• 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 Preventive Medicine and Public Health
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• v.34 no.1
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• pp.80-88
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• 2001

Objectives : In an epidemiologic study on the health impact of Agent Orange exposure, the valid estimation of exposure level is the most important step. Based on recent studies, we examined the correlation between exposure levels categorized by personal exposure estimates and serum 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD, Dioxin), exploring the possibility of utilizing the exposure level as a surrogate for the estimate of exposure to agent orange. Methods : During the study period (Jan 1996-Feb 1996), blood specimens of 745 subjects taken randomly among 1,329 persons and kept frozen, were analyzed for 2,3,7,8-TCDO and six other dioxin congeners. The serum dioxin and congeners were measured in 1998 by CDC, adjusted for serum lipids. We categorized the total exposure scores into five groups based on Agent Orange exposure data collected by interview and military records. Pearson and Spearman's correlation coefficients & multiple regression analysis were used to identify the relationship of the exposure level categorized with serum concentration of 2,3,7,8-TCDD, and six other dioxin congeners. Results : Dioxin and the other congeners, except 1,2,4,6,7,8-HpCDD, showed significant correlations to exposure categories (p<0.005): 2,3,7,8-TCDD and OCDD showed positive correlations, whereas the other congeners did negative. The values of 2,3,7,8-TCDD differed according to exposure category and proportionally increased from the low exposure group to the high, a dose-response relationship, even after other possible confounding variables were adjusted for. In multiple regression analysis, age$(\beta=0.033)$, dioxin$(\beta=0.433)$, 1,2,3,7,8-PeCDD$(\beta=-0.998)$, 1,2,3,4,7,8-HxCDD$(\beta=-0.773)$, 1,2,3,6,7,8-HxCDD$(\beta=0.255)$, 1,2,3,7,8,9-HxCDD$(\beta=-3.468)$, 1,2,3,4,6,7,8-HpCDD$(\beta=0.109)$ we re found to be significantly related to the total exposure score(p<0.005). Conclusion : This study demonstrated that the use of such categorizations as a surrogate measure of agent orange exposure in identifying exposure degrees in a health impact study is valid.

• 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 Korean Society of Community Living Science Conference
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• 2005.06a
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• pp.169-169
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• 2005

• Journal of Microbiology and Biotechnology
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• v.10 no.3
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• pp.281-286
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• 2000

2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD), a ubiquitous environmental contaminant, causes a variety of adverse effects on the male reproductive system in rats. The effect of green tea extract (GTE) was investigated on the testicular function in Spragure-Dawley rats after a single exposure of 10$\mu\textrm{g}$ TCDD/kg body weight. The exposure of rat to TCDD significantly increased the weights of the epididymis and ventral prostate, yet significantly decresed the weight of the seminal vesicle when compared to the controls (p<0.05). In a combined treatment of TCDD with GTE, the organ weight changes caused by TCDD treatment disappeared. Significant decreases in sperm motility and sperm numbers were observed in the TCDD-treated rats, when compared to the control (p<0.05). GTE treatment reversed the decrease of sperm motility and sperm numbers caused by TCDD. There were no differences in sperm morphology, histological changes of the reproductive organs, and spermatogenesis between all the treated groups. In the ventral prostate and seminal vesicle, TCDD increased the CYP1A1 mRNA level, however, it did not affect the estrogen receptor $\beta$ (ER-$\beta$) mRNA level. GTE treatment did not influence the effect of TCDD on the levels of CYP1A1 and Er-$\beta$ mRNA. These results seem to indicate that green tea protects the testicular function against TCDD-induced reproductive toxicity, not because of a receptor-mediated mechanism but rather due to a secondary change of testes or accessory sex organs.

• Toxicological Research
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• v.25 no.1
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• pp.35-40
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• 2009

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and related halogenated aromatic hydrocarbons elicit a diverse spectrum of biochemical and toxic responses in laboratory animals and mammalian cells in culture. Toxicity and carcinogenicity of TCDD is well established but the molecular mechanism is still poorly understood. Here, we found the noble responsive genes to TCDD using the differential display analysis. Treatment of HepG2 cells with TCDD showed a significantly different mRNA expression pattern from the untreated cells in differential display analysis. The differentially displayed bands were isolated and used as probes in dot blot and Northern blot analyses. Of thirty-five isolated differentially displayed bands, only two bands were confirmed as positive in dot blot and Northern blot analyses. The nucleotides sequences of these clones were analyzed and the search of Genebank database revealed that one clone is highly homologous with RanBP2 (Ras-related nuclear protein binding protein2; 92%) and the other is an unknown gene. RanBP2 is a nucleoporin with SUMO E3 ligase activity that functions in both nucleocytoplasmic transport and mitosis and its role as a novel tumor suppressor has been recently proposed. Thus, these results may suggest the clue elucidating the toxic mechanism of TCDD through RanBP2.

