McMartin K E
Alcohol Clin Exp Res. 1984 Mar-Apr;8(2):172-8. doi: 10.1111/j.1530-0277.1984.tb05831.x.
A common complication of chronic alcohol abuse is folic acid deficiency, which can result from poor dietary intake and from a direct effect of ethanol on folate metabolism, such as the acute decrease in serum folate levels. Ethanol (4 g/kg body weight) was administered orally to male Sprague-Dawley rats to study the rat as a suitable animal model for the acute effects of ethanol. The concentration of folate in the urine, determined by Lactobacillus casei assay, as well as the amount of urinary folate excretion were markedly increased 4 hr after ethanol administration. After 14 hr, the total plasma folate level was significantly depressed to 50% of control levels. No significant changes were observed in the total folate levels in the liver and red cell nor in the levels of individual hepatic folate monoglutamate derivatives determined by high pressure liquid chromatography assay. These results indicate that acute ethanol administration to rats produces a marked increase in the urinary excretion of folate compounds, which leads to a decrease in plasma folate levels. The acute decrease in plasma folate levels in ethanol-treated rats is similar to that seen in humans and suggests that the rat is an appropriate model for the study of the acute effects of ethanol on folate metabolism.
慢性酒精滥用的一种常见并发症是叶酸缺乏，这可能源于饮食摄入不足以及乙醇对叶酸代谢的直接影响，比如血清叶酸水平的急性下降。给雄性斯普拉格-道利大鼠口服乙醇（4克/千克体重），以研究该大鼠作为乙醇急性效应的合适动物模型。通过干酪乳杆菌测定法测定的尿中叶酸浓度以及尿中叶酸排泄量在给予乙醇4小时后显著增加。14小时后，血浆总叶酸水平显著降低至对照水平的50%。通过高压液相色谱测定法测定，肝脏和红细胞中的总叶酸水平以及肝脏中单个叶酸单谷氨酸衍生物的水平均未观察到显著变化。这些结果表明，给大鼠急性给予乙醇会导致叶酸化合物尿排泄显著增加，进而导致血浆叶酸水平降低。乙醇处理的大鼠血浆叶酸水平的急性下降与人类相似，这表明大鼠是研究乙醇对叶酸代谢急性效应的合适模型。
