McGuffin R, Goff P, Hillman R S
Br J Haematol. 1975 Oct;31(2):185-92. doi: 10.1111/j.1365-2141.1975.tb00849.x.
Studies of the rate of depletion of serum and tissue methylated and non-methylated folates were carried our in rats maintained for long periods on either a folate deficient (sucrose-water/sulphathiazole) diet or a deficient diet plus high alcohol intake. By means of implantation of a feeding gastrostomy tube, it was possible to sustain constant blood ethanol levels of between 50 and 300 mg/dl for 3-4 weeks with relatively normal calorie intake and without death of the animal. Using this animal model, which closely resembles severe alcoholism in man, a very rapid depression in serum 5-methyl tetrahydrofolate was observed similar to that reported in alcoholic man. At the same time, release of folates from liver stores was umimpaired by alcohol ingestion. Liver folate store depletion rates were identical for alcoholic and folate starved animals. The explanation for the sudden alcohol suppression of serum folate levels must, therefore, be sought at a point in the internal metabolic sequences of folate other than the delivery of folate stores to plasma.
对长期食用叶酸缺乏（蔗糖水/磺胺噻唑）饮食或缺乏饮食加大量酒精摄入的大鼠进行了血清及组织中甲基化和非甲基化叶酸消耗率的研究。通过植入饲管造瘘术，在相对正常的热量摄入且动物无死亡的情况下，有可能使血液乙醇水平维持在50至300毫克/分升之间3至4周。使用这种与人类严重酗酒非常相似的动物模型，观察到血清5-甲基四氢叶酸迅速下降，这与酒精中毒患者的情况类似。同时，酒精摄入并未损害肝脏储存叶酸的释放。酒精性和叶酸缺乏动物的肝脏叶酸储存消耗率相同。因此，血清叶酸水平突然受到酒精抑制的原因，必须在叶酸内部代谢序列中除叶酸从储存库输送到血浆之外的某个点去寻找。
