• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.6
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• pp.1349-1354
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• 1999

This study was carried out to investigate the protective effect of Korean red ginseng water extract (KRG WE) on clinical chemical parameters in male guinea pigs acutely exposed to 2,3,7,8 tetrachlorodibenzo p dioxin(TCDD). Forty male guinea pigs(200 $\pm$20g) were divided into 4 groups. Normal controls(group 1) received vehicle and saline; group 2(single TCDD treated) received TCDD(5 g/kg, single dose) intraperitoneally; group 3 received KRG WE(200mg/kg, i.p.) for 2 weeks from 1 week before TCDD exposure; group 4 received KRG WE for 1 week since the day of TCDD exposure. Increase in body weight was retarded greatly by TCDD exposure. Body weight of animals in group 2 was significantly decreased starting 2 days after TCDD exposure. However, body weight of animals in group 3 increased throughout the experimental period, although the increasing rate was slower than that of group 1. Decrease in body weight was not observed during the experimental period in group 4. Increases in blood glucose, amylase, lipase, total cholesterol, triglyceride, GOT, GPT, and LDH levels by TCDD intoxication were significantly attenuated by the KRG WE treatment(p<0.05). These results provide a strong evidence that Korean red ginseng might be a useful protective agent against TCDD, an endocrine disruptor.

• Korean Journal of Pharmacognosy
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• v.32 no.2 s.125
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• pp.121-127
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• 2001

The effect of bear bile on 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD)-induced hepatotoxicity was investigated in 6-week-old C57BL/6 male mice. Bear bile (100 mg/kg or 500 mg/kg) was administered orally daily for 4 weeks, respectively. From the second week, $10\;{\mu}g/kg$ of TCDD was administered to the bear bile-treated animals orally once a week for 3 weeks (a total of $30\;{\mu}g/kg$). There were no specific clinical findings and significant body weight changes in all groups. Although the livers in TCDD-treated mice appeared a severe hypertrophy and many necrotic foci, and changed to yellow-brown color in gross findings, these lesions were remarkably reduced by bear bile administration. The elevated serum activities of alanine transaminase, aspartate transaminase, alkaline phosphatase, and lactate dehydrogenase due to TCDD were significantly decreased by bear bile treatment (P<0.05). The lipid peroxidation induced by TCDD was significantly prevented by bear bile administration (P<0.05). In histological examinations, there were a moderate necrosis of hepatic cells around central veins, severe cytoplasmic vacuolizations, inflammatory cell infiltrations, and remarkable fatty changes in the liver of TCDD-treated animals. However, the lesions were dose-dependently inhibited by the bear bile treatments. These findings indicate that bear bile may have a protective effect against TCDD-induced hepatotoxicity in mice.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.211.2-211.2
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• 2003

Saururus Chinensis Baill (Saururaceae) has been used as folk medicine for analgesics, beriberi, edema, hepatitis, and icterus, etc. Hepatoprotective effects of Saururus chinensis Baill (SCB) administration on function of the biochemical parameters in liver of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treated rats were investigated. After 7 days from TCDD(1$\mu\textrm{g}$/kg) injection, SCB(200mg/kg) was administered into rats intraperitoneally for 4 week.s We examined the antioxidative enzymatic activity by measuring the level of AST and ALT in serum and SOD, Catalase, GPx, GSH and GSSG in liver tissue of rats. (omitted)

• Journal of Environmental Health Sciences
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• v.35 no.4
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• pp.259-268
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• 2009

This study was carried out to investigate the protective effect of Red Ginseng Saponins on 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induced toxicities in guinea pigs ($200{\pm}10$ g). Normal control (NC) group guinea pigs ($200{\pm}10$ g) received vehicle and saline, while the TCDD-treated (TT) group was given water-extract (WE), saponin fraction (SF) and non-saponin fraction (NSF). Korean red ginseng fractions were administered from 1 week before TCDD-exposure for 4 weeks. Body weight loss and deteriorated clinical parameters related to sugar metabolism and liver function such as lipase and AST, respectively, these were significantly reduced by both saponin and non-saponin fractions. However, increase of lipase was attenuated by the saponin fraction in a dose-dependent manner. Only AST was affected by the saponin fraction. The results suggest that saponins are active substances in the Korean red ginseng water extract against TCDD induced toxicities in Guinea pigs.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.4
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• pp.782-787
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• 2002

