Oxidative Stress Contributes to Cytoskeletal Protein Degradation of Esox lucius through Activation of Mitochondrial Apoptosis during Postmortem Storage

Xue Li; Pingping Liu; Yunfeng Zhao; Lianfu Zhang; Jian Zhang

doi:10.3390/foods11091308

Oxidative Stress Contributes to Cytoskeletal Protein Degradation of Esox lucius through Activation of Mitochondrial Apoptosis during Postmortem Storage

Foods. 2022 Apr 29;11(9):1308. doi: 10.3390/foods11091308.

Authors

Xue Li¹, Pingping Liu¹, Yunfeng Zhao¹, Lianfu Zhang^{1

2}, Jian Zhang¹

Affiliations

¹ School of Food Science and Technology, Shihezi University, Shihezi 832003, China.
² State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Collaborative Innovation Center of Food Safety and Quality Control in Jiangsu Province, Jiangnan University, Wuxi 214122, China.

Abstract

This study investigated the role of oxidative stress in the mitochondrial apoptotic pathways and structural protein degradation of fish during postmortem storage by measuring oxidative stress levels, mitochondrial antioxidant enzyme activity, mitochondrial dysfunction, apoptotic factors, and structural protein degradation (n = 3). The results revealed that reactive oxygen species (ROS) increased gradually within the first 12 h and then decreased (p < 0.05) in mitochondria. Lipid peroxidation was increased, and superoxide dismutase, catalase, and glutathione peroxidase activities were decreased in mitochondria (p < 0.05). Furthermore, oxidative stress induced mitochondrial membrane opening, mitochondrial swelling, as well as the depolarization of mitochondrial potential. This led to an increase in the release of cytochrome c from mitochondria and caspase-3 activation. Ultimately, oxidative stress promoted small protein degradation (troponin-T and desmin) and induced myofibril susceptibility to proteolysis. These observations confirmed that oxidative stress mediated the activation of mitochondrial apoptotic factors-promoted protein degradation, initiating the deterioration of fish muscle through the mitochondrial apoptotic pathway.

Keywords: caspases; cytochrome c; mitochondrial apoptosis; myofibril protein; reactive oxygen species.

Grants and funding

This study was supported by the National Natural Science Foundation of China [grant number 31960460], the Innovative team building plan of key realm projects in Xinjiang Corps [grant number 2019CB007] and the Research platform projects of Shihezi University [grant number KYPT201904].