• Title/Summary/Keyword: toxicological study

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The Study on the drug pharmacokinetics according to the progression of liver disease

  • Sohn, Soo-Jung;Choi, Hong-Serck;Ahn, Mee-Ryung;Chung, Hye-Joo;Yoo, Tae-Moo;Lee, Min-Ho;Park, Moon-Seung;Shin, In-Chul;Kim, Ju-ll
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.308.1-308.1
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    • 2003
  • We underwent this study to know correlation between the amount of portosysternic shunt/hepatic fibrosis and bioavailability parameters such as AUC, Cmax, Tmax and t1 /2 of high extraction ratio drug, propranolol, in CCl4-induced liver cirrhosis model of rats. This study describes the bioavaility study of propranolol(5 mg/kg), Shunt Index using thallium-201 per rectum scintigraphy to to measure the amount of portosystemic shunt indirectly and intrahepatic hydroxyproline content performed in the CCl4-induced liver cirrhosis model of rats. (omitted)

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13-weeks toxicity study of fructus of Aristolochiae contorta in SD rat

  • Hwang, Myung-Sil;Park, Mi-Sun;Moon, Gi-Young;Lee, Ji-Sun;Yum, Young-Na;Cho, Dae-Hyun;Yang, Ki-Hwa
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2002.11b
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    • pp.158-158
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    • 2002
  • The potential toxicological effects of aristolochic acid (AA), a natural component in Aristolochiaceae family, were investigated. The 13-week toxicity study consisted of groups of 10 SD rat/sex administrated water containing 0, 0.05, 0.5, or 5 mg/kg per day AA (Study 1). The tested groups were terminated on Test Day 90 due to mortality and overt clinical signs of toxicity.(omitted)

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Toxicogenomics Study on TK6 Human Lymphoblast Cells Treated with Mitomycin C

  • Kim, Joo-Hwan;Koo, Ye-Mo;Lee, Woo-Sun;Suh, Soo-Kyung;Kang, Jin-Seok;Han, Eui-Sik;Kim, Seung-Hee;Park, Sue-N.
    • Molecular & Cellular Toxicology
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    • v.3 no.3
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    • pp.165-171
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    • 2007
  • Mitomycin C (MMC), an antitumor antibiotic isolated from Streptomyces caespitosus, is used in chemotherapy of gastric, bladder and colorectal cancer. MMC is activated in vivo to alkylate and crosslink DNA, via G-G interstrand bonds, thereby inhibiting DNA synthesis and transcription. This study investigates gene expression changes in response to MMC treatment in order to elucidate the mechanisms of MMC-induced toxicity. MMC was admistered with single dose (0.32 and 1.6 ${\mu}M$) to TK6 cells. Applied Biosystem's DNA chips were used for identifying the gene expression profile by MMC-induced toxicity. We identified up- or down-regulated 90 genes including cyclin M2, cyclin-dependent kinase inhibitor 1A (p21, cip1), programmed cell death 1, tumor necrosis factor (ligand) superfamily, member 9, et al. The regulated genes by MMC associated with the biological pathways apoptosis signaling pathway. Further characterization of these candidate markers related to the toxicity will be useful to understand the detailed mechanism of action of MMC.

The Effects of Diallyl Disulfide on Antimetastatic Potential of B16-F10 Murine Melanoma Cells (B16-F10 Murine Melanoma 세포의 암전이 억제에 미치는 Diallyl Disulfide의 효과)

  • Kang, Mi-Kyung;Jun, Hye-Seung;Yum, Yung-Na;Hwang, Myung-Sil;Park, Mi-Sun;Kim, Ok-Hee
    • Toxicological Research
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    • v.22 no.4
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    • pp.349-356
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    • 2006
  • Diallyl disulfide (DADS), an oil-soluble organosulfur compound in garlic has been reported to suppress tumor growth and to induce apoptosis in cancer. In the present study, we investigated the effects of DADS on pulmonary metastasis of B16-F10 murine melanoma cells. DADS (i.p. 40 mg/kg) significantly (p<0.05) reduced the number of pulmonary metastatic nodules (48%) in experimental pulmonary metastasis assay. We also found that DADS inhibited adhesion, invasion and migration of B16-F10 melanoma cells in a dose-dependent manner. To study the antimetastatic potential of DADS, we performed the effects of DADS on matrix metalloproteinase activity. DADS significantly inhibited the expression of matrix metalloproteinase-2 activity in B16-F10 cells by gelatin zymography. These results suggest that DADS prevent metastasis in part through suppression of migration of B16-F10 melanoma cells by Inhibiting matrix metalloproteirase-2 responsible for degradation of extracellar matrix.