细胞凋亡对宰后肌肉嫩化作用机理的研究进展

嫩度是决定肉食用品质的重要指标。宰后肉的嫩度发生不连续变化,严重降低了消费者的购买意愿,因此阐明宰后嫩化机理一直是肉品科学领域的研究热点。自“凋亡”的概念引入至宰后肌肉嫩化过程后一直广受关注,动物被屠宰放血后,活性氧（reactive oxygen species,ROS）大量累积,ATP（adenosine triphosphate）逐渐耗尽,必然导致细胞死亡。宰后肌细胞死亡和肌肉嫩化都是在一系列调控因子作用下激活肌肉内源酶,并由内源酶水解蛋白质破坏细胞结构,因此这两个生化过程被认为高度相关。本文综述了宰后肌细胞主要以凋亡的形式死亡,分析了除凋亡外,宰后早期产生少量ROS时细胞会通过自噬启动自身防御系统,宰后后期ATP逐渐耗尽肌细胞可能从凋亡转变为坏死;明确了线粒体通路是宰后肌肉中细胞凋亡酶激活的关键路径,线粒体死亡因子释放是细胞内死亡级联反应的总开关,其开放状态直接决定着细胞以何种途径进行死亡,并进一步从线粒体膜通透化和内膜嵴重构两方面,讨论了宰后线粒体损伤诱导凋亡因子的释放机理;综述了线粒体损伤变化及其对嫩化过程的影响,并从线粒体通过参与能量代谢影响肌肉pH以及通过释放凋亡因子调控细胞凋亡酶活性两方面分析了其潜在机理;探讨了宰后肌肉线粒体与内质网间相互作用以影响Ca²⁺信号传导以及细胞凋亡过程,或与溶酶体相互作用,破坏溶酶体膜稳定性,使其释放组织蛋白酶以激活线粒体Bax和Bid而加速线粒体膜通透性;综述了细胞凋亡酶在宰后早期被激活,并参与部分肌原纤维蛋白的有限降解,但随着宰后时间的延长,ATP逐渐耗尽等因素导致细胞凋亡酶失活,因此细胞凋亡酶只参与宰后早期的嫩化过程。综述内容可为完善宰后肌肉嫩化过程提供理论参考。

Research Progress on Mechanisms of Apoptosis to Postmortem Tenderization in Muscle

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.