmonary disease lung tissues. Methods: BEAS-2B and A549 cells grown under serum-free conditions were treated with or without TCDD (0.15 nM and 6.5 nM) for 24 hours after transfection of pCMV-NCOA7 isoform 4. Expression levels of cytochrome P4501A1 (CYP1A1), IL-6, and IL-8 were measured by quantitative real-time polymerase chain reaction. Results: The transcriptional activities of CYP1A1 and inflammatory cytokines were strongly induced by TCDD treatment in both BEAS-2B and A549 cell lines. The NCOA7 isoform 4 oppositely regulated the transcriptional activities of CYP1A1 and inflammatory cytokines between BEAS-2B and A549 cell lines. Conclusion: Our results suggest that NCOA7 could act as a regulator in the TCDD-AhR signaling pathway with dual roles in normal and abnormal physiological conditions.

• Molecular & Cellular Toxicology
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• 제2권1호
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• pp.35-47
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• 2006

2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) are well known as the most toxic environmental compound in these days. Many researches are reported that dioxin produces multiple toxic effects, such as endocrine toxicity, reproductive toxicity, immunotoxicity and cancer. In this study, we carried to discover novel evidence for previously unknown gene expression patterns in human exposed to dioxin by using radioactive cDNA microarray. 548 workers who were divided into experimental and control groups according to their urinary Naphthol levels were enrolled in our study. Blood mRNA in human was isolated, and the gene expression profiles were analyzed by cDNA microarray. Gene expression analysis identified 52 genes which exhibited a significant change. In our study, most notably, genes involved in cell cycle, cell proliferation, signal transduction and apoptosis in human exposed to dioxin, such as CCND3, TSHR, and EFRN5, were up-regulated. In the current study, we observed gene expression of people that are exposed to dioxin using radioactive cDNA microarray. Through these results, we suggest when objects are exposed to toxic compounds, such as dioxin, the radioactive cDNA microarray may be using in sensitively detecting of cancerous change.