The purpose of this study was to examine the role of mitochondria in postmortem calcium homeostasis and its effect on proteolysis and tenderness. We hypothesized that mitochondria buffer cytosolic calcium levels and delay the activation of calpain-1 and subsequently the development of meat tenderness. To test this hypothesis, pre-rigor bovine longissimus thoracis et lumborum muscle samples were injected with DS16570511 to inhibit mitochondrial calcium uptake. Free calcium, tenderness, texture profile analysis (TPA), calpain-1 activity, and proteolysis were evaluated over a 336 h aging period. Inhibition of mitochondrial calcium uptake increased (P < .0001) cytosolic calcium concentration and calpain-1 autolysis and activity at 24 h compared to control steaks. Further, tenderness and TPA at 168 and 336 h, calpastatin degradation at 24 h, and proteolysis at 168 h were all enhanced (P < .05) in the treated steaks. Collectively, these data indicate that inhibition of mitochondrial calcium uptake can enhance postmortem proteolysis and tenderization through an early activation of calpain-1.

这项研究的目的是检查线粒体在死后钙稳态中的作用及其对蛋白水解和嫩度的影响。我们假设线粒体缓冲了胞质钙水平，并延迟了calpain-1的激活以及随后肉嫩的发展。为了验证这一假设，给DS16570511注射了严紧牛前胸廓和腰部肌肉样品，以抑制线粒体钙的摄取。在336小时的老化过程中评估了游离钙，嫩度，质地特征分析（TPA），钙蛋白酶1活性和蛋白水解作用。抑制线粒体钙摄取增加（P <.0001）与对照牛排相比，在24 h时胞浆钙浓度和calpain-1的自溶和活性。此外， 在处理过的牛排中，在168和336 h时的嫩度和TPA，在24 h时钙蛋白酶抑素的降解以及在168 h时的蛋白水解都得到了增强（P <0.05）。总体而言，这些数据表明，通过早期激活calpain-1，抑制线粒体钙的摄取可以增强死后蛋白水解和嫩化。