• Proceedings of the Korean Society of Embryo Transfer Conference
• /
• 2001.05a
• /
• pp.25-26
• /
• 2001

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2001.10a
• /
• pp.191-192
• /
• 2001

Although the incidence rates of gastric cancer and liver cancer, the most common cancers in Korea, are tending decrease, lung cancer is on the increase every year as cause of cancer death as well as incidence rate in Korea. And cigarette smoke is believed to be responsible for 90% of lung cancer. Many investigators have reported an association between genetic polymorphism of cytochromes P-450 (CYPs) or glutathoine S-transferase (GSTs) and susceptibility to lung cancer.(omitted)

• Proceedings of the Korean Society of Plant Biotechnology Conference
• /
• 2003.04a
• /
• pp.94-94
• /
• 2003

• Molecular & Cellular Toxicology
• /
• v.2 no.4
• /
• pp.236-243
• /
• 2006

Microarray analysis of gene expression has become a powerful approach for exploring the biological effects of drugs, particularly at the stage of toxicology and safety assessment. Acetaminophen (APAP) has been known to induce necrosis in liver, but the molecular mechanism involved has not been fully understood. In this study, we investigated gene expression changes of APAP using microarray technology. APAP was orally administered with a single dose of 50 mg/kg or 500 mg/kg into ICR mice and the animals were sacrificed at 6, 24 and 72 h of APAP administration. Serum biochemical markers for liver toxicity were measured to estimate the maximal toxic time and hepatic gene expression was assessed using high-density oligonucleotide microarrays capable of determining the expression profile of >30,000 well-substantiated mouse genes. Significant alterations in gene expression were noted in the liver of APAP-administered mice. The most notable changes in APAP-administered mice were the expression of genes involved in apoptosis, cell cycle, and calcium signaling pathway, cystein metabolism, glutatione metabolism, and MAPK pathway. The majority of the genes upregulated included insulin-like growth factor binding protein 1, heme oxygenase 1, metallothionein 1, S100 calcium binding protein, caspase 4, and P21. The upregulation of apoptosis and cell cycle-related genes were paralleled to response to APAP. Most of the affected gene expressions were returned to control levels after 72 hr. In conclusion, we identified potential hepatotoxicity makers, and these expressions profiling lead to a better understanding of the molecular basis of APAP-induced hapatotoxicity.

• Molecular & Cellular Toxicology
• /
• v.3 no.2
• /
• pp.98-106
• /
• 2007

Genotoxic stress triggers a variety of biological responses including the transcriptional activation of genes regulating DNA repair, cell survival and cell death. In this study, we investigated to examine gene expression profiles and genotoxic response in TK6 cells treated with DNA damaging agents MNNG (N-methyl-N'-nitrosoguanidine) and hydrogen peroxide $(H_2O_2)$. We extracted total RNA in three independent experiments and hybridized cRNA probes with oligo DNA chip (Applied Biosystems Human Genome Survey Microarray). We analyzed raw signal data with R program and AVADIS software and identified a number of deregulated genes with more than 1.5 log-scale fold change and statistical significancy. We indentified 14 genes including G protein alpha 12 showing deregulation by MNNG. The deregulated genes by MNNG represent the biological pathway regarding MAP kinase signaling pathway. Hydrogen peroxide altered 188 genes including sulfiredoxins. These results show that MNNG and $H_2O_2$ have both uniquely regulated genes that provide the potential to serve as biomarkers of exposure to DNA damaging agents.

• 한국생물공학회:학술대회논문집
• /
• 2005.04a
• /
• pp.383-383
• /
• 2005

• Proceedings of the PSK Conference
• /
• 2002.10a
• /
• pp.245.2-246
• /
• 2002

We studied on the antiproliferative effects of bile acids and their derivatives on HepG2 human hepatocellular carcinoma cells. Ursodeoxycholic acid (UDCA) and its synthetic derivative HS-1030. and chenodeoxycholic acid (CDCA) and its synthetic derivatives. HS-1199 and HS\ulcorner200, were used. We focused on the regulation of cell cycle and induction of apoptosis by these bile acid derivatives. (omitted)

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2004.11a
• /
• pp.112-112
• /
• 2004

• Proceedings of the Korean Society of Plant Biotechnology Conference
• /
• 2003.04a
• /
• pp.95-95
• /
• 2003

• BMB Reports
• /
• v.34 no.3
• /
• pp.259-261
• /
• 2001