• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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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)

• 대한생식의학회:학술대회논문집
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• 대한불임학회 2004년도 제47차 추계학술대회
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• pp.17-20
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• 2004

• Environmental Analysis Health and Toxicology
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• 제25권3호
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• pp.241-251
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• 2010

Crucian carp (Carassius auratus) has been used as the sentinel species for POPs (Persistent Organic Pollutants) monitoring in aquatic environment. However, there is little information for dioxin toxicity and especially, early life stage toxicity in crucian carp have been never carried out. In this study, we investigated several toxic effects for 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) in fertilized egg obtained by natural fertilization from crucian carp. The embryos at 3 h post-fertilization (hpf) were treated with 0.039, 0.156, 0.625, and 2.5 (${\mu}g/L$) TCDD by waterborne exposure for 60 minutes and changed with fresh water 2 times per day. Fertilized eggs started hatching at 51 hpf and TCDD exposed embryo showed decrease of hatching rate in a dose-dependent manner at 75 hpf. Pericardial edema was continuously observed in larvae exposed to TCDD from hatching start time (51 hpf), followed by the onset of mortality. In addition, AhR-related gene, CYP1A was clearly increased by TCDD in a dose dependent manner. These results indicated that fertilized eggs obtained from crucian carp have the TCDD related gene regulation and a distinct TCDD developmental toxicity syndrome by TCDD exposure. Therefore, we suggested that early life stage test in crucian carp could be used as test methods on dioxins toxicity.

• Environmental Analysis Health and Toxicology
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• 제11권3_4호
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• pp.75-87
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• 1996

There are numerous and evidential findings that TCDD (2, 3, 7, 8-tetrachlorodibenzo-Pdioxin, or dioxin) is a potential carcinogen and general toxin in rodents. flowever, human risk assessment for dioxin exposure has been a topic of debate, owing in part to the large animal interspecies differences in its toxicity. We review dioxin-related reports indicating its toxicity, toxic effects in animal, and human epidemiologic findings. The intent of this paper does not provide a causal inference about chronic human diseases related to dioxin exposure. This summary would give a valuable clue for a researcher to conduct or design a further dioxin-related study.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.115.3-116
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• 2003

Saururus chinensis Baill (Saururaceae) is a perennial plant that has been used in the treatment of edema, jaundice and gonorrhea in Korean folk medicine. This study was carried out to investigate the inhibitive effects of Saururus chinensis Baill (SCB) on lipid metabolism in Sprague-DaweIy rat(SD-rat) accutely exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD). After 7 days from TCDD(1$\mu$g/kg) injection, SCB(200mg/kg) was administered into rats intraperitoneally for 4 weeks. (omitted)

• Molecular & Cellular Toxicology
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• 제1권3호
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• pp.164-171
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• 2005

Toxicological studies have an object of detecting adverse effects of a chemical on an organism based on observed toxicity marker (i.e., serum biochemical markers and chemical-specific gene expression) or phenotypic outcome. To date, most toxicogenomic studies concentrated on hepatic toxicity. cDNA microarray analysis enable discrimination of the responses in animals exposed to different classes of hepatotoxicants. In an effort to further characterize the mechanisms of 2, 3, 7, 8,-Tetrachlorodibenzo-p-dioxin (TCDD or dioxin)-mediated toxicity, comprehensive temporal-responsive microarray analyses were performed on hepatic tissue from Sprague-Dawley rats treated with TCDD. Hepatic gene expression profiles were monitored using custom DNA chip containing 490 cDNA clones related with toxicology. Gene expression analysis identified 26 features which exhibited a significant change. In this study, we observed that the genes related with oxidative stress in rats exposed to Dioxin, such as CYPIIA3 and glutathione S-transferase, were up-regulated at 24hr after exposure. In this study, we carried out to discover novel evidence for previously unknown gene expression patterns related to mechanism of hepatic toxicity in rats exposed to dioxin, and to elucidate the effects of dioxin on the gene expression after exposure to dioxin.

