Hepatic folate metabolism in the chronic alcoholic monkey.
Hepatic folate metabolism in the chronic alcoholic monkey.
复制标题
慢性酒精猴的肝脏叶酸代谢。
DOI：
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发表时间：
1981
期刊：
影响因子：
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通讯作者：
C. Halsted
中科院分区：
文献类型：
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作者：
T. Tamura;J. Romero;J. Watson;E. J. Gong;C. Halsted
为了评估肝脏叶酸代谢改变在慢性酒精中毒叶酸缺乏症发病机制中的作用，在给予50%能量乙醇2年的猴子和对照猴子中比较了示踪剂量的3 H-PteGlu的肝脏代谢。长期乙醇喂养导致轻度肝损伤，肝脏叶酸水平显著降低。示踪剂剂量后获得的肝活检的色谱研究表明，还原，甲基化，还原叶酸和多聚谷氨酰叶酸的合成的还原，甲基化的过程没有受到长期乙醇喂养。乙醇喂养组的肝脏氚水平显著降低。这些研究表明，长期乙醇摄入后观察到的肝脏叶酸水平降低是由于长期乙醇摄入后观察到的肝脏叶酸水平降低是由于肝脏中保留叶酸的能力降低，而叶酸的减少和进一步代谢不受影响。
To assess the role of altered hepatic folate metabolism in the pathogenesis of the folate deficiency of chronic alcoholism, the hepatic metabolism of a tracer dose of 3H-PteGlu was compared in monkeys given 50% of energy as ethanol for 2 years and in control monkeys. Long-term ethanol feeding resulted in mild hepatic injury, with a significant decrease in hepatic folate levels. Chromatographic studies of liver biopsies obtained after the tracer dose indicated that the processes of reduction, methylation, and formylation of reduced folate and the synthesis of polyglutamyl folates were not affected by long-term ethanol feeding. Hepatic tritium levels were significantly decreased in the ethanol-fed group. These studies suggest that the decrease in hepatic folate levels observed after long-term ethanol ingestion is due to a decrease in hepatic folate levels observed after long-term ethanol ingestion is due to a decreased ability to retain folates in the liver, whereas reduction and further metabolism of folates is not affected.