This study was carried out to investigate the protective effect of chitosan on lipid peroxidation and key lipid parameters in Sprague-Dawley rat (SO rat) accutely exposured to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Male SO rats received single intraperitoneal (ip) injection of TCDD (40 j.lg/kg), and were given diet containing 3 or 5% chitosan for 4 weeks from 1 week before TCDD treatment. The gain in body weight was less in group treated with TCDD than in CON group, while that of Ch/H+ TCDD group (5% chitosan diet) increased. The decrease in liver and testis weight caused by TCDD was prevented by high dietary intake of chitosan (5% chitosan). Serum (total cholesterol, triglyceride, HDL-C, and LDL-C) and liver lipid parameters (total lipid, total cholesterol, and triglyceride) were significantly elevated in TCDD-induced rats, but these parameters excluding HDL-C were significantly reduced in high dietary intake of chitosan (5% chitosan). These findings suggest that chitosan is believed to be a possible protective effect against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rat.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.125-125
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• 2002

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the best characterized environmental pollutants and is capable of causing a wide variety of toxicities including teratogenesis. TCDD has been known to increase as well as to decrease proliferation rates depending on the experimental conditions.(omitted)

• Toxicological Research
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• v.15 no.1
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• pp.89-93
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• 1999

2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD) is known to induce cytochrome p450 1A1 and to activate c-Src kinase and p21 Ras. This study examined the molecular interactions of adaptor proteins including Shc, Grb2, and Sos in rat primary hepatocytes and their relationship to the induction of CYP1A1 by TCDD. TCDD induced CYP1A1 level and EROD activity in a dose-dependent mode. Sos/Grb2 association isincreased by TCDDㅑㅜ a dose dependent mode. Tyrosine phosphorylated Shc, mainly p152, onloads to Grb2/Sos complex upon TCDD stimulation. The electrophoretic mobility shift of Sos is showed by TCDD. These results indicate that TCDD modulated the molecular interaction features of adaptor compoes proteins including Shc, Grb2, and Cnl in early signaling pathway of TCDD-mediated CYP 1A1 induction of rat primary hepatocyte.

• Biomedical Science Letters
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• v.18 no.1
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• pp.1-9
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• 2012

Differentially expressed genes by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were identified in order to evaluate them as dioxin-sensitive markers and crucial signaling molecules to understand dioxin-induced toxic mechanisms in human bronchial cells. Gene expression profiling was analyzed by cDNA microarray and ten genes were selected for further study. They were cytochrome P450, family 1, subfamily B, polypeptide 1 (CYP1B1), S100 calcium binding protein A8 (calgranulin A), S100 calcium binding protein A9 (calgranulin B), aldehyde dehydrogenase 1 family, member A3 (ALDH6) and peroxiredoxin 5 (PRDX5) in up-regulated group. Among them, CYP1B1 was used as a hallmark for dioxin and sharply increased by TCDD exposure. Down-regulated genes were IK cytokine, interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), nuclease sensitive element binding protein 1 (NSEP1), protein tyrosine phosphatase type VI A, member 1 (PTP4A1), ras oncogene family 32 (RAB32). Although up-regulated 4 genes in microarray were coincided with northern hybridization, down-regulated 5 genes showed U-shaped expression pattern which is sharply decreased at lower doses and gradually increased at higher doses. These results introduce some of TCDD-responsive genes can be sensitive markers against TCDD exposure and used as signaling cues to understand toxicity initiated by TCDD inhalation in pulmonary tissues.

• 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

• Molecular & Cellular Toxicology
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• v.1 no.2
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• pp.78-86
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• 2005

Dioxins, especially 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD or dioxin), are ubiquitous environmental contaminants. TCDD is known that it has toxic effects in animals and humans, including chloracne, immune, reproductive and developmental toxicities, carcinogenicity, wasting syndrome and death. TCDD induces a broad spectrum of biological responses, including disruption of normal hormone signaling pathways, reproductive and developmental defects, immunotoxicity, liver damage, wasting syndrome and cancer. Many researches showed that TCDD induces gene expression of transcriptional factors related cell proliferation, signal transduction, immune system and cell cycle arrest at molecular and cellular levels. These toxic actions of TCDD are usually mediated with AhR (receptor, resulted from cell culture, animal and clinical studies). cDNA microarray can be used as a highly sensitive and informative marker for toxicity. Additionally, microarray analysis of dioxin-toxicity is able to provide an opportunity for the development of candidate bridging biomarkers of dioxin-toxicity. Through microarray technology, it is possible to understand the therapeutic effects of agonists within the context of toxic effects, classify new chemicals as to their complete effects on biological systems, and identify environmental factors that may influence safety.