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乙醛修饰的血清蛋白与重度饮酒者生化指标之间的相关性。

Correlations between serum proteins modified by acetaldehyde and biochemical variables in heavy drinkers.

作者信息

Wickramasinghe S N, Marjot D H, Rosalki S B, Fink R S

机构信息

Department of Haematology, St Mary's Hospital Medical School, London.

出版信息

J Clin Pathol. 1989 Mar;42(3):295-9. doi: 10.1136/jcp.42.3.295.

DOI:10.1136/jcp.42.3.295
PMID:2703546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1141872/
Abstract

A strong and highly significant correlation was observed between serum aspartate transaminase (AST) activity and an index of the cytotoxic activity associated with serum proteins modified by acetaldehyde in a group of 24 heavy drinkers. A weaker but significant correlation (R = 0.564, p = 0.008) was found between total serum creatine kinase activity and this index of serum cytotoxicity. As it is likely that the concentration of circulating modified protein was largely determined by the quantity of free acetaldehyde generated in the liver and that the AST activity was mainly derived from damaged hepatocytes, the data indicate a correlation between hepatic acetaldehyde generation and hepatocyte damage. This correlation may indicate either that increased quantities of acetaldehyde are released by damaged hepatocytes or that acetaldehyde is hepatotoxic in vivo. As only the creatine kinase isoenzyme present in skeletal muscle (CK-MM) was demonstrable in the serum in all but one of our patients, the data also suggest that circulating modified serum proteins may be toxic towards skeletal muscle cells.

摘要

在一组24名重度饮酒者中,观察到血清天冬氨酸转氨酶(AST)活性与乙醛修饰的血清蛋白相关的细胞毒性活性指标之间存在强烈且高度显著的相关性。总血清肌酸激酶活性与该血清细胞毒性指标之间存在较弱但显著的相关性(R = 0.564,p = 0.008)。由于循环中修饰蛋白的浓度很可能在很大程度上由肝脏中产生的游离乙醛量决定,且AST活性主要源自受损肝细胞,这些数据表明肝脏乙醛生成与肝细胞损伤之间存在相关性。这种相关性可能表明受损肝细胞释放出的乙醛量增加,或者乙醛在体内具有肝毒性。由于除一名患者外,我们所有患者的血清中仅能检测到骨骼肌中存在的肌酸激酶同工酶(CK-MM),这些数据还表明循环中的修饰血清蛋白可能对骨骼肌细胞有毒性。

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本文引用的文献

1
Inhibition of glycoprotein secretion by ethanol and acetaldehyde in rat liver slices.
Biochem Pharmacol. 1980 Jan 1;29(1):35-8. doi: 10.1016/0006-2952(80)90240-3.
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Depressed hepatic glutathione and increased diene conjugates in alcoholic liver disease. Evidence of lipid peroxidation.酒精性肝病中肝谷胱甘肽水平降低及二烯共轭物增加。脂质过氧化的证据。
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Alcoholic cardiomyopathy. II. The inhibition of cardiac microsomal protein synthesis by acetaldehyde.酒精性心肌病。II. 乙醛对心脏微粒体蛋白质合成的抑制作用。
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Rates of metabolism of ethanol to acetate by human neutrophil precursors and macrophages.人类中性粒细胞前体和巨噬细胞将乙醇代谢为乙酸盐的速率。
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The capacity of macrophages from different murine tissues to metabolise ethanol and generate an ethanol-dependent non-dialysable cytotoxic activity in vitro.来自不同小鼠组织的巨噬细胞在体外代谢乙醇并产生乙醇依赖性非透析性细胞毒性活性的能力。
Alcohol Alcohol. 1987;22(1):31-9.
9
Supernatants from ethanol-containing macrophage cultures have cytotoxic activity.含乙醇的巨噬细胞培养上清液具有细胞毒性活性。
Alcohol Alcohol. 1986;21(3):263-8.
10
Role of macrophages in the pathogenesis of alcohol induced tissue damage.巨噬细胞在酒精诱导的组织损伤发病机制中的作用。
Br Med J (Clin Res Ed). 1987 May 2;294(6580):1137-9. doi: 10.1136/bmj.294.6580.1137.