TY - JOUR AB - Antimycin A (AMA) inhibits the growth of various cells via stimulating oxidative stress-mediated death. However, little is known about the anti-growth effect of AMA on normal primary lung cells. Here, we investigated the effects of AMA on cell growth inhibition and death in human pulmonary fibroblast (HPF) cells in relation to reactive oxygen species (ROS) and glutathione (GSH) levels. AMA inhibited the growth of HPF cells with an IC50 of ~150 µM at 24 h. AMA induced a G1 phase arrest of the cell cycle and it also triggered apoptosis accompanied by the loss of mitochondrial membrane potential (MMP; ∆Ψm). AMA increased ROS levels including O2᛫- in HPF cells from the early time point of 25 min. It induced GSH depletion in HPF cells in a dose-dependent manner. Z-VAD (a pan-caspase inhibitor) did not significantly prevent cell death and MMP (∆Ψm) loss induced by AMA. N-acetylcysteine (NAC; an antioxidant) attenuated cell growth inhibition, death and MMP (∆Ψm) loss in AMA-treated HPF cells and NAC generally decreased the ROS level in these cells as well. Vitamin C enhanced cell growth inhibition, death, GSH depletion and O2᛫- levels in 100 µM AMA-treated HPF cells whereas this agent strongly attenuated these effects in 200 µM AMA-treated cells. In conclusion, AMA inhibited the growth of HPF cells via apoptosis as well as a G1 phase arrest of the cell cycle. AMA-induced HPF cell death was related to increased ROS levels and GSH depletion. AD - Department of Physiology, Medical School, Research Institute for Endocrine Sciences, Chonbuk National University, Jeonju 561-180, Republic of Korea AU - Park,Woo ,Hyun AU - You,Bo ,Ra DA - 2016/02/01 DO - 10.3892/ijo.2015.3276 EP - 820 IS - 2 JO - Int J Oncol KW - human pulmonary fibroblast anti­mycin A cell death reactive oxygen species glutathione PY - 2016 SN - 1019-6439 1791-2423 SP - 813 ST - Antimycin A induces death of the human pulmonary fibroblast cells via ROS increase and GSH depletion T2 - International Journal of Oncology TI - Antimycin A induces death of the human pulmonary fibroblast cells via ROS increase and GSH depletion UR - https://doi.org/10.3892/ijo.2015.3276 VL - 48 ER -