College of Food Science and Engineering, Gansu Agricultural University, Lanzhou, 730070, P. R. China.
Animal Husbandry and Veterinary Institute of Haibei Prefecture, Haibei, 812200, P. R. China.
J Sci Food Agric. 2023 Jan 30;103(2):514-523. doi: 10.1002/jsfa.12161. Epub 2022 Aug 17.
Adenosine monophosphate-activated protein kinase (AMPK) is instrumental in the initiation of early postmortem glycolysis and the advent of pale, soft, and exudative (PSE) meat when cellular energy is altered. However, conflicting studies show that AMPK activation without corresponding energy level changes in PSE meat challenges this long-held notion. Here, we examined the effects of reactive oxygen species (ROS)-mediated oxidative stress on AMPK activation in the context of glycolysis, protein solubility, and water-holding capacity (WHC) in the postmortem yak longissimus dorsi (LD) muscle. Further, we explored the mechanisms underlying these effects.
Hydrogen peroxide (H O ) significantly augmented the degree of oxidative stress, increasing the production of ROS and malondialdehyde excessive production and reducing the activity of the anti-oxidants superoxide dismutase and glutathione peroxidase. In turn, oxidative stress dramatically promoted AMPK activation and glycolysis by increasing glycogen depletion and promoting hexokinase and phosphofructokinase activity. Subsequently, lactic acid accumulation increased, leading to a rapid decline in pH, which aggravated protein solubility degree and centrifugal loss in the early postmortem yak LD muscle. Importantly, these changes caused by oxidative stress were eliminated by the AMPK inhibitor. Mechanistically, oxidative stress elevated calcium ion (Ca ) levels, which mobilized calcium/calmodulin-dependent protein kinase β (CaMKKβ) and AMPK. Rescue experiments confirmed that the increases were attenuated using Ca and CaMKKβ chelators, respectively.
These results indicated that oxidative stress caused by ROS hastened early-stage postmortem glycolysis and reduced the WHC of yak meat. These effects were likely mediated by the alternative and energy-independent CaMKKβ/AMPK signaling pathway. © 2022 Society of Chemical Industry.
腺苷单磷酸激活蛋白激酶 (AMPK) 在细胞能量改变时，对启动死后早期糖酵解和苍白、柔软、渗出 (PSE) 肉的出现起着重要作用。然而，相互矛盾的研究表明，PSE 肉中 AMPK 的激活而没有相应的能量水平变化，对这一长期存在的观点提出了挑战。在这里，我们研究了活性氧 (ROS) 介导的氧化应激对糖酵解、蛋白质溶解度和死后牦牛背最长肌保水性 (WHC) 中 AMPK 激活的影响。此外，我们还探讨了这些影响的机制。
过氧化氢 (H O ) 显著增加了氧化应激的程度，增加了 ROS 的产生和丙二醛的过度产生，降低了抗氧化剂超氧化物歧化酶和谷胱甘肽过氧化物酶的活性。反过来，氧化应激通过增加糖原耗竭和促进己糖激酶和磷酸果糖激酶的活性，显著促进 AMPK 的激活和糖酵解。随后，乳酸积累增加，导致 pH 值迅速下降，从而加剧了早期死后牦牛背最长肌的蛋白质溶解度和离心损失。重要的是，AMPK 抑制剂消除了氧化应激引起的这些变化。从机制上讲，氧化应激会升高钙离子 (Ca ) 水平，从而动员钙/钙调蛋白依赖性蛋白激酶 β (CaMKKβ) 和 AMPK。挽救实验证实，分别使用 Ca 和 CaMKKβ 螯合剂可以减弱这些增加。
这些结果表明，ROS 引起的氧化应激加速了早期的死后糖酵解，降低了牦牛肉的 WHC。这些影响可能是通过替代的、不依赖能量的 CaMKKβ/AMPK 信号通路介导的。© 2022 化学工业协会。
