Abstract
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.
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