• 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.

• Toxicological Research
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• v.19 no.4
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• pp.325-330
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• 2003

The effects of estrogen on apoptosis induced by 2,3,7,8-tetrachlorodibenzo-p-doxin (TCDD) were examined in cultured MCF-7 cells. TCDD stimulated apoptosis and inhibited the expression of bcl-2 gene in MCF-7 cells grown in the media supplemented with 10% fetal bovine serum. However, TCDD failed to induce apoptosis if cells were grown in the media deprived of all estrogen-like compounds. Removal of estrogen-like compounds from the growth media also led to the activation of bcl-2 gene expression in cells treated with TCDD. Combined treatment of estrogen with TCDD abrogated the binding of Aryl hydrocarbon Receptor (AhR)-TCDD complex to Dioxin response element (DRE) of bcl-2 gene leading to the inhibition of bcl-2 gene expression as well as stimulation of apoptosis. The present study suggests that the binding of estrogen receptor (ER)-estrogen complex to the estrogen responsive element (E) interferes with the binding of AhR- TCDD complex to the DRE and inhibits the bcl-2 expression.