Antimycin A as a mitochondrial electron transport inhibitor prevents the growth of human lung cancer A549 cells

Abstract

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 microM 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 microM AMA induced apoptosis of approximately 17% in view of annexin V-staining cells. The dose of 50 microM AMA also induced loss of the mitochondrial membrane potential (DeltaPsi(m)) of approximately 38%. The intracellular reactive oxygen species (ROS) levels including O2(.-) 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.