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

Identifieur interne : 001165 ( Main/Merge ); précédent : 001164; suivant : 001166

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

Auteurs : JIALI TANG [États-Unis] ; Cameron Faustman [États-Unis] ; Richard A. Mancini [États-Unis] ; Mark Seyfert [États-Unis] ; Melvin C. Hunt [États-Unis]

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RBID : Pascal:06-0423421

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English descriptors

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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Pascal:06-0423421

Le document en format XML

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<div type="abstract" xml:lang="en">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.</div>
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