• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.11a
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• pp.51-58
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• 2002

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.42-58
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• 2002

Acute Cd exposure produces hepatotoxicity, whereas chronic Cd exposure produces nephrotoxicity, hematotoxicity, immunotoxicity and bone damage. Previous experiments suggest that the low-molecular-weight, metal-binding protein metallothionein (MT) in liver protects against liver injury, but is responsible for the kidney injury observed after chronic Cd exposure.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.107-114
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• 2002

Cholestatic liver injury results from the accumulation of toxic bile salts within the liver. The aim of the present study was to understand the mechanism of bile salts-induced hepatocellular apoptosis in bile duct-ligated (BDL) rats, using Western blot and immunohistochemical analysis.(omitted)

• Korean Journal of Veterinary Pathology
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• v.1 no.1
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• pp.13-25
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• 1997

The anticarcinogenic effects of dimethyl disulfide(DMDS, methyl disulfide)and diallyl disulfide(DADA, allyl disulfide) were studied in a 28 weeks rat multi-organ carcinogenesis model. neoplastic and preneoplastic lesions were observed in the liver kidney thyroid gland esophagus duodenum colon, rectum and adrenal gland. Tesults showed that neoplastic lesions in the kidney liver and thyroid gland were inhibited by DADS but those in the liver and colon were enhanced by DMDS when compared to positive control group. incidence of neoplastic lesions in the other organs were not changed by DMDS or DADS exposure. While GST-p positive foci in the liver were increased by DMDS, DADS had no effect. There was no significant histopathological lesion in DMDS or DADS treated group without pretreatment with carcinogens.

• Environmental Analysis Health and Toxicology
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• v.7 no.1_2
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• pp.35-43
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• 1992

Mugwort has been used as a Korean folk medicine in treating liver diseases acting as an analgesics, sedative, diuresis, choleretics. This study was perfomed to evaluate the effect of mugwort extracts on the changes of enzyme activities, lipid accumulation of the serum and liver, when hepatotoxicity was induced by benzo(a)pyrene. The results are as follows: 1. Mugwort water extract administration prevented the increase of serum and liver AST, ALT, LDH, ${\gamma}$-GTP, liver ALP activities and bilirubin content caused by B(a)P injection. 2. The increase of serum and liver ALT, LDH, ${\gamma}$-GTP, serum AST activities and liver bilirubin contents in B(a)P treated group were decreased by mugwort methanol extract treatment. 3. Serum and liver total cholesterol, phospholipid, triglyceride level and serum HDL-cholesterol level were increased by B(a)P treatment. After combined treatment of mugwort water and methanul extracts, these lipid content were significantly decreased. 4. The hepatotropic effect of mugwort water extract and after-treatment against B(a)P induced hepatotoxicity was superior to that of methanol extract and pretreatment.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.136-136
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• 2004

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.135-135
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• 2004

• Molecular & Cellular Toxicology
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• v.3 no.2
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• pp.137-144
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• 2007

The mechanism of cytotoxicity of doxifluridine, a prodrug fluorouracil (5-FU), has been ascribed to the misincorporation of fluoropyrimidine into RNA and DNA and to the inhibition of the nucleotide synthetic enzyme thymidylate synthase. Increased understanding of the mechanism of 5-FU has led to the development of strategies that increases its anticancer activity or predicts its sensitivity to patients. Using GeneChip?? Rhesus Macaque Genome arrays, we analyzed gene expression profiles of doxifluridine after two weeks repeated administration in cynomolgus monkey. Kegg pathway analysis suggested that cytoskeletal rearrangement and cell adhesion remodeling were commonly occurred in colon, jejunum, and liver. However, expression of genes encoding extracellular matrix was distinguished colon from others. In colon, COL6A2, COL18A1, ELN, and LAMA5 were over-expressed. In contrast, genes included in same category were down-regulated in jejunum and liver. Interestingly, MMP7 and TIMP1, the key enzymes responsible for ECM regulation, were overexpressed in colon. Several studies were reported that both gene reduced cell sensitivity to chemotherapy-induced apoptosis. Therefore, we suggest they have potential as target for modulation of 5-FU action. In addition, the expression of genes which have been previously known to involve in 5-FU pathway, were examined in three organs. Particularly, there were more remarkable changes in colon than in others. In colon, ECGF1, DYPD, TYMS, DHFR, FPGS, DUT, BCL2, BAX, and BAK1 except CAD were expressed in the direction that was good response to doxifluridine. These results may provide that colon is a prominent target of doxifluridine and transcriptional profiling is useful to find new targets affecting the response to the drug.

• Proceedings of the Korean Society of Toxicology Conference
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• 1998.10a
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• pp.55-55
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• 1998

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.314.1-314.1
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• 2001