Contribution of cathepsin, calpain and proteasome to the post-mortem proteolysis and tenderisation

Qian Zhang ； Xiaoying Luo ； Qiufeng Ruan ； Shanbai Xiong

《International Core Journal of Engineering》 7卷12期 (2021/12) Pp. 549-562

https://doi.org/10.6919/ICJE.202112_7(12).0077

摘要

Tenderness is one of the most important evaluation indicators of meat quality, and endogenous enzymes in post-mortem muscles play key roles in degradation of myofibrils and tenderness improving. Cathepsin is the first endogenous enzymes family found to be positive in post-mortem ageing, and most studies are focus on cathepsin B, D, H and L. Calpain is the major contributor to post-mortem muscle tenderness, and owns calpastatin to control proteolysis precisely. Proteasome is controversial involving in ageing process, but increasing evidence emerged on the 20S core particle degradation of structural protein even under extreme conditions. In this paper, the characteristics, action mechanism and influencing factors of the three endogenous enzymes were reviewed, and the process of their involvement in meat ageing and tenderness improving was analysed, in order to provide theoretical basis for meat processing.

關鍵字

Cathepsin ； calpain ； proteasome ； post-mortem ； ageing ； tenderness

參考文獻

Koohmaraie M., Geesink G. H. Contribution of post-mortem muscle biochemistry to the delivery of consistent meat quality with particular focus on the calpain system[J]. Meat Science, 2006, 74:34-43.

Purslow P. P. New developments on the role of intramuscular connective tissue in meat toughness[J]. Review of Food Science and Technology, 2014, 5:133-153.

Ouali A. Proteolytic and physicocohemical mechanisms involved in meat texture development, Biochimie, 1992, 74: 251-265.

Ahmed Z, Donkor O, Street W A, et al. Calpains-and cathepsins-induced myofibrillar changes in post-mortem fish: Impact on structural softening and release of bioactive peptides[J]. Trends in Food Science & Technology, 2015,45(1):130-146.

Kane B, Petrovich D R, Stern R O and Farber J L. ATP depletion and loss of cell integrity in anoxic hepatocytes and silica treated macrophages.Cell Physiol,1985,249 (3) :256-266