• 한국지하수토양환경학회지:지하수토양환경
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• 제9권3호
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• pp.20-26
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• 2004

2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD)로 오염된 토양의 현장 광분해 정화 과정에서 가장 중요한 이동 메커니즘인 지표에서의 증발 및 광분해에 의한 유기 용매의 이류 상방향 이동에 대한 수식화와 모델 개발을 수행하였다. 각 유체 분포에 대한 다상 유동 효과, 구동력으로서의 중력, k-S-p 관계의 정확한 묘사를 위한 van Genutchen 방정식을 포함한 유한요소법 기반의 수치 모델을 제안하였다. 실험실 규모의 비포화 토양 컬럼 내 용매 이동에 중요한 영향을 미치는 인자들을 조사하기 위하여 수행한 계산의 결과들을 제시하였다. 중력은 고투수성 토양의 유체 분포와 증발에 상당한 영향을 미쳤다. 토양의 종류 또한 증발 과정 중 유체 포화도 분포에 큰 영향을 미친다. 용매의 이류 이동량은 증발량이 증가할수록 초기 물 포화도가 감소할수록 증가하였다. 본 연구에서 수행한 시뮬레이션은 개발된 모델이 토양 환경 내에서 유기 용매의 이류 이동에 영향을 미치는 다양한 인자들의 영향을 분석하는데 유용함을 보여준다.

• 생명과학회지
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• 제11권4호
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• pp.346-353
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• 2001

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) a prototype of the highly toxid halogenated arylhydrocarbons, bioaccumulates in the food chain and induces a complex spectrum of pathological responses. However, its effect on the nerve system is relatively not well studied. In this study we evaluated TCDDs cytotoxicity on the cortical cell and investigated its effect on the expression 2,3-cyclic nucleotide 3-phosphodiesterase(CNPase), a marker for oilgodendrocytes, The survival rates of 4 DIV cortical cells, that are dissociated from E18 rat cortex and maintained in the presence of TCDD, were 88.8, 83.6, 78.5, and 78.6%(5,10, 20 and 50 nM, respectively) where the reduction in 20 and 50mM TCDD were statistically very significant(p<0.01). Imunocytochemistry of cultured cells revealed that the intensities of immunostaining with an anti-CNP1&2 antibody depended on the concentrations of the toxin. Immunoblot analysis also showed differential expression of CNP1 and CNP2 in the presence of TCDD; the CNP1 expression was dose-dependently decreased. Interestingly, the expression of CNP2 in the presence if TDCC; the CNP1 expression was dose-dependently decreased. Interestingly, the expression of CNP2 fluctuated with the TCDD concentration. These results indicated that CNP1 and 2 are differentially regulated by TCDD, implying the functions of oligodendrocytes are modulated by the toxin.

• Toxicological Research
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• 제19권4호
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• pp.325-330
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• 2003

The effects of estrogen on apoptosis induced by 2,3,7,8-tetrachlorodibenzo-p-doxin (TCDD) were examined in cultured MCF-7 cells. TCDD stimulated apoptosis and inhibited the expression of bcl-2 gene in MCF-7 cells grown in the media supplemented with 10% fetal bovine serum. However, TCDD failed to induce apoptosis if cells were grown in the media deprived of all estrogen-like compounds. Removal of estrogen-like compounds from the growth media also led to the activation of bcl-2 gene expression in cells treated with TCDD. Combined treatment of estrogen with TCDD abrogated the binding of Aryl hydrocarbon Receptor (AhR)-TCDD complex to Dioxin response element (DRE) of bcl-2 gene leading to the inhibition of bcl-2 gene expression as well as stimulation of apoptosis. The present study suggests that the binding of estrogen receptor (ER)-estrogen complex to the estrogen responsive element (E) interferes with the binding of AhR- TCDD complex to the DRE and inhibits the bcl-2 expression.

• Environmental Analysis Health and Toxicology
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• 제24권1호
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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.