Abstract
The objective of this study was to investigate the mechanism underlying lysosome-mediated apoptosis, the cross-talk between the lysosomes and mitochondria, and the effect of the pathway on bovine longissimus muscle tenderness during 7 d post-mortem aging through the observation and analysis of longissimus dorsi (LD) muscles of six crossbred cattle. Results showed that an elevated reactive oxygen species level ( P < 0.05) can damage lysosomal membrane stability ( P < 0.05) through accumulating redox-active iron of bovine muscle during post-mortem aging. In addition, the activities of cathepsins B and D increased with post-mortem aging ( P < 0.05). Moreover, cathepsin B and D activated Bid and Bax in the mitochondria ( P < 0.05). Activated Bid and Bax triggered mitochondrial membrane permeability ( P < 0.05) and further activated caspase-9 and caspase-3 ( P < 0.05), leading to apoptosis. Ultimately, the tenderness of bovine muscle was improved during post-mortem aging ( P < 0.05). Importantly, cathepsin D plays a crucial role in the lysosomal-mitochondrial apoptotic pathway and tenderness in post-mortem muscle. These findings provide new insights into the apoptotic pathway of bovine muscle during post-mortem aging.
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