Preedy V R, Siddiq T, Why H, Richardson P J
Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, London, U.K.
Alcohol Alcohol. 1994 Mar;29(2):141-7.
Ethanol ingestion can induce a variety of metabolic changes in the heart, and recent studies have even suggested that moderate ethanol intake confers cardio-protective effects in reducing mortality due to coronary artery disease. However, in this review we explore the consequences of excessive ethanol intake or alcohol misuse. We investigate the epidemiology of alcohol misuse, and thereafter present evidence supporting the existence of a specific alcoholic heart muscle disease (AHMD). The prevalence of AHMD is described and the contributing mechanisms are discussed. These include the involvement of free radicals, defects in intermediary metabolism and the formation of acetaldehyde adducts. Special attention has been paid to ethanol-induced changes in protein turnover. Our studies show that ethanol impairs the protein synthetic pathways, affecting the contractile proteins per se, as well as the subcellular organelles as exemplified by the mitochondria. Acetaldehyde appears to be a particularly potent toxin. The experiments described in this review emphasize the need for investigative studies in intact models. The mechanisms inherent in the pathogenesis of AHMD may be applicable to other heart muscle disorders.
摄入乙醇可在心脏诱导多种代谢变化，近期研究甚至表明适度摄入乙醇在降低冠状动脉疾病所致死亡率方面具有心脏保护作用。然而，在本综述中，我们探讨过量摄入乙醇或酒精滥用的后果。我们调查酒精滥用的流行病学，之后展示支持特定酒精性心肌病（AHMD）存在的证据。描述了AHMD的患病率并讨论了其促成机制。这些机制包括自由基的参与、中间代谢缺陷以及乙醛加合物的形成。特别关注了乙醇诱导的蛋白质周转变化。我们的研究表明，乙醇损害蛋白质合成途径，影响收缩蛋白本身以及以线粒体为例的亚细胞器。乙醛似乎是一种特别强效的毒素。本综述中描述的实验强调了在完整模型中进行研究的必要性。AHMD发病机制中固有的机制可能适用于其他心肌疾病。
