Vilpo J A
Laboratory of Molecular Hematology, Biocenter, Oulu, Finland.
Mutat Res. 1988 May;193(3):207-17. doi: 10.1016/0167-8817(88)90031-4.
The expression of the DNA base-excision-repair enzyme uracil-DNA glycosylase in the human hematopoietic system followed a tightly regulated pattern: high enzyme activities were recorded in proliferating bone marrow progenitor cells and in peripheral blood T- and B-cells, both groups of cells requiring the integrity of their genetic information for their proper function. The blood quiescent immunocompetent cells retained their DNA-uracil exclusion capacity, even in the oldest age groups. Peripheral blood mature end cells, granulocytes, platelets and red cells had little activity, consistent with the fact that these cells are anuclear or short-lived, so that no template-primer functions of their DNA are required. Uracil-DNA glycosylase expression is high in all types of human leukemia, providing a selective advantage for survival of leukemic cells. Overall results show that a deficiency of this DNA base-excision-repair pathway is not likely to be an etiopathogenetic factor in the formation of non-random or other chromosomal abnormalities or in the leukemogenesis itself.
DNA碱基切除修复酶尿嘧啶-DNA糖基化酶在人类造血系统中的表达遵循严格调控的模式：在增殖的骨髓祖细胞以及外周血T细胞和B细胞中记录到高酶活性，这两组细胞正常功能均需要其遗传信息的完整性。血液中静止的免疫活性细胞即使在年龄最大的群体中也保留了其DNA尿嘧啶排除能力。外周血成熟终末细胞、粒细胞、血小板和红细胞活性很低，这与这些细胞无细胞核或寿命短暂的事实一致，因此不需要其DNA的模板-引物功能。尿嘧啶-DNA糖基化酶在所有类型的人类白血病中表达都很高，为白血病细胞的存活提供了选择性优势。总体结果表明，这种DNA碱基切除修复途径的缺陷不太可能是非随机或其他染色体异常形成或白血病发生本身的病因学因素。
