肿瘤坏死因子（TNF）可激活多形核中性粒细胞（PMN）以抑制肿瘤细胞增殖。这种细胞停滞活性可以通过向实验中加入红细胞（RBC）来阻止。TNF诱导PMN细胞停滞活性是由过氧化氢（H2O2）介导的。RBC具有两条主要途径以解毒H2O2，一个是通过过氧化氢酶，另一个是通过谷胱甘肽氧还原循环。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。通过AT去除过氧化氢酶的RBC不再保护Raji肿瘤细胞免受PMN细胞停滞活性的影响。然而，通过NE去除还原谷胱甘肽对RBC保护肿瘤靶细胞没有影响。因此，RBC可以保护肿瘤细胞免受TNF激活的PMN介导的细胞停滞活性，并且这种保护是由过氧化氢酶而不是谷胱甘肽产生的。

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.