Effects of mitochondrial lipid molecules on release of ROS and beef muscle oxidation: a perspective on membrane...

The release of postmortem mitochondrial reactive oxygen species (ROS) contributes to muscle oxidative deterioration. Six LuXi yellow male cattle (22 months, 450 kg) were selected and each Psoas major muscles were divided into two: (1) in a NaCl solution and (2) in a mitoquinone solution. The release mechanism of beef ROS was explored from the perspectives of mitochondrial structure and lipid molecules. 3994 lipid species matched with 44 lipid classes were identified. These lipids encompass glycerophospholipids, sphingolipids, and glycerides. The linear mixed analysis model found significant interaction between treatment and storage time on phosphatidylethanolamine (PE, P = 0.0374), triglycerides (TG, P < 0.01), Ceramide (Cer, P = 0.016), sphingomyelin (SM, P = 0.048) and acylcarnitine AcCa (P < 0.01). Importantly, glycerol phospholipids such as PE, cardiolipin (CL), phosphatidylcholine (PC), and TG constitute the basic structure of mitochondrial membrane. Cylindrical lipids PC and SM are conducive to membrane stability, while conical lipids PE and CL increase membrane elasticity, ensuring mitochondrial integrity and preventing excessive ROS release. Simultaneously, mitoquinone may inhibit the production of ROS by mitochondrial complexes. This study found that compared to sodium chloride group, mitoquinone treatment may reduce the level of ROS in postmortem muscle and inhibited the rapid increase of thiobarbituric acid reactive substances (TBARS) and carbonyls (P < 0.05). These results indicate that changes in critical mitochondrial lipid molecules are closely related to the generation and release of mitochondrial ROS, thereby altering lipid and protein oxidation of postmortem muscles and beef quality.