The Lymphocyte as a Marker of Past Nutritional Status: Persistence of Abnormal Lymphocyte Deoxyuridine (dU) Suppression Test and Chromosomes in Patients with Past Deficiency of Folate and Vitamin B12 *
The Lymphocyte as a Marker of Past Nutritional Status: Persistence of Abnormal Lymphocyte Deoxyuridine (dU) Suppression Test and Chromosomes in Patients with Past Deficiency of Folate and Vitamin B12 *
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淋巴细胞作为过去营养状况的标志：过去缺乏叶酸和维生素 B12 的患者持续存在异常淋巴细胞脱氧尿苷 (dU) 抑制试验和染色体 *
DOI：
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发表时间：
1978
影响因子：
6.5
通讯作者：
V. Herbert
中科院分区：
文献类型：
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作者：
K. Das;V. Herbert
在正常受试者的骨髓细胞或 PHA 刺激的淋巴细胞的短期悬浮培养物中，非放射性脱氧尿苷 (dU) 抑制放射性胸苷 ([3H]TdR) 或其类似物 [125I] 脱氧尿苷 ([125I]Udr) 掺入 DNA。叶酸或维生素 B12 缺乏的患者的这两种细胞系统中，脱氧尿苷 (dU) 的正常抑制都会受到损害，但可以通过适当的维生素来纠正。对因维生素 B12 或叶酸缺乏而导致巨幼细胞贫血的患者在治疗前后进行了研究。当治疗使骨髓形态以及血清和红细胞维生素水平恢复正常时，dU抑制试验和骨髓中的染色体变化也得到纠正。然而，治疗后长达84天的时间里，淋巴细胞的dU抑制试验和染色体变化仍然异常。根据治疗前存在的维生素缺乏情况，通过适当的体外添加叶酸、甲基叶酸和维生素 B12 来纠正这些异常的淋巴细胞 dU 抑制试验。这些研究表明，异常的淋巴细胞 dU 抑制试验可以在体外通过适当的维生素纠正，并且淋巴细胞中特征性的染色体异常（当骨髓中不存在这些异常时）表明过去缺乏维生素 B12 或叶酸。这些变化可用于对接受“霰弹枪”疗法的患者的这些缺陷进行回顾性诊断。他们进一步支持循环未刺激淋巴细胞的概念：(1) 不含有大量维生素 B12 或叶酸； (2)反映淋巴细胞生成时患者的维生素状况； (3) 在旨在诊断当前骨髓和其他非淋巴细胞细胞系营养状态的 dU 抑制试验中不能替代骨髓。这些研究进一步证明，选择性营养缺乏可能发生在同一个人的一种细胞系中，而不是另一种细胞系中，并指出需要对影响各种人类细胞系营养输送、吸收和利用的因素进行更多研究。这些研究还提供了评估循环淋巴细胞年龄的新方法。
In short‐term suspension cultures of bone marrow cells or PHA‐stimulated lymphocytes from normal subjects, non‐radioactive deoxyuridine (dU) suppresses the incorporation of radioactive thymidine ([3H]TdR) or its analogue, [125I]deoxyuridine ([125I]Udr), into DNA. This normal suppression by deoxyuridine (dU) is impaired in both of these cell systems from patients with deficiency of folate or vitamin B12, and corrected by the appropriate vitamin. Patients with megaloblastic anaemia due to deficiency of vitamin B12 or folate were studied before and after treatment. When treatment had returned to normal the bone marrow morphology and the serum and red cell vitamin levels, then the dU suppression test and chromosomal changes in the bone marrow were also corrected. However, the dU suppression test and chromosomal changes remained abnormal in lymphocytes as long as 84 d after therapy. These abnormal lymphocyte dU suppression tests were corrected by the appropriate in vitro additions of folic acid, methylfolate and vitamin B12, depending on the vitamin deficiency present before therapy. These studies suggest that an abnormal lymphocyte dU suppression test corrected by the appropriate vitamin in vitro, and characteristic chromosome abnormalities in lymphocytes, when these are absent in the bone marrow, indicate past deficiency of vitamin B12 or folate. These changes can be used for retrospective diagnosis of these deficiencies in patients treated by ‘shotgun’ therapy. They further support the concepts that circulating unstimulated lymphocytes: (1) do not incorporate appreciable amounts of vitamin B12 or folic acid; (2) reflect the vitamin status of the patient at the time the lymphocytes were generated; and (3) cannot replace bone marrow in dU suppression tests aimed at diagnosis of current marrow and other non‐lymphocyte cell line nutrient status. These studies add to the evidence that selective nutrient deficiency may occur in one but not another cell line in the same person, and point to the need for more studies on factors affecting nutrient delivery, uptake, and utilization by various human cell lines. These studies also provide a new approach to evaluation of circulating lymphocyte age.