Hibernation-induction peptide and cell death: [ d-Ala 2, d-Leu 5]enkephalin blocks Bax-related apoptotic processes

Abstract

The psychostimulant methamphetamine, both in vivo and in vitro, caused a mitochondrial cytochrome c release, the translocation of Bax from cytosol into mitochondrion, and the oligomerization of Bax. These effects by methamphetamine were blocked by a neuroprotective and hibernation-induction δ opioid peptide [ d-Ala 2, d-Leu 5]enkephalin (DADLE). These results suggest that methamphetamine causes apoptosis by affecting the dynamics of Bax and that the neuroprotective property of DADLE may be due partly to its ability to potently block Bax-related apoptotic processes.