• Environmental Mutagens and Carcinogens
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• v.24 no.3
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• pp.143-150
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• 2004

In mammalian, cytochrome P4501A1 (CYP1A1) is very important for metabolism of xenobiotics such as PAHs(Polycyclic aromatic hydrocarbon) and heterocyclic amine, and it is induced by environmental contaminants such as PAHs, TCDD(2,3,7,8-tetrchlorodibenzo-p-dioxin) and 3-MC (3-methylcholanthrene). In fish, like mammalian, when it is exposed to environmental contaminants, they cause specific and sensitive induction of CYP1A. Therefore, induction of CYP1A in fish and mammalian is widely used as a biomarker for exposure of environmental contaminants. In this study, to compare the function of Cyp1a1 in fish with it in mammalian, we have used rainbow trout(Oncorhynchys mykiss) hepatoma cells (RTH-149) and mouse hepatocyte (Hepa-I). in order to examine induction of Cyp1a1 by TCDD, we have used the bioassay system. We examined effects of TCDD on the Cyp1a1-luciferase reporter gene activity, 7-ethoxyresorufin O-deethylase(EROD) activity and Cypa mRNA level.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.300-311
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• 1998

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), one of the most notorious toxic environmental pollutants, induces various toxic effects in many organs including testes and is regarded as an endocrine disruptor. Korean ginseng, on the other hand, has been well known for its preventive effects on lox- ins, diabetes melltus and hyperlipidemia. We investigated, histopathologically, the effect of Korean Red ginseng water extract (KR-WE) on guinea pig testes damaged by TCDD. Ninety guinea pigs were divided into 6 groups: normal control (NC) group received vehicle and saline; TCDD,1191kg b.w., was administered intraperitoneally to the single dose TCDD-treated (77) group; 100 mghg b.w.16 and 200mg1kg b.w./d KR-WE were injected intraperitoneally to the preventive groups (PIOO and P2OO, respectively) for 28 days from 1 week before TCDD injection, and to the therapeutic groups (CIOO and C2OO, respectively) for 14 days since 1 week after TCDD administration. Increment of body weight was retarded to a larger extent by TCDD. Moreover, body weight of the 77 group decreased significantly 7 days after TCDD exposure, while that of preventive groups kept increasing. Decrease in body weight was not observed in KR-WE-treated groups. Weight decrease in testes caused by TCDD was remarkably protected by KR-WE. Testicles in 77 group displayed decreased tubular size and maturation arrest at the primary or secondary spermatocyte stage. On the other hand, maturation arrest in germ cells by TCDD was improved in KR-WE treated groups. Almost complete protection of the testes was observed in PIOO and P2OO groups. In addition, the therapeutic effect was noticed in C 100 and C2OO groups. These results provided strong evidence that Korean Red ginseng might be a useful agent for the prevention and treatment of testicular damage induced by environmental pollutants.

• Korean Journal of Environmental Biology
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• v.21 no.2
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• pp.170-176
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• 2003

The effect of xenobiotics on cytochrome P450 (CYP) and 7-ethoxyresorufin-O-deethylase (EROD) in hepatopancreatic microsome of surf clam, Coelomactra anti-quata, were investigated. The microsome isolated from the digestive gland of the surf clam, collected from the east coast of Korea, was in vitro exposed to p, p -DDT (0.1,0.4 and 1.0 mM) for 30 min and 2,3,7,8-TCDD (0.01, 0.04 and 0.1 ppb) and PCB-153 (0.01, 0.04 and 0.1 ppb) for 7 hr. In the case of DDT exposure, the CYP content and EROD activity of 1.0 mM exposure group increased up to about 117% and 120% of the DMSO solvent control group after 10 min. exposure, respectively. After 2 hr exposure of TCDD, the CYP content and EROD activity were also induced to the range of 103∼110% and 121∼139%, respectively. The PCB-153 exposure group showed 107∼115% of CYP content and 129∼140% of EROD activity after 2 hr exposure. Three test chemicals apparently induced CYP and EROD activity in the microsome of surf clam. The inducing potentials depend en the test chemicals.

• Journal of Digital Convergence
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• v.11 no.4
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• pp.339-350
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• 2013

The decreased body, liver, kidney, spleen and testis weights of guinea pigs by TCDD (2,3,7,8-tetracholorodibenzo-${\rho}$-dioxin) treatment (TT) were statistically significantly increased after treating red ginseng saponin fraction (SF) (p>0.01). After treated with SF, the decreased hematocrits values and numbers of RBC and platelet, activity of amylase and lactate dehydrogenase, levels of uric acid, total protein and albumin by TT were increased, and the increased numbers of WBC, levels of triglyceride, total cholesterol (TC), LDL-cholesterol, HDL-cholesterol, creatinine, blood urea nitrogen, calcium and phosphorus, activities of creatinine kinase, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were decreased after treated with SF. And they all had a statistical significance (p>0.01) except for RBC, WBC, platelet, blood glucose, TC, calcium and albumin. From these results, we knew that SF mollified the acute toxicity induced by TCDD in guinea pigs.