Appearance of shortened Bcl-2 and Bax proteins and lack of evidence for apoptosis in rat forebrain after severe experimental traumatic brain injury

To investigate whether apoptosis plays a role in traumatic brain injury (TB I), we examined the expression of Bcl-2 and Bax proteins and the release of mitochondrial cytochrome c in rat brains using Western blot analysis. Bcl- 2 at the predicted 26 kDa was not detected in controls and TBI groups. Howe ver, at 1 h post-TBI, a shortened Bcl-2 protein with a molecular size of si milar to 14.5 kDa was detected in the injured hemisphere (R). At 4 and 12 h post TBI, an additional bcl-2 band (similar to 10 kDa) was detected in R. Both bands disappeared at 14 days postinjury. The predicted 21-kDa band of Bax was detected in both controls and TBI animals. In addition, two shorten ed Bax proteins (similar to 18 kDa) were detected after TBI. The time cours e of appearance was similar to that of Bcl-2 described above. In the presen t study, neither cytochrome c release from mitochondria nor DNA fragmentati on was detected in the forebrains of sham and TBI groups. Treatment of anim als with an antioxidant N-acetylcysteine administered ip greatly diminished the levels of shortened Bcl-2 and Bax proteins. These findings suggest tha t the induction of shortened Bcl-2 and Bax proteins in rat brains may be as sociated with reactive oxygen species generated after TBI. (C) 2001 Academi c Press.