Study on the effect of reactive oxygen species-mediated oxidative stress on the activation of mitochondrial apoptosis and the tenderness of yak meat

Abstract

This study investigated the effect of reactive oxygen species-mediated oxidative stress on activation of mitochondrial apoptosis and tenderness of yak meat during postmortem ageing. Oxidative stress degree, Ca²⁺ levels, membrane permeability transition pore opening, mitochondrial membrane potential, apoptotic factors and the shear force were examined. Results showed that the ROS generated by H₂O₂ significantly increased mitochondrial oxidative stress by decreasing the activities of superoxide dismutase, catalase and glutathione peroxidase, and increasing lipid peroxidation. Furthermore, oxidative stress enhanced Ca²⁺ production and cytochrome c release, changed the levels of Bcl-2 family proteins and activated caspase-9 and -3 activities. Ultimately, oxidative stress increased the apoptosis rate and tenderness of yak meat. These observations confirmed that ROS-mediated oxidative stress participates in the activation of the apoptotic cascade reaction involving Ca²⁺ and Bcl-2 family proteins. The results further suggested that ROS-mediated oxidative stress plays a significant role in meat tenderization through the mitochondrial apoptotic pathway.

Keywords: Bcl-2 family proteins; Cytochrome c (PubChem CID: 16057918); DCFH-DA (PubChem CID: 104913); GSH (PubChem CID: 124886); Glycerol (PubChem CID: 753); H(2)O(2) (PubChem CID: 784); JC-1 (PubChem CID:5492929); Mitochondrial apoptosis; NAC (PubChem CID: 12035); Oxidative stress; Reactive oxygen species; SDS (PubChem CID: 3423265); SOD (PubChem CID: 11963501); Tenderness; Tris (PubChem CID: 6503); Yak meat.