Deacon R, Perry J, Lumb M, Chanarin I
Biochem J. 1985 Apr 1;227(1):67-71. doi: 10.1042/bj2270067.
N2O oxidizes and inactivates cob[I]alamin, and animals exposed in this way serve as models for cobalamin 'deficiency'. Such animals show a fall in activity of glycinamide ribotide transformylase and a rise in that of 5-amino-4-imidazolecarboxamide ribotide transformylase. The fall in glycinamide ribotide transformylase activity was prevented by parenteral 5'-methylthioadenosine derived from methionine. Methylthioadenosine in turn is converted into formate. Activity of glycinamide ribotide transformylase recovers after 7 days despite continued N2O inhalation, and this is probably related to restoration of methionine synthesis by induction of betaine:homocysteine transmethylase.
一氧化二氮会氧化并使钴胺素[I]失活,以这种方式暴露的动物可作为钴胺素“缺乏”的模型。这类动物的甘氨酰胺核苷酸转甲酰酶活性下降,而5-氨基-4-咪唑甲酰胺核苷酸转甲酰酶活性上升。甲硫氨酸衍生的肠胃外5'-甲硫基腺苷可防止甘氨酰胺核苷酸转甲酰酶活性下降。甲硫基腺苷继而转化为甲酸。尽管持续吸入一氧化二氮,但7天后甘氨酰胺核苷酸转甲酰酶活性仍会恢复,这可能与通过诱导甜菜碱:同型半胱氨酸转甲基酶来恢复甲硫氨酸合成有关。