Fragmentation of cellular DNA is a nonspecific indicator of responsiveness to tumor necrosis factor.

B Y Rubin, S L Anderson, R M Lunn, G R Hellermann, L J Smith
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Abstract

Tumor necrosis factor (TNF) or lymphotoxin (LT) treatment of cells sensitive to the anticellular action of TNF results in the degradation of their cellular DNA into fragments that are multiples of about 200 base pairs. The specificity of this DNA fragmenting effect was examined. The DNA of cells dying either as a result of exposure to interferon-gamma (IFN-gamma) or as a result of having exhausted their culture media was observed to be fragmented into multiples of 200 base pairs. Antibody to TNF or LT failed to block the IFN-gamma-mediated DNA fragmentation and antibodies to IFN-gamma, TNF, and LT failed to block the DNA fragmentation observed in the cells dying as a result of having exhausted their culture media. Thus the fragmentation of cellular DNA appears to be nonspecific effect of cell death that can be induced by a variety of treatments.

细胞DNA的断裂是对肿瘤坏死因子反应性的非特异性指标。
肿瘤坏死因子(TNF)或淋巴毒素(LT)治疗对TNF的抗细胞作用敏感的细胞导致其细胞DNA降解成约200个碱基对的倍数片段。研究了这种DNA片段化效应的特异性。由于暴露于干扰素- γ (ifn - γ)或由于耗尽其培养基而死亡的细胞的DNA被观察到分裂成200个碱基对的倍数。TNF或LT抗体不能阻断ifn - γ介导的DNA片段,ifn - γ、TNF和LT抗体不能阻断因培养基耗尽而死亡的细胞中观察到的DNA片段。因此,细胞DNA的断裂似乎是细胞死亡的非特异性效应,可以通过各种治疗诱导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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