Tritsch G L, Niswander P W
Immunol Commun. 1981;10(1):1-8. doi: 10.3109/08820138109050681.
During phagocytosis and membrane perturbation, mouse macrophages generate superoxide in direct proportion to their intracellular adenosine deaminase activity. It is proposed that since adenosine deaminase controls the amount of substrate available to xanthine oxidase, and the latter produces superoxide during turnover of its substrates, the purine salvage pathway is an important contributor to the superoxide requirement of macrophages. It is further proposed that this may be the basis for the mechanism of the association of adenosine deaminase deficiency with immunodeficiency.
在吞噬作用和膜扰动过程中,小鼠巨噬细胞产生的超氧化物与其细胞内腺苷脱氨酶活性成正比。有人提出,由于腺苷脱氨酶控制着黄嘌呤氧化酶可利用的底物量,而黄嘌呤氧化酶在其底物周转过程中产生超氧化物,因此嘌呤补救途径是巨噬细胞超氧化物需求的重要贡献者。进一步提出,这可能是腺苷脱氨酶缺乏与免疫缺陷关联机制的基础。