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1 August 2001 Evidence that bcl-2 is the Target of Three Photosensitizers that Induce a Rapid Apoptotic Response
David Kessel, Michelle Castelli
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We originally proposed that the subcellular target for one class of photosensitizing agents was the mitochondrion. This classification was based on effects that occur within minutes of irradiation of photosensitized cells: rapid loss of the mitochondrial membrane potential (ΔΨm), release of cytochrome c into the cytosol and activation of caspase-3. These effects were followed by the appearance of an apoptotic morphology within 30–90 min. Fluorescence localization studies on three sensitizers initially classified as ‘mitochondrial’ revealed that these agents bind to a variety of intracellular membranes. The earliest detectable effect of photodamage is the selective loss of the antiapoptotic protein bcl-2 leaving the proapoptotic protein bax undamaged. Bcl-2 photodamage can be detected directly after irradiation of cells at 10°C. Subsequent warming of cultures to 37°C results in loss of ΔΨm, release of cytochrome c and activation of caspase-3. The latter appears to amplify the other two effects. Based on results reported here we propose that the apoptotic response to these photosensitizers is derived from selective photodamage to the antiapoptotic protein bcl-2 while leaving the proapoptotic protein bax unaffected.

David Kessel and Michelle Castelli "Evidence that bcl-2 is the Target of Three Photosensitizers that Induce a Rapid Apoptotic Response," Photochemistry and Photobiology 74(2), 318-322, (1 August 2001).<0318:ETBITT>2.0.CO;2
Received: 27 February 2001; Accepted: 1 May 2001; Published: 1 August 2001

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