Gansauge S, Gansauge F, Gause H, Poch B, Schoenberg M H, Beger H G
Department of General Surgery, University of Ulm, Germany.
FEBS Lett. 1997 Mar 3;404(1):6-10. doi: 10.1016/s0014-5793(97)00059-8.
The role of reactive oxygen species (ROS) generated by hypoxanthine/xanthine oxidase (HX/XO) in the induction of apoptosis was studied in the human fibroblast cell line WI38. Apoptosis but not necrosis was observed in proliferating fibroblasts after 48 h incubation with 1 mM HX and 0.05 U/ml XO. Induction of apoptosis was hindered by catalase. Cell-cycle analysis revealed a reduction of cells in the S/G2 phase 24 and 48 h after stimulation, suggesting that ROS induce a G1 arrest in proliferating fibroblasts. This was supported by an accumulation of p53 and the cdk inhibitor p21WAF1/CIP1. Since apoptosis was not inducible in senescent fibroblasts our data indicate that ROS mainly induces apoptosis in proliferating cells.
研究了次黄嘌呤/黄嘌呤氧化酶（HX/XO）产生的活性氧（ROS）在人成纤维细胞系WI38中诱导细胞凋亡的作用。在用1 mM HX和0.05 U/ml XO孵育48小时后，在增殖的成纤维细胞中观察到细胞凋亡而非坏死。过氧化氢酶可抑制细胞凋亡的诱导。细胞周期分析显示，刺激后24小时和48小时，S/G2期的细胞减少，这表明ROS在增殖的成纤维细胞中诱导G1期停滞。p53和细胞周期蛋白依赖性激酶抑制剂p21WAF1/CIP1的积累支持了这一点。由于衰老的成纤维细胞中不能诱导细胞凋亡，我们的数据表明ROS主要在增殖细胞中诱导细胞凋亡。
