Mitochondrial and endoplasmic reticulum stress pathways regulate tenderness of post-mortem chicken muscle

Apoptosis is closely associated with meat tenderization and calcium chloride (CaCl2) and tea polyphenols (TP) have been shown to have a positive effect on meat tenderness. To examine the mechanism by which apoptosis regulates meat tenderness, chicken breasts were treated with 50 mM CaCl2 and 5 mg/mL TP during 5 days of post-mortem ageing where corresponding tender indexes were measured. The results demonstrated that the shear force was highly reduced by 30.74% and 53.64% in chicken breasts treated with CaCl2 and TP, respectively, which promoted postmortem degradation of troponin-T and desmin as well as destruction of myofibrils. Western blot analysis demonstrated that CaCl2 and TP treatments resulted in the activation of calpain-1, caspase-12, -9 and -3, cleavage of PARP, increased the Bax/Bcl-2 ratio, and reduced Bcl-xL levels. In addition, BiP, p-IRE1, and XBP1 factors associated with the endoplasmic reticulum (ER) pathway, were activated during apoptosis. This suggests that the mitochondrial and ER pathways were involved in the induction of apoptosis by CaCl2 and TP during post-mortem ageing. Moreover, ultrastructural damage occurring in mitochondria and nuclei was observed in the morphological features of apoptosis. Consequently, these results suggest that CaCl2 and TP promote meat rejuvenation during ageing process by activating apoptosis via mitochondrial and ER pathways. [Display omitted] •CaCl2 and TP reduce shear force to improve chicken breast tenderness.•CaCl2 and TP damage myofibril fibers and degrade troponin-T and desmin.•Calpain-1 and its downstream pathway are activated by CaCl2 and TP.•Endoplasmic reticulum and mitochondrial pathway involve tenderness regulation.