PRESENCE OF NONOXIDATIVE ETHANOL-METABOLISM IN HUMAN ORGANS COMMONLY DAMAGED BY ETHANOL ABUSE
PRESENCE OF NONOXIDATIVE ETHANOL-METABOLISM IN HUMAN ORGANS COMMONLY DAMAGED BY ETHANOL ABUSE
复制标题
DOI：
10.1126/science.3941913
复制
发表时间：
1986-01-31
期刊：
影响因子：
56.9
通讯作者：
LANGE, LG
中科院分区：
文献类型：
--
作者：
LAPOSATA, EA;LANGE, LG
乙醛是乙醇氧化代谢的最终产物，它会导致酒精引起的肝脏疾病，但不能解释胰腺、心脏或大脑等器官的损伤，因为这些器官的氧化代谢很少或不存在;也不能解释慢性酗酒者中发现的各种器官损伤模式。因此，其他生化介质可能是重要的酒精诱导的器官损伤的发病机制。发现许多人体器官通过最近描述的非氧化途径代谢乙醇，形成脂肪酸乙酯。缺乏氧化酒精代谢但经常被酒精滥用损害的器官具有高脂肪酸乙酯合成活性，并显示出脂肪酸乙酯的大量瞬时积累。因此，非氧化乙醇代谢，除了氧化途径可能是重要的病理生理学乙醇诱导的疾病在人类。
Acetaldehyde, the end product of oxidative ethanol metabolism, contributes to alcohol-induced disease in the liver, but cannot account for damage in organs such as the pancreas, heart, or brain, where oxidative metabolism is minimal or absent; nor can it account for the varied patterns of organ damage found in chronic alcoholics. Thus other biochemical mediators may be important in the pathogenesis of alcohol-induced organ damage. Many human organs were found to metabolize ethanol through a recently described nonoxidative pathways to form fatty acid ethyl esters. Organs lacking oxidative alcohol metabolism yet frequently damaged by ethanol abuse have high fatty acid ethyl ester synthetic activities and show substantial transient accumulations of fatty acid ethyl esters. Thus nonoxidative ethanol metabolism in addition to the oxidative pathway may be important in the pathophysiology of ethanol-induced disease in humans.