4.7 Article

Exploring the potential effect of phospholipase A2 antibody to extend beef shelf-life in a beef liposome model system

期刊

MEAT SCIENCE
卷 198, 期 -, 页码 -

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.meatsci.2022.109091

关键词

Phospholipase A2; Anti-phospholipase A2; Phospholipid; Antioxidant capacity; Lipid oxidation; Lipidomics

资金

  1. KSU Global Food System Initiative
  2. National Science Foundation
  3. K-IDeA Networks of Biomedical Research Excellence (INBRE) of National Institute of Health [P20GM103418]
  4. Kansas State University
  5. USDA National Institute of Food and Agriculture, Hatch project [1003222]

向作者/读者索取更多资源

This study aimed to investigate the impact of phospholipase A2 (PLA2) and its antibody (aPLA2) on phospholipid hydrolysis, lipid oxidation, and antioxidant capacity in beef. The results showed that PLA2 decreased key phospholipid classes and increased the release of polyunsaturated fatty acids (FFAs). Despite exhibiting strong antioxidant capacity, PLA2 treatment led to increased lipid oxidation. On the other hand, aPLA2 treatment showed potential in reducing lipid oxidation.
The objective of this study was to elucidate the effect of phospholipase A2 (PLA2) and a PLA2 antibody (aPLA2) on phospholipid (PL) hydrolysis in beef and to understand how the altered PL composition may affect lipid oxidation and antioxidant capacity of beef in an in vitro system. Various combinations of PLA2 and aPLA2 were introduced to a beef liposome model system and exposed to a retail display. The PL and free fatty acid (FFA) profiles, antioxidant capacity and lipid oxidation were measured for the liposome system. Key PL classes were reduced and the release of polyunsaturated FFAs was increased with the inclusion of PLA2 in the treatments (P < 0.05). There was no inhibition of PL hydrolysis with the addition of aPLA2. PLA2 showed strong antioxidant capacity in the liposome system (P < 0.01), but lipid oxidation still increased in samples treated with PLA2 throughout the retail display (P < 0.01). Finally, aPLA2 treatments demonstrated potential to decrease lipid oxidation (P < 0.01).

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