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Antimycin A induces apoptosis in As4.1 juxtaglomerular cells

2007; Elsevier BV; Volume: 251; Issue: 1 Linguagem: Inglês

10.1016/j.canlet.2006.11.002

1872-7980

Grace Park, Yong-Whan Han, Sang‐Wook Kim, Suhn-Hee Kim, Kyung-Woo Cho, Sung-Zoo Kim,

ATP Synthase and ATPases Research

Antimycin A, an inhibitor of electron transport in mitochondria, has been used as reactive oxygen species (ROS) generator in the biological system. Here, we investigated the in vitro effect of antimycin A on apoptosis in As4.1 juxtaglomerular cells. Antimycin A efficiently induced apoptosis in As4.1 cells as evidenced by flow cytometric detection of sub-G1 DNA content, annexin V binding assay and DAPI staining. This apoptotic process was accompanied by loss of mitochondrial transmembrane potential (ΔΨm), Bcl-2 decrease, caspase-3 activation and PARP cleavage. All of caspase inhibitors tested in this experiment failed to rescue As4.1 cells from antimycin A-induced cell death at the time of 48 h in view of sub-G1 cells and annexin V positive staining cells. However, with regard to the mitochondrial membrane potential (ΔΨm), pan caspase inhibitor (Z-VAD-FMK) and caspase-3 inhibitor (Z-DEVD-FMK) at the concentration of 25 μM noticeably decreased the loss of mitochondrial membrane potential (ΔΨm) in antimycin A-treated cells. Taken together, we have demonstrated that antimycin A as an inhibitor of electron transport in mitochondria potently induces apoptosis in As4.1 juxtaglomerular cells.