Spontaneous Ultra-Weak Photon Emission and Delayed Luminescence during Carbon Tetrachloride-Induced Liver Injury and Repair in Mouse

DOI Web Site Web Site 被引用文献1件 参考文献33件
  • Kim Jungdae
    Biomedical Physics Laboratory 25-414, School of Physics, Seoul National University
  • Lim Jaekwan
    Biomedical Physics Laboratory 25-414, School of Physics, Seoul National University
  • Lee Byung-Cheon
    Biomedical Physics Laboratory 25-414, School of Physics, Seoul National University
  • Kim Yong-ung
    College of Pharmacy, Seoul National University
  • Lee Seung Ki
    College of Pharmacy, Seoul National University
  • Cheun Byeung Soo
    Department of Molecular Biology, College of Medicine, Kyung Hee University
  • Soh Kwang-Sup
    Biomedical Physics Laboratory 25-414, School of Physics, Seoul National University

この論文をさがす

抄録

Spontaneous ultra-weak photon emission and delayed luminescence were measured from the mouse liver injured by carbon tetrachloride (CCl4), a hepatotoxic chemical. After carbon tetrachloride in olive oil (4 ml/kg) was injected intraperitoneally into ICR mouse, spontaneous photon emission and delayed luminescence using metal halide lamp was measured from the excised liver. Twenty-four hours after injection, spontaneous photon emission from the livers was 69.3 ± 21.2 counts/min/cm2, which was two times higher than that from controls of 29.5 ± 5.9 counts/min/cm2. However, 72 hr after injection, spontaneous photon emission from the livers was lowered to 37.0 ± 14.9 counts/min/cm2. These observations were closely correlated with those of the activities of aspartate aminotransferase (AST/GOT) and alanine aminotransferase (ALT/GPT), which were released in the course of hepatocellular death. Delayed luminescence also showed clear distinction in its time course of relaxation between the carbon tetrachloride-treated and control groups. On the basis of these observations, we suggest that these photon emissions are involved in the process of death and/or proliferation of liver cells after acute exposure to carbon tetrachloride with sublethal doses. Further, these photon emissions might be originated from the process of lipid peroxidation and consequent radical scavenging by antioxidant enzymes in injured liver tissue. This model study might provide a basis for the analysis of hepatotoxicant induced liver injury and repair by means of measurements of the photon emissions. <br>

収録刊行物

被引用文献 (1)*注記

もっと見る

参考文献 (33)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