• Biomedical Science Letters
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• v.7 no.4
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• pp.197-203
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• 2001

This study was carried out to investigate the effect of crude ginseng saponin (CGS) on clinical pathological parameters in adult female guinea pigs exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). A total of 80 guinea pigs (800$\pm$20 g) were divided into 8 groups: group 1 (normal control group) was given vehicle (com oil containing small amount of acetone and DMSO) and saline; group 2 (single TCDD-treated) received TCDD (1 $\mu\textrm{g}$/kg, i.p.) and saline (i.p.); groups 3 and 4 were administered CGS at daily i.p. doses of 10 and 20 mg/kg for 4 weeks, respectively; groups 5 and 6 were administered CGS (10 and 20 mg/kg, respectively) for 5 weeks starting 1 week before TCDD-exposure; groups 7 and 8 were administered CGS (10 and 20 mg/kg, respectively) for 3 weeks from 1 week after TCDD-exposure. CGS was prepared by Diaion HP-20 adsorption chromatography. Body weight of G2 was significantly decreased from the 2nd week after TCDD-exposure (p<0.01). Body weights of the CGS-treated groups were also decreased by TCDD-exposure, but the weight loss was greatly retarded compared with that of G2. Increase in blood glucose, amylase, lipase, total cholesterol. triglyceride, AST and LDL-cholisterol levels by TCDD exposure was significantly attenuated by the CGS-treatment (p<0.05). From these results, we found that saponin the main active ingredient of ginseng, played a protective role against TCDD-induced toxicity in not only male but female guinea pigs.

• Biomedical Science Letters
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• v.26 no.2
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• pp.66-74
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• 2020

This study was carried out to investigate the protective effect of crude saponin from Platycodon grandiflorum on Clinical chemical parameters in male rats acutely exposed to 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD). Crude saponin was prepared from Korean Platycodon grandiflorum with Diaion HP-20 adsorption chromatography after extraction of 80% ethanol at 75℃. The crude saponin was confirmed by thin layer chrmatography. When compared with ginseng saponins, the crude saponin had both a few number of saponins and a broad distribution. Forty male rats (200±20 g) were divided into 4 groups. Normal control (NC) group received vehicle and saline; TCDD-treated (TT) group received TCDD (40 ㎍/kg, single dose) intraperitoneally; Platycodon grandiflorum saponin (PG5 and PG10) groups received crude saponin 5 mg/kg and 10 mg/kg (p.o), respectively, for 2 weeks before 1 week of TCDD-exposure. Increase of body weight was retarded greatly by TCDD-exposure. Body weight of animals in TT group was significantly decrease after 2 days of TCDD-exposure. However, body weights of animals in PG groups increased through the experimental perimental period, although the increasing rate was slower than that of NC group. Increases in contents of blood glucose, total cholesterol and triglyceride (TG) and activities of amylase, lipase, AST, ALT and LDH by toxic action of TCDD were significantly attenuated by crude saponin from Platycodon grandiflorum (P<0.05). In conclusion, these results suggest that crude saponin prepared from Korean Platycodon grandiflorum might be a member of useful protective agents against TCDD, which is one of the environmental hormones.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.125-125
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• 2001

B cell has been identified as the sensitive cellular target responsible for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) -induced immune suppression. In isolated cell systems, the differentiation of B cells into antibody secreting plasma cells is believed to be inhibited by TCDD. We also have previously demonstrated IgM secretion was suppressed by TCDD in LPS-activated murine B cell line, CH12.LX.(omitted)

• Environmental Mutagens and Carcinogens
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• v.24 no.2
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• pp.91-98
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• 2004

Although 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) is a powerful carcinogen in several species, limited model system exist to study carcinogenicity of this compound at cellular level. To enhance our under-standing of carcinogenicity of TCDD at cellular level, we investigated micronucleus (MN) frequency as a index of genetic toxicity and whether TCDD can transform the human cells in culture. Normal human cell lines, skin keratinocyte HaCaT, Chang liver and breast MCF10A cells were used. TCDD did not affect the cell viability of the Chang liver, HaCaT and MCF10A cells. The frequency of micronucleus was increased after treatment of TCDD for 24hr in Chang liver and HaCaT cells, but not changed in MCF10A cells. And we observed putative transformed cells in Chang liver cells exposed to 1 $\mu$M TCDD for 2 weeks. The putative transformed cells were also observed in HaCaT cells with subsequent exposure to TCDD (0.1, 1, 10, 100 nM) for 2 weeks after initial exposure to MNNG, but not observed in MCF10A cells. Collectively, these results indicate that the ability of TCDD to induce micronuclei may be involved in cellular transformation of Chang liver and HaCaT cells. Our putative TCDD-transformed cells of Chang liver and HaCaT are expected to provide a clue to the elucidation of TCDD-induced transformation pathway.

• Natural Product Sciences
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• v.14 no.2
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• pp.73-80
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• 2008

The authors screened the pharmacological effects of 50% ethanol extracts of Yacon on spermatogenesis in rats. Numbers of sperm in animals treated with 25, 50, or 100 mg/kg/day for 6 weeks of Yacon tuber extracts (YTE) were approximately 1.51, 1.61 and 1.78 times higher, respectively, than in the untreated control group. Moreover, the spermatogenic effect of Yacon leaf extract was found to be $1.03{\sim}1.38$ times higher than that of YTE. The ameliorative effect of Yacon tuber extracts on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced toxicities in the rat were also investigated. Rats were assigned to three groups (6 rats/group), a control group, a TCDD exposed group, and a group treated with Yacon tuber extract (YTE) after TCDD exposure (TCDD/YTE group). 40 ${\mu}g/kg$ of TCDD was injected i.p., and 200 mg/kg/day of YTE was also administered for 4 weeks by oral gavage. The TCDD/YTE group showed a significant increase in sperm number as compared with the TCDD exposed group. In conclusion, TCDD induced testicular toxicity was significantly ameliorated by YTE. The results of the present study suggest that Yacon extract is a possible therapeutic for the treatment of spermatogenic disorder.

