Effect of mitochondrial apoptotic activation through the mitochondrial membrane permeability transition pore on yak meat tenderness during postmortem aging

- We examine the caspases in the apoptosis pathway of yak meat during postmortem aging.
- CsA can inhibit the opening of the mitochondrial membrane permeability transition pore.
- The cytochrome c is released from mitochondria to cytoplasm via MPTP.
- MPTP mediates the activation of the mitochondrial apoptosis pathway of yak meat during postmortem aging.
- ROS generation and Ca2+ overloading may paly a significant role in opening the MPTP.

The effect of membrane permeability transition pore dependent mitochondrial apoptotic activation on yak meat tenderness was investigated. Results indicate that MPTP opening increased significantly and the mitochondrial membrane potential decreased markedly in the early aging process (P < 0.05). Cytochrome c was released from the mitochondria to the cytoplasm via the MPTP in the early period. Meanwhile, the activation of procaspase-9 occurred earlier than that of procaspase-3. Cyclosporin A suppressed the MPTP opening, depolarization of the mitochondrial membrane potential, activities of caspase-9 and caspase-3, apoptosis rate, myofibril fragmentation index, reactive oxygen species generation, and Ca2+ levels. These results demonstrated that MPTP mediated the release of cytochrome c in the mitochondrial apoptotic pathway. Furthermore, yak meat tenderness was improved by mitochondrial apoptotic pathway during aging. MPTP opening may be influenced by the ROS generation and Ca2+ overloading in yak meat during postmortem aging.