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Changes in mitochondrial membrane potential during oxidative stress-induced apoptosis in PC12 cells

1997; Wiley; Volume: 50; Issue: 3 Linguagem: Inglês

10.1002/(sici)1097-4547(19971101)50

1097-4547

Takumi Satoh, Yasushi Enokido, Hitoshi Aoshima, Yasuo Uchiyama, Hiroshi Hatanaka,

ATP Synthase and ATPases Research

We examined the effects of various types of oxidative stress on cell survival and on mitochondrial membrane potential (ΔΨm) in PC12 cells transfected with BCL-2. Several types of oxidative stress such as exposure to hydrogen peroxide, 13-L-hydroperoxylinoleic acid, and xanthine + xanthine oxidase triggered apoptotic nuclear condensation and DNA fragmentation in normal PC12 cells. These types of oxidative stress induced significant increases in level of reactive oxygen species (ROS) before cell death. By contrast, BCL-2 prevented the apoptosis induced by these oxidative stresses. However, BCL-2 did not reduce ROS levels, indicating that it functions downstream of ROS generation. We measured ΔΨm as a potential target of ROS during oxidative stress–induced cell death. Hydrogen peroxide, 13-L-hydroperoxylinoleic acid, and xanthine + xanthine oxidase induced a significant loss of ΔΨm simultaneously with cell death. BCL-2 prevented the decrease in ΔΨm as well as apoptosis induced by oxidative stress. These observations suggest that the oxidative stress triggers apoptosis associated with both increased generation of ROS and decreases in level of ΔΨm and that BCL-2 prevents cell death as well as Δ Ψm but not ROS production. J. Neurosci. Res. 50:413–420, 1997. © 1997 Wiley-Liss, Inc.