Lumb M, Perry J, Deacon R, Chanarin I
Br J Haematol. 1982 Jun;51(2):235-42.
Rats were injected with [2-14C]H4PteGlu daily for 3 d and thereafter one group left in air and a second group in an atmosphere of nitrous oxide/oxygen (1/1). Nitrous oxide inactivates cobalamin. The N2O-treated rats excreted large amounts of L. casei-active folate into the urine. The urinary folate co-chromatographed with authentic 3H-labelled 5-methyltetrahydrofolate. Both groups of animals excreted 14C-labelled breakdown products in the urine but there was no evidence of increased folate catabolism in the N2O-treated rats. It was concluded that the folate deficiency that develops in the N2O-treated rat is due to massive urinary loss of folate. This appears to be secondary to impaired cellular uptake of folate which leads to a raised plasma folate level.
大鼠每天注射[2-¹⁴C]四氢叶酸谷氨酸，持续3天，之后一组置于空气中，另一组置于一氧化二氮/氧气（1/1）的气氛中。一氧化二氮会使钴胺素失活。经一氧化二氮处理的大鼠向尿液中排泄大量对干酪乳杆菌有活性的叶酸。尿中的叶酸与 authentic ³H标记的5-甲基四氢叶酸共色谱。两组动物的尿液中均排泄出¹⁴C标记的分解产物，但没有证据表明经一氧化二氮处理的大鼠叶酸分解代谢增加。得出的结论是，经一氧化二氮处理的大鼠出现的叶酸缺乏是由于叶酸大量经尿液流失。这似乎继发于细胞对叶酸摄取受损，从而导致血浆叶酸水平升高。
