Antimycin A as a mitochondrial electron transport inhibitor prevents the growth of human lung cancer A549 cells
Antimycin A as a mitochondrial electron transport inhibitor prevents the growth of human lung cancer A549 cells
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DOI：
10.3892/or_00000061
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发表时间：
2008-09-01
期刊：
影响因子：
4.2
通讯作者：
Park, Woo Hyun
中科院分区：
文献类型：
--
作者：
Han, Yong Hwan;Kim, Suhn Hee;Park, Woo Hyun
抗霉素A（AMA）抑制细胞色素B和C之间的线粒体电子传递。本研究探讨了AMA对人肺腺癌A549细胞生长的影响及其与细胞周期和凋亡的关系。2-100 μ M AMA处理A549细胞72 h，细胞生长受到明显抑制。DNA流式细胞仪检测显示，AMA可轻微诱导细胞周期G1期阻滞72 h。鉴于膜联蛋白V染色细胞，用50 μ M AMA处理诱导的凋亡类似于17%。50 μ M AMA的剂量也诱导了线粒体膜电位（Delta Psi（m））的损失，损失率接近38%。AMA处理的A549细胞内活性氧（ROS）水平，包括O-2（中心点-）显着增加。结论：AMA通过诱导细胞周期阻滞和凋亡抑制A549细胞的生长。AMA处理的A549细胞的生长抑制伴随着ROS水平的增加。
Antimycin A (AMA) inhibits mitochondrial electron transport between cytochromes b and c. We evaluated the effects of AMA on the growth of human pulmonary adenocarcinoma A549 cells in relation to cell cycle and apoptosis. Treatment with 2-100 mu M AMA significantly inhibited the cell growth of A549 for 72 h. DNA flow cytometry indicated that AMA slightly induced a G1 phase arrest of the cell cycle for 72 h. Treatment with 50 mu M AMA induced apoptosis of similar to 17% in view of annexin V-staining cells. The dose of 50 mu M AMA also induced loss of the mitochondrial membrane potential (Delta Psi(m)) of similar to 38%. The intracellular reactive oxygen species (ROS) levels including O-2(center dot-) were significantly increased in AMA-treated A549 cells. In conclusion, AMA inhibited the growth of A549 cells via inducing cell cycle arrest as well as triggering apoptosis. Growth inhibition in AMA-treated A549 cells was accompanied by an increase in ROS levels.