Valentine W N, Paglia D E, Fink K, Madokoro G
J Clin Invest. 1976 Oct;58(4):926-32. doi: 10.1172/JCI108545.
Lead intoxication is accompanied by an acquired deficiency of erythrocyte pryimidine-specific, 5'-nucleotidase. Genetically determined deficiency of this enzyme is associated with chronic hemolysis, marked basophilic stippling of erythrocytes on stained blood films, and unique intraerythrocytic accumulations of pyrimidine-containing nucleotides. The present report documents that lead-induced deficiency when sufficiently severe gives rise to findings similar to the hereditary disorder. Whereas pyrimidine-containing nucleotides are virutally absent in the erythrocytes of normal and reticulocyte-rich blood, 12% of erythrocyte nucloetides in the blood of a patient with lead intoxication contained cytidine. Nucleotidase activity was about 25% that in normal erythrocytes and 15% or less of that expected in comparable reticulocyte-rich blood. The distribution of nucleotidase activity in patient erythrocytes is unknown, and much more severe deficiency could have been present in subsets of the cell populations analyzed. The findings indicate that the hemolytic anemia and increased basophilic stippling characteristic of certain cases of lead intoxication may share a common etiology with essentially identical features of the genetically determined disorder.
铅中毒伴有获得性红细胞嘧啶特异性5'-核苷酸酶缺乏。这种酶的遗传性缺乏与慢性溶血、染色血涂片上红细胞明显的嗜碱性点彩以及含嘧啶核苷酸在红细胞内的独特蓄积有关。本报告证明，当铅诱导的缺乏足够严重时，会产生与遗传性疾病相似的表现。在正常和富含网织红细胞的血液的红细胞中几乎不存在含嘧啶核苷酸，而一名铅中毒患者血液中12%的红细胞核苷酸含有胞苷。核苷酸酶活性约为正常红细胞的25%，在可比的富含网织红细胞的血液中预期活性的15%或更低。患者红细胞中核苷酸酶活性的分布情况未知，在所分析的细胞群体亚群中可能存在更严重的缺乏。这些发现表明，某些铅中毒病例的溶血性贫血和嗜碱性点彩增加的特征可能与遗传性疾病的基本相同特征具有共同的病因。
