The effects of freeze–thaw and sonication on mitochondrial oxygen consumption, electron transport chain-linked metmyoglobin reduction, lipid oxidation, and oxymyoglobin oxidation

Mitochondria potentially influence Mb redox stability in meat by (1) decreasing partial oxygen pressure via oxygen consumption, (2) mitochondrial electron transport chain (ETC)-linked reduction of MetMb, and/or (3) oxidation of mitochondrial membrane lipid. The objective of this study was to investigate the effect of freeze–thaw and sonication treatments on mitochondrial oxygen consumption, ETC-dependent MetMb reducing activity, lipid oxidation, and Mb redox stability. Mitochondria were frozen and thawed (−18 °C for 2 h and 4 °C for 0.5 h) for 3 cycles, or sonicated for 30 s with a sonic dismembrator. State III oxygen consumption rate (OCR) was decreased by both treatments at pH 7.2, and by sonication only at pH 5.6 (P < 0.05). There was no effect on state IV OCR (P > 0.05). Respiratory control ratio (RCR) was decreased by freeze–thaw and sonication at pH 7.2 and 5.6 (P < 0.05). Sonication increased mitochondrial lipid oxidation and MetMb formation (P < 0.05); a similar effect was observed in sonicated samples in the presence of ascorbic acid and ferric chloride (P < 0.05). Sonication also decreased mitochondrial ETC-dependent MetMb reduction (P < 0.05). These results suggested that sonication treatment had the potential to affect Mb stability via mitochondrial lipid oxidation and/or ETC-mediated MetMb reduction, but the effect on myoglobin stability by freeze–thaw treatment was minimal.