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目的：了解氧自由基的产生与ＴＮＦ抗肿瘤活性之间的关系。方法：采用３Ｈ－ＴｄＲ摄入法测定ＴＮＦ对胃癌细胞株Ｘ－１０８、卵巢癌细胞株３ＡＯ和ＡＯ肿瘤细胞的杀伤活性；用细胞色素Ｃ氧化法测定靶细胞经ＴＮＦ刺激后产生的超氧离子水平。结果：ＴＮＦ对Ｘ－１０８、ＡＯ有较明显的杀伤活性，３Ｈ－ＴｄＲ摄入量的降低与ＴＮＦ浓度的增加一致，而３ＡＯ则对ＴＮＦ呈明显的抵抗。Ｘ－１０８细胞株在经ＴＮＦ处理８ｈ后即可检测出超氧离子，并且在２４ｈ后达到高峰。Ｘ－１０８和ＡＯ细胞内超氧离子的水平与ＴＮＦ的剂量有关。对于抵抗ＴＮＦ的３ＡＯ卵巢癌细胞株，其超氧离子的水平与对照组无明显差别。阿霉素能够增强ＴＮＦ诱导氧自由基的能力。结论：ＴＮＦ的受体后效应——自由基的产生可能是ＴＮＦ杀伤靶细胞的重要机制之一。
Objective: To understand the relationship between the production of oxygen free radicals and the antitumor activity of TNF. Methods: 3H-TdR uptake method was used to determine the killing activity of TNF on gastric cancer cell line X-108, ovarian cancer cell line 3AO and AO tumor cells; cytochrome C oxidation method was used to measure the superoxide ion produced by target cells stimulated by TNF. Level. RESULTS: TNF showed significant killing activity against X-108 and AO. The decrease of 3H-TdR intake was consistent with the increase of TNF concentration, while 3AO showed significant resistance to TNF. X-108 cell line could detect superoxide ion after TNF treatment for 8 hours, and peaked at 24 hours. The levels of superoxide ion in X-108 and AO cells are related to the dose of TNF. For 3AO ovarian cancer cell lines resistant to TNF, there was no significant difference in the level of superoxide ion between the control and the AO. Doxorubicin enhances the ability of TNF to induce oxygen free radicals. Conclusion: The post-receptor effect of TNF, the production of free radicals, may be one of the important mechanisms of TNF killing target cells.