Deacon R, Perry J, Lumb M, Chanarin I
MRC Clinical Research Centre, Northwick Park Hospital, Harrow, Middlesex.
Br J Haematol. 1990 Mar;74(3):354-9. doi: 10.1111/j.1365-2141.1990.tb02595.x.
Endogenous formate levels in blood and liver were assayed in rats both after inactivation of cobalamin (Cbl) by exposure to N2O as well as in air-breathing controls. The uptake of [14C]formate by tetrahydrofolate (H4folate) in bone marrow cells and liver homogenate and the incorporation of [14C]formate into purine, pyrimidine, methionine, serine and choline, was measured. There was a significant accumulation of endogenous formate following Cbl inactivation. There was impaired utilization of [14C]formate for single unit carbon (C1 unit) transfers mediated by folate in Cbl-inactivated tissues, other than for synthesis of adenine. The impairment was not accompanied by any accumulation of labelled methylH4folate indicating that methylfolate trapping played no part in impaired single carbon unit transfer. The effect of Cbl lack was a failure to form formylH4folate so that formate accumulated. The reason for this is not known.
在大鼠中，通过暴露于一氧化二氮使钴胺素（Cbl）失活后，以及在呼吸空气的对照大鼠中，测定了血液和肝脏中的内源性甲酸水平。测量了骨髓细胞和肝脏匀浆中四氢叶酸（H4folate）对[14C]甲酸的摄取，以及[14C]甲酸掺入嘌呤、嘧啶、蛋氨酸、丝氨酸和胆碱的情况。Cbl失活后，内源性甲酸有显著积累。在Cbl失活的组织中，除了腺嘌呤合成外，叶酸介导的用于单碳单位（C1单位）转移的[14C]甲酸利用受损。这种损伤并没有伴随着标记的甲基H4folate的任何积累，这表明甲基叶酸捕获在单碳单位转移受损中不起作用。Cbl缺乏的影响是无法形成甲酰H4folate，从而导致甲酸积累。其原因尚不清楚。
