The role of oxidative stress in lamb meat tenderization: Lysosomal-mitochondrial mediated apoptosis during postmortem aging

• Postmortem lysosomal Fenton reaction causes damage to membrane structure • Lysosomal membrane permeability enables the release of cathepsin D into the cytoplasm • Cathepsin D activates BCL2-Associated X to mediate mitochondrial apoptosis • Lysosome-mitochondrial apoptotic pathway improve tenderness of lamb meat This study examined the role of the lysosomal-mitochondrial apoptosis pathway in the tenderization of lamb meat during postmortem aging. Upon injection into lamb meat, deferoxamine (DFO) reduced oxidative damage to lysosomes, inhibited the permeability of the mitochondrial membrane, reduced apoptosis, and altered the tenderness of meat. The decline in lysosomal membrane permeabilization (LMP) led to an increase in cathepsin D levels. BH3 interacting domain death agonist (Bid) and BCL-2-associated X protein (Bax) levels in the early post-slaughter period further impaired mitochondrial membrane stability and induced apoptosis. Reduction level of Cytochrome c (Cyt-c), the expression of cysteinyl aspartate specific proteinase (caspase-9, caspase-3), and the increase in apoptosis were higher in the control group than in the DFO group ( P < 0.05). The increase in the myofibril fragmentation index(MFI) and the decrease in pH value and shear stress ( P < 0.05) demonstrated that the tenderness of lamb meat was improved after treatment. Correlation analysis showed that lysosomal-mediated mitochondrial apoptosis had a positive effect on the tenderness of lamb meat during postmortem aging.