Parry T E, Blackmore J A
Br J Haematol. 1976 Dec;34(4):567-73. doi: 10.1111/j.1365-2141.1976.tb03602.x.
The serum "uracil+uridine" level, expressed as uracil, has been measured in 21 cases of vitamin B12 deficiency, in which the serum folate was normal, and compared with the level in 97 normal subjects. The level in the vitamin B12 deficient group (11.9 mumol/1). was significantly lower than in the controls (15.7 mumol/1., P less than 0.005). Nine of the former were complicated by stystemic illness but the clinical and haematological features in the remaining 12 were consistent with the diagnosis of pernicious anaemia in relapse. The serum uracil level in this group was even lower (10.21 mumol/1., P less than 0.01). This finding is unexpected in view of the generally accepted indirect role of vitamine B12 in the methylation of deoxyuridine monophosphate to deoxythymidine monophosphate. Reasons are given for not accepting these results as reflecting the main biochemical lesion in vitamin B12 deficiency. Although they do not give direct support to an impairment in the methylation of deoxyuridine monophosphate, they do not exclude it as they test only one possible metabolic pathway and moreover they could represent the result of more than one action of vitamin B12 on uracil metabolism. They do show, however, that some aspect of uracil metabolism other than methylation is affected in vitamin B12 deficiency in man.
已对21例血清叶酸正常的维生素B12缺乏症患者测定了以尿嘧啶表示的血清“尿嘧啶+尿苷”水平，并与97名正常受试者的水平进行了比较。维生素B12缺乏组的水平（11.9微摩尔/升）显著低于对照组（15.7微摩尔/升，P<0.005）。前者中有9例并发全身性疾病，但其余12例的临床和血液学特征与复发的恶性贫血诊断相符。该组的血清尿嘧啶水平甚至更低（10.21微摩尔/升，P<0.01）。鉴于普遍认为维生素B12在脱氧尿苷单磷酸甲基化为脱氧胸苷单磷酸过程中起间接作用，这一发现出人意料。文中给出了不接受这些结果反映维生素B12缺乏主要生化病变的原因。尽管这些结果没有直接支持脱氧尿苷单磷酸甲基化受损，但由于它们仅测试了一种可能的代谢途径，而且它们可能代表维生素B12对尿嘧啶代谢多种作用的结果，所以也不能排除这种可能性。然而，它们确实表明，人类维生素B12缺乏会影响尿嘧啶代谢中除甲基化以外的某些方面。