• YAKHAK HOEJI
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• v.50 no.4
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• pp.220-227
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• 2006

The therapeutic effect of tissue cultured root of mountain ginseng (Panax ginseng) (tcMG) on 2,3,7,8-tetrachlorodaibenzo-p-dioxin (TCDD) induced toxicity in rat was investigated. The rats were assigned into three groups (10 rats/group), control, TCDD exposed group and tcMG treated group after TCDD exposed. $50\;{\mu}g/kg$ of TCDD was injected by i.p. for TCDD exposed group and 30 mg/kg of tcMG saponin was administered for 4 weeks by oral gavage for tcMG treated group. The weights of body, spleen, kidney, thymus, testes and epididymides were decreased in the single TCDD treatment. However these organs was significantly recovered by tcMG saponin except thymus (p<0.05). tcMG decreased the level of hepatic demage maker enzymes, AST and ALP. It also lowered total cholesterol and triglyceride. The level of serum triglyceride was significantly decreased in tcMG saponin treated group compared with the control. Histopathological examination revealed morphological change in the liver spleen, thymus and testes of TCDD treated rats. However they were relatively well preserved in the tcMG treatment group. In conclusion, TCDD induced toxicity was some repaired by tcMG. tcMG may be useful for prevention and treatment of TCDD induced toxicity.

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.94-94
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• 2003

Endocrine disrupters (EDs) are exogenous chemicals that interfere with the production, releasing, metabolism, excretion, binding of natural hormones, and whole endocrine systems. EDs are very dangerous since they are extremely stable, not easily degraded, and accumulated in fat and tissue. 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) is known as the most toxic EDs. Therefore, this study was conducted to investigate the effects of TCDD on proliferation of human breast cancer (MCF-7) and endometrial adenocarcinoma (Hec-1B) cells. 10, 100, and 1000 nM of TCDD were treated with steroid free condition. Viable cell counting, MTT, and BrdU assay was performed to investigate cell proliferation. Apoptosis was investigated using DNA laddering. Although, DNA fragmentation as the evidence of apoptosis was not detected, all of these cell lines showed restricted proliferation at 48 hrs after 100 and 1000 nM TCDD treatments. Recently, it has been reported that the expression of transforming growth factor $\beta$s (TGF-$\beta$s) are increased in TCDD treatment and also involved in regulation of cell cycle. Therefore, these results were considered that the decreased cell prolifcration by TCDD is related to the expression of TGF-$\beta$s.

• Environmental Mutagens and Carcinogens
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• v.26 no.3
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• pp.77-85
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• 2006

2,3,7,8-Tetrachlorodibenzo-$\rho$-dioxin(TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although TCDD is recognized as potent carcinogens, relatively little is known about their role in the tumor promotion and carcinogenesis. It is known that TCDD can increase of cancer risk from various types of tissue by a mechanism possibly involving the aryl hydrocarbon receptor (AhR) activation. In this study, effects of TCDD on cellular proliferation of normal human skin and lung fibroblasts, Detroit551 and WI38 cells were investigated. In addition, to enhance our understanding of TCDD-mediated carcinogenesis, we have investigated process in which expression of Erk1/2, cyclinD1, oncogene such as Ha-ras and c-myc, and their cognate signaling pathway. TCDD that are potent activators of AhR-mediated activity was found to induce significant increase of cytochrome P4501A1 mRNA expression, suggesting a presence of functional AhR. These results support that CYP1A1 enzyme may be involved in the generation of TCDD-induced toxicity. Moreover mitogen-activated protein kinases (MARKs) phosphorylation and cyclin D1 overexpression are induced by TCDD, which corresponded with the progression of cellular proliferation. However, TCDD did not affected Ha-ras and c-myc mRNA expression. Taken together, it seems that TCDD are could be a part of cellular proliferation in non-tumorigenic normal human cells such as Detroit551 and WI38 cells through the upregulation of MAPKs signaling pathway regulating growth of cell population. Therefore, AhR-activating TCDD could potentially contribute to tumor promotion and Detroit551 and WI38 cells have been used as a detection system of tumorigenic effects of TCDD.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.6
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• pp.469-476
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• 2012

2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) is an environmental toxicant with a polyhalogenated aromatic hydrocarbon structure and is one of the most toxic man-made chemicals. Exposure to 2,3,7,8-TCDD induces reproductive toxicity, immunotoxicity, and hepatotoxicity. In this study, we evaluated how 2,3,7,8-TCDD-induced hepatotoxicity affect the expression of heat shock proteins and antioxidant enzymes using the real-time polymerase chain reaction (PCR) in rat. 2,3,7,8-TCDD increased heat shock protein (Hsp27, ${\alpha}$-B-crystallin, Mortalin, Hsp105, and Hsp90s) and antioxidant enzymes (SOD-3, GST and catalase) expression after a 1 day exposure in livers of rats, whereas heat shock protein (${\alpha}$-B-crystallin, Hsp90, and GRP78) and antioxidant enzymes (SOD-1, SOD-3, catalase, GST, and GPXs) expression decreased on day 2 and then slowly recovered back to control levels on day 8. These results suggest that heat shock proteins and antioxidant enzymes were induced as protective mechanisms against 2,3,7,8-TCDD induced hepatotoxicity, and that prolonged exposure depressed their levels, which recovered to control levels due to reduced 2,3,7,8-TCDD induced hepatotoxicity.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.178-178
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• 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)