Tettamanti Gianluca, Malagoli Davide, Ottaviani Enzo, de Eguileor Magda
Department of Structural and Functional Biology, University of Insubria, Via J.H. Dunant 3, 21100 Varese, Italy.
Cell Biol Int. 2008 Feb;32(2):287-92. doi: 10.1016/j.cellbi.2007.10.011. Epub 2007 Nov 12.
Oligomycin A, an inhibitor of mitochondrial ATP synthase, provokes simultaneous and different responses in IPLB-LdFB insect cell line. The oligomycin A treatment causes mitochondrial loss, increase in reactive oxygen species (ROS), destabilization/reorganization of the actin microfilaments and, finally, autophagic cell death. We speculate that oligomycin A affects the mitochondria and that the impairment of these organelles leads to the generation of ROS in quantities that exceed the antioxidant capacity of the cell. This in turn would lead to a feedback loop of increased mitochondrial impairment, amplification of ROS production and the removal of damaged organelles through autophagy.
