Suppr超能文献

肝脏疾病中乙醇代谢酶的活性

Activities of ethanol-metabolizing enzymes in liver diseases.

作者信息

Nuutinen H U

出版信息

Scand J Gastroenterol. 1986 Aug;21(6):678-84. doi: 10.3109/00365528609011100.

Abstract

The activities of hepatic alcohol (ADH), aldehyde (ALDH), and lactate dehydrogenases were measured in 69 patients with various liver diseases (15 controls, 20 with alcoholic and 8 with non-alcoholic fatty liver, 13 with alcoholic cirrhosis, 2 with alcoholic hepatitis, 3 with cryptogenic and 3 with primary biliary cirrhosis, and 5 with acute or chronic hepatitis). The specific activities of all these enzymes were decreased in both alcoholic and non-alcoholic liver diseases. The activities of ADH and low-Km ALDH were significantly decreased both in alcoholic (ADH, 7.22 mU/mg protein, p less than 0.001; low-Km ALDH, 5.00 mU/mg protein, p less than 0.001) and in other liver diseases (ADH, 10.70 mU/mg protein, p less than 0.001; low-Km ALDH, 6.80 mU/mg protein, p less than 0.005) when compared with controls (ADH, 20.87 mU/mg protein; low-Km ALDH, 14.41 mU/mg protein). The hepatic protein content was significantly (p less than 0.001) increased in alcoholic fatty degeneration but not in alcoholic cirrhosis or other liver diseases. The results suggest that in man alcohol- and acetaldehyde-metabolizing enzymes are not induced by chronic alcohol consumption. On the contrary, the hepatic activities of these enzymes appeared to be lower in alcoholic than in non-alcoholic liver diseases. Consequently, in addition to liver injury alcohol may also directly affect the synthesis or breakdown of alcohol-metabolizing enzymes.

摘要

对69例患有各种肝脏疾病的患者(15例对照者、20例酒精性脂肪肝患者、8例非酒精性脂肪肝患者、13例酒精性肝硬化患者、2例酒精性肝炎患者、3例隐源性肝硬化患者、3例原发性胆汁性肝硬化患者以及5例急性或慢性肝炎患者)的肝脏乙醇脱氢酶(ADH)、乙醛脱氢酶(ALDH)和乳酸脱氢酶活性进行了测定。在酒精性和非酒精性肝脏疾病中,所有这些酶的比活性均降低。与对照者(ADH,20.87 mU/mg蛋白;低Km ALDH,14.41 mU/mg蛋白)相比,酒精性疾病(ADH,7.22 mU/mg蛋白,p<0.001;低Km ALDH,5.00 mU/mg蛋白,p<0.001)以及其他肝脏疾病(ADH,10.70 mU/mg蛋白,p<0.001;低Km ALDH,6.80 mU/mg蛋白,p<0.005)中ADH和低Km ALDH的活性均显著降低。酒精性脂肪变性时肝脏蛋白含量显著增加(p<0.001),但酒精性肝硬化或其他肝脏疾病时则无增加。结果表明,在人类中,慢性饮酒不会诱导酒精和乙醛代谢酶。相反,酒精性肝脏疾病中这些酶的肝脏活性似乎低于非酒精性肝脏疾病。因此,除了肝损伤外,酒精还可能直接影响酒精代谢酶的合成或分解。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验