Expression of bcl-2 inhibits cellular radical generation.
Bcl-2 expression in neural cells has been shown to inhibit apoptotic death in association with a decrease in reactive oxygen species. We present the results of a study that used electron spin resonance (ESR) measurements to evaluate the level of hydroxyl radical production in bcl-2 expressing GT1-7 cells and control cells. Incubation of cell monolayers with the spin trap N-t-alpha-phenylnitrone (PBN), and measurements of the hydroxyl radical production at different timepoints, revealed a higher radical production in control cells than in bcl-2 expressing cells, even in the absence of insult. The ESR signal was suppressed by addition of ethanol, indicating that the trapped radical was indeed hydroxyl radical. The mechanism by which the expression of bcl-2 leads to a decrease in cellular production of hydroxyl radical is unknown.
Wiedau-Pazos
M
M
Department of Neurology, University of California, Los Angeles 90024-1769, USA.
Trudell
J R
JR
Altenbach
C
C
Kane
D J
DJ
Hubbell
W L
WL
Bredesen
D E
DE
D000818:Animals; D002460:Cell Line; D002470:Cell Survival; D004578:Electron Spin Resonance Spectroscopy; D005609:Free Radicals / Q000037:antagonists & inhibitors / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000096:biosynthesis; D015870:Gene Expression; D017665:Hydroxyl Radical / Q000378:metabolism*; D009474:Neurons; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis*; D019253:Proto-Oncogene Proteins c-bcl-2; D011519:Proto-Oncogenes; D013113:Spin Labels
D005609:Free Radicals; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D013113:Spin Labels; D017665:Hydroxyl Radical; D019204:GTP-Binding Proteins