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J.Health Sci., 51(2), 155-160, 2005
Spontaneous Ultra-Weak Photon Emission and Delayed Luminescence during Carbon
Tetrachloride-Induced Liver Injury and Repair in Mouse
Jungdae Kim,*, a Jaekwan
Lim,a Byung-Cheon
Lee,a Yong-ung
Kim,b Seung Ki
Lee,b Byeung Soo Cheun,c and Kwang-Sup
Soha
aBiomedical Physics Laboratory 25-414, School of Physics, Seoul National University, San 56-1, Sillim-dong, Gwanak-gu, Seoul
151-747, Korea, bCollege of Pharmacy, Seoul National University, San 56-1, Sillim-dong, Gwanak-gu, Seoul 151-742, Korea,
and cDepartment of Molecular Biology, College of Medicine, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul
130-701, Korea
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.
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