A specific radioimmunoassay for 5'-deoxyadenosyl cobalamin in serum.

A specific radioimmunoassay for 5'-deoxyadenosyl cobalamin in serum.
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血清中 5-脱氧腺苷钴胺素的特异性放射免疫测定。

DOI:
10.1111/j.1365-2141.1988.tb02414.x
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发表时间:
1988
影响因子:
6.5
通讯作者:
Polu,S
Polu,S
中科院分区:
医学2区
文献类型:
--
作者:
Quadros,EV;Rothenberg,SP;Polu,S

文献摘要

相似文献

用5‘-脱氧腺苷钴胺(Cb1)抗血清建立了5’-脱氧腺苷钴胺(ADO-Cbl)的放射免疫分析方法。在1:100或更高的稀释度下,抗血清不与标记的甲基-羟基、硫基或氰基-Cbl结合,这些Cbl类似物即使在100倍的浓度下也不竞争放射免疫分析。30名正常人的Ado-Cbl的血清浓度(范围和平均±SD)分别为47-134和81±16 pg/ml,总Cbl的对应值为189-610和355±144 pg/ml。甲基Cbl的计算值为142-476 pg/ml和274±127pg/ml,变异系数分别为46%和21%。5例健康者的ADO-Cbl浓度在正常范围内(75-95pg/ml),总Cbl浓度正常值较低(189-217pg/ml)。在两名低Cbl(118和170pg/ml)且无任何Cbl缺乏临床证据的受试者中,ADO-Cbl正常(分别为63和95pg/ml)。6例低总Cbl(57±25pg/ml)患者和6例临床Cbl缺乏症患者的血清ADO-Cbl和甲基Cbl浓度分别为35±12pg/ml和22±22pg/ml。这与每个辅因的正常平均值的差异非常显著(P<0.001)。Cbl缺乏症的甲基Cbl浓度下降幅度相对较大(分别为92%和57%),使Cbl缺乏症患者的Ado-Cbl相对浓度增加到总Cbl的61%。虽然低血清甲基Cbl是Cbl缺乏症的敏感指标,但它可能不像血清Ado-Cbl降低那样特异。在无临床Cbl缺乏症的情况下,组织储备以外的因子(S)可将血清甲基Cbl降至95%可信限以下。
A specific radioimmunoassay for 5′‐deoxyadenosyl cobalamin (ado‐Cbl) has been developed using an antiserum raised to this cobalamin (Cbl). At a 1:100 or greater dilution the antiserum did not bind radiolabelled methyl‐hydroxo‐, sulphito‐ or cyano‐Cbl and these Cbl analogues did not compete in the radioimmunoassay even at 100‐fold higher concentration.The serum concentration (range and mean ± SD) of ado‐Cbl in 30 normal subjects was 47–134 and 81 ± 16 pg/ml. The corresponding values for total Cbl in these sera were 189–610 and 355 ± 144 pg/ml, and the computed values for methyl‐Cbl were 142–476 and 274 ± 127 pg/ml. The coefficient of variation was substantially greater for methyl‐Cbl than for ado‐Cbl (46% v. 21%, respectively). The ado‐Cbl concentration was in the normal range (75–95 pg/ml) in five healthy subjects with a low normal concentration (189–217 pg/ml) of total Cbl. In two subjects with low total Cbl (118 and 170 pg/ml) and without any clinical evidence of Cbl deficiency, ado‐Cbl was normal (63 and 95 pg/ml. respectively). Thus, in this group, low methyl‐Cbl accounted for the lower total Cbl.The concentration (mean ± SD) of serum ado‐Cbl and methyl‐Cbl in six patients with low total Cbl (57 ± 25 pg/ml) and clinical evidence for Cbl deficiency was 35 ± 12 pg/ml and 22 ± 22 pg/ml, respectively. This difference from the normal mean for each cofactor was highly significant (P<0.001). The decrease in the concentration of methyl‐Cbl in Cbl deficiency was relatively greater than the decrease in ado‐Cbl (92% v. 57%, respectively) which raised the relative concentration of ado‐Cbl in Cbl deficiency to 61% of the total Cbl. Although a low serum methyl‐Cbl is a sensitive indicator of Cbl deficiency, it may not be as specific as a decrease in serum ado‐Cbl. Factor(s) other than tissue stores of Cbl may lower serum methyl‐Cbl below the 95% confidence limit in the absence of clinical Cbl deficiency.