• Journal of Life Science
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• v.13 no.4
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• pp.457-462
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• 2003

Houttuynia Cordata thunb has been used as folk medicine for analgesics, beriberi, edema, hepatitis and icterus etc. We investigated, the effects of Houttuynia Cordata thunb administration on protective in liver of 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) treated rats. Seven days after the injection of TCDD(1${\mu}g$/kg), Houttuynia Cordata thunb (200mg/kg) was administered into rats intraperitoneally for four weeks. We examined the antioxidative enzymatic activity by measuring the level of GOT, GPT in serum and MDA, GSH, GSSG, GPx, SOD and Catalase in liver tissue of rats. GOT activity of Houttuynia Cordata thunb and TCDD administered group(HTT) showed 49.00% of inhibitive effect compared to TCDD-treated abnormal group(TTA). GPT level of HTT group was decreased to the level of Non TCDD-treated group(NTT). MDA content in the TTA group was 1.27 times increased compared to NTT group. HTT group was inhibited by 69.53% compared to TTA group. GSH contents in HTT group was 1.91 times increased compared to TTA group. GSSG contents in HTT group was 46.72% decreased compared to TTA group. SOD and Catalase in TTA group were lower than in NTT group, but SOD and Catalase in HTT group were increased by 82% and 55.45% respectively compared to TTA group.

• Toxicological Research
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• v.23 no.2
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• pp.135-142
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• 2007

Formononetin is an isoflavonoid phytoestrogen found in certain foodstuffs such as soy and red clover. In this study, we examined the action of formononetin with the carcinogen activation pathway mediated through the aryl hydrocarbon receptor (AhR) in MCF-7 breast carcinoma cells. Treating the cells with formononetin alone caused the accumulation of CYP1A1 mRNA as well as elevation in CYP1A1-specific 7-ethoxyresorufin O-deethylase (EROD) activity in a dose dependent manner. However, a concomitant treatment with 7,12-dimethylbenz[a]anthracene (DMBA) and formononetin markedly reduced both the DMBA-inducible EROD activity and CYP1A1 mRNA level. Under the same conditions, formononetin inhibited the DMBA-induced AhR transactivation, as shown by reporter gene analysis using a xenobiotic responsive element (XRE). Additionally, formononetin inhibited both DMBA-inducible nuclear localization of the aryl hydrocarbon receptor (AhR) and metabolic activation of DMBA, as measured by the formation of the DMBA-DNA adducts. Furthermore, formononetin competed with the prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), for binding to the AhR in an isolated rat cytosol. These results suggest that formononetin might be considered as a natural ligand to bind on AhR and consequently produces a potent protective effect against DMBA-induced genotoxicity. Therefore, that's the potential to act as a chemopreventive agent that is related to its effect on AhR pathway as antagonist/agonist.

• Journal of Ginseng Research
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• v.32 no.4
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• pp.382-389
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• 2008

To achieve a better understanding of protective effects of water extracts of Panax ginseng against TCDD-induced toxicities, we monitored physiological and clinical changes in rat for 4 weeks after administrations of each Panax Ginseng extract or TCDD, and co-administration of the two materials. For this study, 120 male Sprague-Dawley (SD) rats weighing 190-210 g each (8 weeks old) were divided into four groups: TCDD-administered, co-administered group with TCDD and ginseng extract, ginseng extract-administered, and control group. The TCDD-administered group received single dose of TCDD in a corn oil vehicle ($25\;{\mu}g/kg$ body weight) by intraperitoneal administration on Day 1. The Panax ginseng extracts-administered group received intraperitoneally 100 mg/kg body weight every other day for one month. For the co-administered group with TCDD and ginseng extracts, Panax ginseng extracts were intraperitoneally administered to rats at 100 mg/kg body weight every other day for one month after a single intraperitoneal dose of $25\;{\mu}g$ of TCDD/kg body weight on Day 1. Panax ginseng extracts attenuated the mortality induced by TCDD administration. The extracts also slightly attenuated the TCDD-induced body weight loss. Administration of TCDD alone increased liver weight at 2, 5, and 16 days after administration of TCDD. Administration of Panax ginseng extracts rather decreased liver weight through whole the experimental period, but which was statistically insignificant. Administration of TCDD alone at $25\;{\mu}g/kg$ body weight increased both serum enzyme activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) at 32 days, indicating that liver damage occurred maximally at that time. Ginseng extract administration caused insignificant changes in serum ALT, but gradually decreased in AST as the exposure time increased. Coadministration of TCDD and ginseng extracts caused serum AST activity to significant recovery to normal value at 16 days and 32 days after exposure to TCDD. The extracts also significantly decreased the TCDD-induced ALT activity after 16 days of TCDD administration. These results suggest that Panax ginseng extracts may possess a protective effect against TCDD-induced toxicities including hepatotoxicity in rats.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.13
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• pp.5149-5153
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• 2014

Background: Chlorophenols (CPs) and related phenoxyacetic acids (PAs) are pesticide groups contaminated with highly toxic 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) during production. PAs and CPs exposure is associated with risk of cancer, but the situation regarding lung cancer has not been clearly defined. We proposed a meta-analysis of published researches to evaluate relationship between chronic exposure to PAs and CPs in pesticide production workplaces and the risk of lung cancer. Materials and Methods: After searching PubMed, Scopus, Scholar Google, Web of Sciences until August 2013, the association between chronic PAs and CPs exposure in production workplace and lung cancer was studied in 15 cohort studies. The standardized mortality rate (SMR) and 95% confidence intervals (CI) were collected from the papers. We used random or fixed-effects models, Egger test, funnel plot and meta regression in our analysis. Results: Five papers with six reports were included in the final analysis. The standardized mortality rate for lung cancer from the random model was 1.18 (95% CI: 1.03-1.35, p=0.014) with moderate heterogeneity. Publication bias was not found for included studies in meta-analysis (p=0.9). Conclusions: Our findings has strengthen the evidence of lung cancer from chronic exposure to chlorophenol related compounds (PAs, CPs).