Amber I J, Hibbs J B, Taintor R R, Vavrin Z
VA Medical Center, Salt Lake City, UT 84148.
J Leukoc Biol. 1988 Feb;43(2):187-92. doi: 10.1002/jlb.43.2.187.
Culture medium conditioned by incubation with murine cytotoxic activated macrophages causes release of iron-55 label from viable murine EMT-6 tumor cells as well as inhibition of DNA replication and aconitase activity. These metabolic changes occur in parallel with L-citrulline, nitrate, and nitrate synthesis from L-arginine by EMT-6 cells. Protein synthesis is required for activation of this effector mechanism. Once the effector pathway is induced in EMT-6 cells in the presence of amino acids, L-arginine is the only amino acid required for its function. Arginase inhibits the effector mechanism, which is additional evidence for its specific L-arginine requirement. The results show induction, in a non-macrophage cell line, of a novel effector pathway which, in addition to other effects, inhibits cellular proliferation.
与鼠细胞毒性活化巨噬细胞共同孵育的培养基会导致活的鼠EMT - 6肿瘤细胞释放铁 - 55标记物，并抑制DNA复制和乌头酸酶活性。这些代谢变化与EMT - 6细胞从L - 精氨酸合成L - 瓜氨酸、硝酸盐和亚硝酸盐的过程同时发生。激活这种效应机制需要蛋白质合成。一旦在氨基酸存在的情况下在EMT - 6细胞中诱导出效应途径，L - 精氨酸是其发挥功能所需的唯一氨基酸。精氨酸酶抑制效应机制，这是其对L - 精氨酸有特定需求的额外证据。结果表明，在非巨噬细胞系中诱导出了一种新的效应途径，该途径除了其他作用外，还能抑制细胞增殖。
