Ornithine carbamyltransferase is a sensitive marker for alcohol-induced liver injury

被引:17
作者
Murayama, Hiroshi [1 ]
Ikemoto, Masaki [2 ]
Hamaoki, Masaru [1 ]
机构
[1] Yamasa Corp, Diagnost Dept, Chiba 2880056, Japan
[2] Kyoto Univ, Fac Med, Sch Hlth Sci, Kyoto 6068507, Japan
关键词
Alanine aminotransferase; Aspartate aminotransferase; Ornithine carbamyltransferase; Glutamate dehydrogenase; Mitochondria; ACUTE HEPATIC-INJURY; GLUTAMATE-DEHYDROGENASE; RELIABLE MARKER; CELL NECROSIS; SERUM; CARBAMOYLTRANSFERASE; STEATOSIS; DIAGNOSIS; INCREASE; ARGINASE;
D O I
10.1016/j.cca.2008.11.027
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Background: Although mitochondrion-derived markers such as ornithine carbamyltransferase (OCT) and glutamate dehydrogenase (GLDH) have been reported to be good markers for alcohol-induced hepatic injury, their use has been limited due to the notion that mitochondrial markers are less sensitive than cytosol-derived markers. We determined the clinical importance of mitochondrion-derived markers in the evaluation of alcohol-induced hepatotoxicity. Methods: Rats were administered alcohol chronically (5-30% ethanol in drinking water with or without high fat diet feeding for 15 weeks) and hepatic damages were evaluated by serum OCT and GLDH, together with other liver enzymes such as alanine aminotransferase and aspartate aminotransferase. Hepatic content of the enzymes was also evaluated in the chronic ethanol feeding model to confirm whether induction of the enzyme in the liver reflects the serum activity. Results: The serum activities of OCT and GLDH increased significantly by chronic ethanol feeding while other markers did not. Although the hepatic content of OCT and GLDH also increased, the serum activities did not correlate with the hepatic activities and the extent of increase in the liver was much less than in serum. Conclusions: Mitochondrion-derived markers, especially OCT, appeared superior to cytosol-derived markers in the detection of alcohol-induced liver injury. (C) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:100 / 104
页数:5
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