• Title, Summary, Keyword: 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD)

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Protective Effect of Cornu Cervi Parvum Extract on Toxicity Induced by 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Rat (다이옥신-유도 독성에 대한 녹용 추출물의 방어효과)

  • Hwang Seock Yeon;Yang Jin Bae;Chang Cheoul Soo;Lee Young Chan;Lee Hyung Chul
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.16 no.4
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    • pp.674-679
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    • 2002
  • The toxicity and bioaccumulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs) continues to be a focus of research in human and various species. The main human exposure is via the dietary route. This study was carried out to investigate the protective effect of Cornu Cervi Parvum extract on clinical parameters and hepatotoxicity in Sprague-Dawley rat (SD rat) accutely exposured to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Male SD rats received single intraperitoneal (ip) injection of TCDD (40 ㎍/kg), and administered 10 or 20 mg/kg/day of the ethanol extract oral injection 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 C/H+ TCDD group (Cornu Cervi Parvum extract 20 mg/kg/day) increased. The decrease in spleen and testis weight caused by TCDD was prevented by Cornu Cervi Parvum extract 20 mg/kg/day. The fluctuation in BUN content, WBC and platelet count by TCDD intoxication were significantly attenuated by the ethanol extract treatment (20 mg/kg/day for 4 weeks). Treatments of rats with the extract (10 or 20 mg/kg/day) were significantly reduced AST and ALT levels compared with TCDD-treated group. Moderate swelling of hepatocytes, hyperchromatism, acidophilic cytoplasm and cytoplasmic vacuolation were observed in TCDD-treated animals (TCDD group). The administration of EtOH extract 10 or 20 mg/kg along with TCDD significantly alleviated the liver histopathological alteration induced by TCDD. These results suggest that Cornu Cervi Parvum extract can be useful as a protective agent against TCDD, an endocrine disruptor.

IDENTIFICATION OF 2,3,7,8-TETRACHLORODIBENZO-P DIOXIN RESPONSIVE GENES IN HUMAN HACAT AND CHANG LIVER CELLS

  • Ryeom, Tai-Kyung;Kang, Ho-Il;Park, Young-Sill;Eom, Mi-Ok;Park, Mi-Sun;Jee, Seung-Wan;Kim, Ok-Hee
    • Proceedings of the Korean Society of Toxicology Conference
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    • pp.129-129
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    • 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)

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Protective Effects of Bear Bile against Hepatotoxicity Induced by 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) in Mice (마우스에서 2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD)에 의해 유발된 간독성에 대한 웅담의 방어효과)

  • Zhang, Hu-Song;Nam, Sang-Yoon;Kang, Jong-Koo
    • Korean Journal of Pharmacognosy
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    • v.32 no.2
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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.

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Protective Effects of Red Ginseng Saponins against to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Induced Toxicity in Guinea Pigs (기니피그에서 홍삼 사포닌의 2,3,7,8-TCDD 독성 방어 효과)

  • Hwang, Seock-Yeon;Lee, Chan-Yong
    • 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.

Effect of Chitosan on the Lipid Metabolism in Treated 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Rats (다이옥신 처리에 대한 키토산이 지질대사에 미치는 효과)

  • Hwang Seock Yeon;Yang Jin Bae;Chang Cheoul Soo;Kim Tae Up;Lee Hyung Chul
    • 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.

Hepatoprotective Effects of Saururus chinensis Baill against 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) Induced Toxicity

  • Lee, Sang-Hun;Kim, Hee-Jin;Lee, Jin-Young;Ha, Bae-Jin
    • Proceedings of the PSK Conference
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    • pp.211.2-211
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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)

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Tumorigenic Effects of 2,3,7,8-Tetrachlorodibenzo-$\rho$-dioxin in Normal Human Skin and Lung Fibroblasts (사람의 정상 피부세포 및 폐세포의 발암에 미치는 2,3,7,8-Tetrachlorodibenzo-$\rho$-dioxin의 영향)

  • Kang, Mi-Kyung;Ryeom, Tai-Kyung;Kim, Kang-Ryune;Kim, Ok-Hee;Kang, Ho-Il
    • 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.

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Effects of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) on Gene Expression in Mouse Skin Carcinogenesis (마우스 피부암 발생과정에 있어서 2,3,7,8-Tetrachlorodibenzo-p­Dioxin (TCDD) 처리에 의한 유전자발현 변화 연구)

  • Ryeom Tai Kyung;Kim Ok Hee;Kong Mi Kyung;Park Mi Sun;Jee Seung Wan;Eom Mi Ok;Kang Ho Il
    • Environmental Mutagens and Carcinogens
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    • v.25 no.1
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    • pp.40-46
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    • 2005
  • 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although the mechanism of carcinogenesis by TCDD is unclear, it is considered to be a non-genotoxic compound and tumor promoter. In our experiment, we investigated the effects of TCDD on gene expression in mouse skin carcinogenesis. We used cDNA microarray to detect the differential gene expression in tumors induced in hairless mouse skin by MNNG plus TCDD protocol. We found that erb-2, c-ets2 and p27$^{kip1}$ were significantly up-regulated, but TNFR2, AKT-l, integrin $\beta$l, maspin, IGF-l, c-raf-l, Rb were significantly down-regulated, in tumor region, respectively. We also found that the expression of 53 genes involved in cen cycle, signal transduction, apoptosis, adhesion molecule, angiogenesis, and invasion, were changed two fold more, in tumor surrounding region. These data suggest that TCDD alters the expression of a large array of genes involved in apoptosis, cytokine production and angiogenesis in mouse skin carcinogenesis.

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ROLE OF CELL CYCLE REGULATORS IN NEUTOTOXIC EFFECTS OF 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN

  • Lee, Yong-Soo;Jin, Da-Qing;Kim, Jung-Ae
    • Proceedings of the Korean Society of Toxicology Conference
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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)

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2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin Induces Recruitment of Shc/Cbl/Grb2/Sos Conplex in Early Signaling Pathway of CYP1A1 Induction in the Primary Culture of Hepatocytes

  • Kim, Bok-Ryang;Park, Rae-Kil;Kim, Dong-Hyun
    • 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.

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