关键词: 宰后嫩化, 细胞凋亡, 细胞凋亡酶, 线粒体损伤, 凋亡因子

Abstract:

Tenderness has been considered as one of the most important eating quality characteristics of meat, while inconsistent changes of tenderness in postmortem (PM) muscles can significantly reduce the purchasing intention. Therefore, investigating mechanism of postmortem muscle tenderization is becoming more and more important in the past decade. Since apoptosis definition was highlighted in the PM tenderization process, it has been widely concerned. Shortly after slaughter, the reactive oxygen species (ROS) was significantly accumulated, and ATP (adenosine triphosphate) was gradually exhausted within muscle fibers, which inevitably led to skeletal cell death. Both PM cell death and meat tenderization refer to the activation of muscle endogenous enzymes by a series of regulatory factors, followed by the degradation of muscle structural proteins. The two biochemical processes are considered to be highly related. PM muscle cells die mainly through apoptosis. Besides, in the early stage of PM, when a small amount of ROS is produced, the cells start their defense system by autophagy and ATP therefore gradually deplete muscle cells in the later stage, which may change from apoptosis to necrosis. It has been documented that mitochondrial pathway is crucial for the apoptosis activation in PM muscles. The release of apoptotic factors from mitochondria is the master node of the intracellular death cascade reaction. The opening status of mitochondrial outer membrane directly determines the way, in which the muscle fiber dies. In this paper, the release mechanism of apoptotic factors induced by PM mitochondrial damage was discussed from the perspectives of mitochondrial membrane permeability and cristae remodeling, and the regulation of mitochondrial damage on PM muscle tenderization was discussed. Moreover the underlying mechanism behind it was also analyzed to reveal the effect of mitochondria on muscle pH regulation through energy metabolism, the release of apoptotic factors and regulation of apoptosis enzyme activity. At the same time, the interaction between mitochondria and endoplasmic reticulum were discussed, focusing on Ca²⁺ signal transduction and cell apoptosis process. The interaction between mitochondria and lysosome was further investigated, by highlighting the stability of lysosomal membrane and the subsequently released cathepsin to activate Bax and Bid to accelerate mitochondrial membrane permeability. Caspases were activated and involved in the limited degradation of some myofibrils in the early stage of PM tenderization, followed by the inactivation resulting from the decreasing ATP or other factors with the extended PM time. Therefore, caspases maybe only involve the early stage of tenderization. This review could provide a theoretical reference for the perfection of PM muscle tenderization investigations.

Key words: postmortem tenderization, apoptosis, caspases, mitochondrial damage, apoptotic factors