Molecular & Cellular Toxicology

  • 제2권1호
  • /
  • Pages.21-28
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  • 2006
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  • 1738-642X(pISSN)
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  • 2092-8467(eISSN)
대한독성유전 단백체학회 (The Korean Society of Toxicogenomics and Toxicoproteomics)
권호 표지

Hepatic Gene Expression Analysis of Gadolinium Chloride Treated Mice

  • Jeong, Sun-Young (Department of Biopotency/Toxicology Evaluation, University of Science & Technology) ;
  • Lim, Jung-Sun (Korea Institute of Toxicology, KRICT) ;
  • Hwang, Ji-Yoon (Korea Institute of Toxicology, KRICT) ;
  • Kim, Yong-Bum (Department of Biopotency/Toxicology Evaluation, University of Science & Technology) ;
  • Kim, Chul-Tae (Department of Anatomy, College of Medicine, Konyang University) ;
  • Lee, Nam-Seob (Department of Anatomy, College of Medicine, Konyang University) ;
  • Yoon, Seok-Joo (Department of Biopotency/Toxicology Evaluation, University of Science & Technology)
  • 발행 : 2006.03.31
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초록

Gadolinium chloride ($GdCl_{3}$) was known to block Kupffer cells and generally its toxicity study based on blocking these cells. Therefore, $GdCl_{3}$ frequently used to study toxic mechanisms of hepatotoxicants inducing injury through Kupffer cells. We also tried to investigate the effect of $GdCl_{3}\;on\;CCl_{4}$ toxicity, typical hepatotoxicants. Administration of $GdCl_{3}$ to mice significantly suppressed AST (asparatate amino transferase), ALT (alanine amino transferase) levels which were increased by $CCl_{4}$ treatment. However, $GdCl_{3}$ didn't inhibit the phagocytotic activity of Kupffer cells. Malondialdehyde (MDA) is a good indicator of the degree of lipid peroxidation. In this study, MDA increased by $GdCl_{3}$ administration not by $CCl_{4}$. To understand the toxicity of $GdCl_{3}$, we analyzed global gene expression profile of mice liver after acute $GdCl_{3}$ injection. Four hundred fifty two genes were differentially expressed with more than 2-fold in at least one time point among 3 hr, 6 hr, and 24 hr. Several genes involved in fibrogenesis regulation. Several types of pro-collagens (Col1a2, Col5a2, Col6a3, and Col13a1) and tissue inhibitor of metal-loproteinase1 (TIMP1) were up regulated during all the time points. Genes related to growth factors, chemokines, and oxidative stress, which were known to control fibrogenesis, were significantly changed. In addition, $GdCl_{3}$ induced abnormal regulation between lipid synthesis and degradation related genes. These data will provide the information about influence of $GdCl_{3}$ to hepatotoxicity.

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