Tang Jiali, Faustman Cameron, Hoagland Thomas A, Mancini Richard A, Seyfert Mark, Hunt Melvin C
Department of Animal Science, University of Connecticut, 3636 Horsebarn Hill Road Ext., Storrs, Connecticut 06269-4040, USA.
J Agric Food Chem. 2005 Feb 23;53(4):1223-30. doi: 10.1021/jf048646o.
The objective of this study was to assess the morphological integrity and functional potential of mitochondria from postmortem bovine cardiac muscle and evaluate mitochondrial interactions with myoglobin (Mb) in vitro. Electron microscopy revealed that mitochondria maintained structural integrity at 2 h postmortem; prolonged storage resulted in swelling and breakage. At 2 h, 96 h, and 60 days postmortem, the mitochondrial state III oxygen consumption rate (OCR) and respiratory control ratio decreased with time at pH 7.2 and 5.6 (p < 0.05). Mitochondria isolated at 60 days did not exhibit ADP-induced transitions from state IV to state III oxygen consumption. Tissue oxygen consumption also decreased with time postmortem (p < 0.05). Mitochondrial oxygen consumption was inhibited by decreased pH in vitro (p < 0.05). In a closed system, mitochondrial respiration resulted in decreased oxygen partial pressure (pO(2)) and enhanced conversion of oxymyoglobin (OxyMb) to deoxymyoglobin (DeoMb) or metmyoglobin (MetMb). Greater mitochondrial densities caused rapid decreases in pO(2) and favored DeoMb formation at pH 7.2 in closed systems (p < 0.05); there was no effect on MetMb formation (p > 0.05). MetMb formation was inversely proportional to mitochondrial density at pH 5.6 in closed systems. Mitochondrial respiration in open systems resulted in greater MetMb and DeoMb formation at pH 5.6 and pH 7.2, respectively, vs controls (p < 0.05). The greatest MetMb formation was observed with a mitochondrial density of 0.5 mg/mL at both pH values in open systems. Mitochondrial respiration facilitated a shift in Mb form from OxyMb to DeoMb or MetMb, and this was dependent on pH, oxygen availability, and mitochondrial density.
本研究的目的是评估死后牛心肌中线粒体的形态完整性和功能潜力，并在体外评估线粒体与肌红蛋白（Mb）的相互作用。电子显微镜显示，线粒体在死后2小时保持结构完整；长时间保存会导致肿胀和破裂。在死后2小时、96小时和60天时，线粒体状态III氧消耗率（OCR）和呼吸控制率在pH 7.2和5.6时随时间下降（p<0.05）。在60天时分离的线粒体未表现出ADP诱导的从状态IV到状态III氧消耗的转变。组织氧消耗也随死后时间下降（p<0.05）。体外pH降低会抑制线粒体氧消耗（p<0.05）。在封闭系统中，线粒体呼吸导致氧分压（pO₂）降低，并促进氧合肌红蛋白（OxyMb）向脱氧肌红蛋白（DeoMb）或高铁肌红蛋白（MetMb）的转化。在封闭系统中，更高的线粒体密度导致pO₂迅速下降，并有利于在pH 7.2时形成DeoMb（p<0.05）；对MetMb形成没有影响（p>0.05）。在封闭系统中，pH 5.6时MetMb形成与线粒体密度成反比。与对照组相比，开放系统中的线粒体呼吸分别在pH 5.6和pH 7.2时导致更多的MetMb和DeoMb形成（p<0.05）。在开放系统中，两种pH值下线粒体密度为0.5 mg/mL时观察到最大的MetMb形成。线粒体呼吸促进了Mb形式从OxyMb向DeoMb或MetMb的转变，这取决于pH、氧可用性和线粒体密度。
