• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2003년도 추계학술대회
• /
• pp.179-179
• /
• 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)

• 대한화학회지
• /
• 제38권11호
• /
• pp.819-826
• /
• 1994

환경시료중 수질시료속에 미량으로 존재하는 다이옥신류를 정량하기 위한 분석법의 연구로써 시료의 유형에 관계없이 적용시킬 수 있는 보다 간단하고 효유적인 전처리 방법을 조사하고 HRGC/HRMS-SIM 방법으로 검출한계를 낮추며 정성과 정량이 동시에 이루어지도록 하였다. 초기농축단계로 dichloromethane(DCM)을 이용한 액체-액체추출법을, 정제단계로 강양이온교환수지, 실리카 직렬 카트리지컬럼, Flotisil 카트리지컬럼을 이용한 고체상 추출법을 사용하였다. 각각의 회수율과 방해물제거에 대한 선택성으로부터 본 분석법의 효율성을 조사했으며 TCDD의 손실없이 페놀류, 농약류, PCB류를 제거, 분리할 수 있었다. 해수 1L에 1,2,3,4-TCDD 10ng을 첨가시킨 다음 농축 및 정제의 모든 단계를 거친 후 평균회수율은 92(${\pm}$1.6)%였다. 또한 광양만에서 채취한 해수시료에 대해 분 분석법을 적용시킨 결과 4.5(${\pm}$1.1)pg/L의 2,3,7,8-TCDD를 검출할 수 있었다.

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

• 한국응용약물학회:학술대회논문집
• /
• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
• /
• pp.89-89
• /
• 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
• /
• 한국환경독성학회 2003년도 추계국제학술대회
• /
• pp.179-179
• /
• 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.

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
• /
• pp.129-129
• /
• 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)

• 한국환경성돌연변이발암원학회:학술대회논문집
• /
• 한국환경성돌연변이발암원학회 2004년도 춘계학술대회
• /
• pp.97-97
• /
• 2004

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2003년도 추계학술대회
• /
• pp.178-178
• /
• 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)

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2003년도 추계학술대회
• /
• pp.190-191
• /
• 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)

• 대한약학회:학술대회논문집
• /
• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
• /
• pp.121.1-121.1
• /
• 2003

Houttuynia cordata Thunb (HCT) is a herbal plant growing in China, Japan and Korea. According to the records of the Chinese medicine, this plant has been used as folk medicine for analgesics, beriberi, edema, hepatitis, icterus, etc. TCDD (2, 3, 7, 8 -tetrachlorodibenzo-p-dioxin), one of the notorious toxic environmental pollutants, damages various organs including liver and is regarded as an endocrine disrupter. After 7 days from TCDD (1$\mu$g/kg) injection, HCT (200 mg/kg) was administered into rats intraperitoneally for 4 weeks. (omitted)