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非球形红细胞性溶血性贫血中红细胞糖酵解及核苷酸代谢的酶缺乏(作者译)

[Enzyme deficiencies in glycolysis and nucleotide metabolism of red blood cells in nonspherocytic hemolytic anemia (author's transl)].

作者信息

Waller H D, Benöhr H C

出版信息

Klin Wochenschr. 1976 Sep 1;54(17):803-21. doi: 10.1007/BF01469302.

Abstract

The detection of enzyme deficiencies in glycolytic and nucleotide metabolism of human red blood cells has enriched the pathophysiological knowledge on the origin of nonspherocytic hemolytic anemias (NSHA). So far for 11 of 13 glycolytic enzymes deficiencies have been described which are connected with alterations of biochemical enzymatic properties. The most frequent enzyme deficiencies are those of GPI and PK. By performance of special electrophoretic techniques genetic studies allow the demonstration of homozygote and double heterozygote defect carriers. Up to now only adenylate kinase and pyrimidine 5' nucleotidase deficiencies have been detected as genetically determined in altered nucleotide metabolism. The metabolic alterations of several enzymopathies have been characterized so well, that the pathophysiological relations between enzyme deficiency and NSHA probably have been found to be a sufficient explanation.

摘要

人类红细胞糖酵解和核苷酸代谢中酶缺陷的检测丰富了关于非球形细胞溶血性贫血(NSHA)起源的病理生理学知识。迄今为止,已描述了13种糖酵解酶中的11种缺陷,这些缺陷与生化酶特性的改变有关。最常见的酶缺陷是葡萄糖磷酸异构酶(GPI)和丙酮酸激酶(PK)的缺陷。通过特殊电泳技术进行的基因研究能够证明纯合子和双重杂合子缺陷携带者。到目前为止,在核苷酸代谢改变中仅检测到腺苷酸激酶和嘧啶5'核苷酸酶缺陷是由基因决定的。几种酶病的代谢改变已得到很好的表征,以至于酶缺陷与NSHA之间的病理生理关系可能已被认为是一个充分的解释。

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