Correlation Analysis of Mitochondrial Tu Translation Elongation Factor and Energy Metabolism in Qinchuan Cattle during Postmortem Aging

Mitochondrial Tu translation elongation factor (TUFM) has been demonstrated to be involved in cellular autophagy during the postmortem aging of Qinchuan beef. This study aimed to explore the relationship between TUFM expression and changes in energy metabolism during this process. Changes in the expression and content of TUFM, the contents of glucose (GLU), lactic acid (LA), adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and the activities of lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), triose phosphate isomerase (TPI), malate dehydrogenase (MDH), and cytochrome c oxidase (COX) in the Longissimus dorsi muscle of Qinchuan cattle were determined at different periods (0, 2, 12, 24, 48, 96, 144 and 192 h) of aging at 4 ℃. The results showed that during postmortem aging, the contents of GLU, ATP, ADP and AMP, and the activities of LDH, SDH and TPI exhibited a decreasing trend. Meanwhile, the expression level of TUFM, MDH activity, and the contents of LA and TUFM showed an initial increase followed by a decrease. The activity of COX exhibited an initial decrease followed by a temporary increase and then a decrease. The various indicators of energy metabolism and TUFM exerted their effects mainly at the early stage of postmortem aging. Pearson’s correlation analysis indicated that the expression level of TUFM was significantly positively correlated with MDH and LA but significantly negatively correlated with ATP, ADP, AMP, LDH, SDH, TPI, COX, and GLU at the early stage (P < 0.01). At the middle and late stages, TUFM expression was significantly positively correlated with all these indicators (GLU, LA, ATP, ADP, AMP, LDH, MDH, SDH, TPI and COX) (P < 0.01). In conclusion, during the early period of postmortem aging, the gradual increase of TUFM expression can provide energy to muscle cells for energy metabolism pathways, which may be possibly due to the positive involvement of TUFM in cellular autophagy. When energy is deficient during the middle and late periods, TUFM may inhibit cellular autophagy to prioritize energy use for important pathways (e.g., energy metabolism pathways) other than cellular autophagy, thereby maintaining cellular homeostasis. In summary, TUFM plays a dual role during the postmortem aging process, in regulating cellular autophagy to provide energy for metabolic pathways, thereby assisting in maintaining the duration of post-mortem energy metabolism.