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논문 기본 정보

자료유형
학술저널
저자정보
Suh, Soo-Kyung (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Jung, Ki-Kyung (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Jeong, Youn-Kyoung (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Kim, Hyun-Ju (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Lee, Woo-Sun (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Koo, Ye-Mo (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Kim, Tae-Gyun (Genetic Toxicology Team, Toxicological Research Department, National Institute of Toxicological Research, Korea Food and Drug Administration) Kang, Jin-Seok Kim, Joo-Hwan Lee, Eun-Mi Park, Sue-Nie Kim, Seung-Hee Jung, Hai-Kwan
저널정보
대한독성유전단백체학회 Molecular & cellular toxicology Molecular & cellular toxicology 제2권 제4호
발행연도
2006.1
수록면
236 - 243 (8page)

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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.
#Toxicogenomics #Acetaminophen #Microarray #Hetotoxicity

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