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酒精对所有器官均有毒性,其是直接毒害骨髓和造成代谢紊乱,间接影响造血,后者导致脂肪肝和门脉高压,以及脂蛋白异常引起细胞膜改变,继而引起溶血。酒精在体内的氧化最主要的是乙醇脱氢酶催化乙醇形成乙醛,此过程中NAD(烟酰胺腺嘌呤二核苷酸)变成NADH(还原型NAD),随后乙醛脱氢酶将乙醛变成醋酸盐的过程也同样产生NADH,而过量的NADH与乙醇的大部分毒性有关。其次是定位作用于质网上的细胞色素P-450依赖性微粒体的乙醇氧化系统(MEOS),其活动性可因慢性大量饮酒而增高,从而增加甘油三酸酯及磷脂的合成,并沉积于肝脏。乙醇对骨髓的毒性作用包括造血祖细胞空泡变性,增殖减低,伴叶酸缺乏的巨幼细胞改变。空泡变性在停饮后3-7天可消失。空泡变性的早幼红细胞
Alcohol is toxic to all organs, which directly poison the bone marrow and cause metabolic disorders, indirectly affecting hematopoiesis. The latter leads to fatty liver and portal hypertension, and abnormal lipoprotein causes cell membrane changes, which in turn leads to hemolysis. Alcohol oxidation in the body is the most important alcohol dehydrogenase to catalyze the formation of ethanol acetaldehyde, NAD (nicotinamide adenine dinucleotide) into NADH (reduced NAD), followed by acetaldehyde dehydrogenase B The conversion of aldehydes to acetates also produces NADH, while excess NADH is associated with most of the toxicity of ethanol. Followed by the localization of the cytosolic P-450-dependent microsomal ethanol oxidation system (MEOS) acting on the cytoplasm, which activity may be increased by chronic heavy drinking to increase the synthesis of triglycerides and phospholipids and to be deposited on liver. Toxic effects of ethanol on bone marrow include degeneration of hematopoietic progenitor cells, reduced proliferation, changes in megaloblastic cells with folic acid deficiency. Degeneration of vacuoles can disappear 3-7 days after stopping drinking. Vacuolar degeneration of young erythrocytes