Shau H Y
Division of Surgical Oncology, UCLA School of Medicine 90024-1782.
Cancer Commun. 1991 Sep;3(9):283-6.
Tumor necrosis factor (TNF) activates polymorphonuclear neutrophils (PMN) to suppress tumor cell proliferation. This cytostatic activity could be blocked by the addition of red blood cells (RBC) into the assay. TNF-induced PMN cytostatic activity was mediated by hydrogen peroxide (H2O2). RBC have two major pathways to detoxify H2O2, one by catalase and the other by the glutathione redox cycle. Therefore, the catalase inhibitor 3-amino-1,2,4-triazole (AT) and the glutathione inhibitor N-ethylmaleimide (NE) were used to assess the role of each anti-oxidant in protecting the tumor target cells. RBC, depleted of catalase by AT, no longer protected Raji tumor cells from PMN cytostatic activity. However, depletion of reduced glutathione by NE had no effect on RBC protection of tumor target cells. Thus, RBC can protect tumor cells from cytostatic activity mediated by TNF-activated PMN, and the protection is a function of catalase, but not glutathione.
肿瘤坏死因子（TNF）激活多形核中性粒细胞（PMN）以抑制肿瘤细胞增殖。将红细胞（RBC）添加到检测中可阻断这种细胞生长抑制活性。TNF诱导的PMN细胞生长抑制活性由过氧化氢（H2O2）介导。RBC有两条主要的H2O2解毒途径，一条通过过氧化氢酶，另一条通过谷胱甘肽氧化还原循环。因此，使用过氧化氢酶抑制剂3-氨基-1,2,4-三唑（AT）和谷胱甘肽抑制剂N-乙基马来酰亚胺（NE）来评估每种抗氧化剂在保护肿瘤靶细胞中的作用。经AT处理而耗尽过氧化氢酶的RBC，不再能保护Raji肿瘤细胞免受PMN细胞生长抑制活性的影响。然而，用NE耗尽还原型谷胱甘肽对RBC对肿瘤靶细胞的保护作用没有影响。因此，RBC可以保护肿瘤细胞免受TNF激活的PMN介导的细胞生长抑制活性的影响，且这种保护作用是过氧化氢酶的功能，而非谷胱甘肽的功能。
