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Hepatic gene expression profiling and lipid homeostasis in mice exposed to seatogenic drug, tetracycline

Title
Hepatic gene expression profiling and lipid homeostasis in mice exposed to seatogenic drug, tetracycline
Authors
Yin H.-Q.Kim M.Kim J.-H.Kong G.Lee M.-O.Kang K.-S.Yoon B.-I.Kim H.-L.Lee B.-H.
Ewha Authors
김형래
SCOPUS Author ID
김형래scopus
Issue Date
2006
Journal Title
Toxicological Sciences
ISSN
1096-6080JCR Link
Citation
vol. 94, no. 1, pp. 206 - 216
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Tetracycline is one of a group of drugs known to induce microvesicular steatosis. In the present study, we investigated the effects of tetracycline on gene expression in mouse liver, using Applied Biosystems Mouse Genome Survey Microarrays. A single oral dose of 0.1 or 1 g/kg tetracycline was administered to male ICR mice, and liver samples were obtained after 6, 24, or 72 h. Histopathological evaluation showed microvesicular steatosis in the high-dose group at 24 h. In total, 96 genes were identified as tetracycline responsive. Their level of expression differed significantly from controls (two-way analysis of variance; p < 0.05), after adjustment by the Benjamini-Hochberg multiple testing correction, and displayed a twofold or greater induction or repression. The largest groups of gene products affected by tetracycline exposure were those involved in signal transduction, nucleic acid metabolism, developmental processes, and protein metabolism. The expression of genes known to be involved in lipid metabolism was examined, using two-sample Student's t-test for each treatment group versus a corresponding control group. The overall net effects on expression of lipid metabolism genes indicated an increase in cholesterol and triglyceride biosynthesis and a decrease in β-oxidation of fatty acids. Our data support a proposed mechanism for tetracycline-induced steatogenic hepatotoxicity that involves these processes. Moreover, we demonstrated global changes in hepatic gene expression following tetracycline exposure; many of these genes have the potential to be used as biomarkers of exposure to steatogenic hepatotoxic agents. © 2006 Oxford University Press.
DOI
10.1093/toxsci/kfl078
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의과대학 > 의학과 > Journal papers
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