人类肝脏疾病会降低缬氨酸分解代谢中甲基丙烯酰辅酶A水合酶和β-羟基异丁酰辅酶A水解酶的活性。
Human liver disease decreases methacrylyl-CoA hydratase and beta-hydroxyisobutyryl-CoA hydrolase activities in valine catabolism.
作者信息
Ishigure K, Shimomura Y, Murakami T, Kaneko T, Takeda S, Inoue S, Nomoto S, Koshikawa K, Nonami T, Nakao A
机构信息
Department of Surgery II, Nagoya University School of Medicine, 466-8550, Nagoya, Japan.
出版信息
Clin Chim Acta. 2001 Oct;312(1-2):115-21. doi: 10.1016/s0009-8981(01)00597-6.
BACKGROUND
Methacrylyl-coenzyme A (MC-CoA) hydratase and beta-hydroxyisobutyryl-coenzyme A (HIB-CoA) hydrolase are key enzymes regulating the toxic concentration of MC-CoA generated in valine catabolism.
MATERIALS AND METHODS
We studied the activities and mRNA expression levels of these enzymes in normal human livers and in human livers with chronic hepatitis, cirrhosis, or hepatocellular carcinoma.
RESULTS
The activities of both enzymes were significantly lower by 36% to 46% in livers with cirrhosis or hepatocellular carcinoma compared with normals, suggesting a decrease in the capability of detoxifying MC-CoA with these diseases. The mRNA levels for both enzymes measured by quantitative polymerase chain reaction were significantly increased in livers with cirrhosis, but were not altered in those with chronic hepatitis or hepatocellular carcinoma when compared with normal livers.
CONCLUSION
Our results suggest that low levels of these enzyme activities in livers with cirrhosis or hepatocellular carcinoma are the result of posttranscriptional regulation in the damaged liver.
背景
甲基丙烯酰辅酶A（MC-CoA）水合酶和β-羟基异丁酰辅酶A（HIB-CoA）水解酶是调节缬氨酸分解代谢中产生的MC-CoA毒性浓度的关键酶。
材料与方法
我们研究了这些酶在正常人类肝脏以及患有慢性肝炎、肝硬化或肝细胞癌的人类肝脏中的活性和mRNA表达水平。
结果
与正常肝脏相比，肝硬化或肝细胞癌患者肝脏中这两种酶的活性均显著降低36%至46%，表明这些疾病中MC-CoA解毒能力下降。通过定量聚合酶链反应测量的这两种酶的mRNA水平在肝硬化患者肝脏中显著升高，但与正常肝脏相比，慢性肝炎或肝细胞癌患者肝脏中的mRNA水平没有变化。
结论
我们的结果表明，肝硬化或肝细胞癌患者肝脏中这些酶活性水平较低是受损肝脏中转录后调控的结果。
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