The changes of intracellular H₂O₂ are an important factor maintaining mitochondria membrane potential of antimycin A-treated As4.1 juxtaglomerular cells

We investigated an involvement of ROS, such as H₂O₂ and O₂{radical dot}^- and GSH in the As4.1 cell death by antimycin A and examined whether ROS scavengers rescue antimycin A-induced As4.1 cell death and its mechanism. Levels of intracellular H₂O₂ and O₂{radical dot}^- were markedly increased in antimycin A-treated cells. Antimycin A reduced the intracellular GSH content. A ROS scavenger, Tiron down-regulated the production of intracellular H₂O₂. However, the reduction of intracellular H₂O₂ level did not change the apoptosis parameters, such as sub-G1 DNA content and annexin V binding. Interestingly, treatment of Tiron could partially prevent the loss of mitochondrial transmembrane potential (ΔΨ_m). Treatment of SOD and catalase also reduced the intracellular H₂O₂ and loss of mitochondrial transmembrane potential (ΔΨ_m) without reducing O₂{radical dot}^- level and apoptosis in antimycin A-treated As4.1 cells. All the ROS scavengers, SOD and catalase did not inhibit GSH depletion induced by antimycin A, resulting in failure of preventing the apoptosis. In addition, all the reagents including antimycin A did not induce any specific phase arrest of cell cycle in As4.1 cells. In summary, these results demonstrate that antimycin A generates potently ROS, H₂O₂ and O₂{radical dot}^- and induces the depletion of GSH content in As4.1 JG cells, and that Tiron, SOD and catalase inhibited partially the loss of mitochondrial transmembrane potential (ΔΨ_m) via the reduction of intracellular H₂O₂ level.