Warner R D, Dunshea F R, Ponnampalam E N, Cottrell J J
Department of Primary Industries, 600 Sneydes Road, Werribee 3030, Australia.
Meat Sci. 2005 Sep;71(1):205-17. doi: 10.1016/j.meatsci.2005.04.008. Epub 2005 May 31.
Metabolic processes in muscle tissue in vivo result in the production of reactive oxygen species and oxidative compounds including superoxide anions and nitric oxide (NO). Reactive oxygen species can react with both lipids and proteins and often have deleterious effects, contributing to the onset of ageing and senescence as well as cell death. Nitric oxide (NO) is a free radical that is constantly produced or released throughout the body by diverse tissues and is known to influence proteolytic activity in human and rodent skeletal muscle as well as being involved in regulation of calcium homeostasis in the muscle cell. The influence of nitric oxide on development of meat tenderness has been studied through postmortem manipulation and also through in vivo studies. The effect of NO on meat tenderness is postulated to be via its regulatory effects on the proteins calpain, cathepsins, ryanodine receptor channel in the sarcoplasmic reticulum (SR) and the sarcoplasmic-endoplasmic release calcium ATPase in the SR. NO is an oxidant although the effects of NO on effector proteins can be distinguished from a direct oxidation reaction. The onset of oxidation in meat postmortem is well known to produce off-odours, discolouration and unacceptable flavours associated with rancidity. Oxidation during the immediate postmortem period appears to inhibit tenderisation during ageing, probably through an inhibitory effect of oxidation on the calpain enzyme. Oxidation of muscle tissue occurring as a result of availability of oxygen during modified atmosphere packaging may also have deleterious consequences for tenderness development during storage of meat prior to retail display. In conclusion, it is proposed that postmortem meat tenderisation is influenced by skeletal muscle's release of NO pre-slaughter and the oxidation of proteases postmortem. This proposal is compatible with the existing tenderness model and will hopefully assist in increasing the accuracy of prediction of meat tenderness. Future directions for research are discussed.
体内肌肉组织中的代谢过程会产生活性氧物种和氧化化合物,包括超氧阴离子和一氧化氮(NO)。活性氧物种可与脂质和蛋白质发生反应,通常具有有害作用,会导致衰老和细胞死亡。一氧化氮(NO)是一种自由基,由身体内不同组织持续产生或释放,已知其会影响人和啮齿动物骨骼肌中的蛋白水解活性,并参与肌肉细胞钙稳态的调节。人们已通过宰后处理以及体内研究,对一氧化氮对肉嫩度发展的影响展开了研究。据推测,NO对肉嫩度的影响是通过其对钙蛋白酶、组织蛋白酶、肌浆网(SR)中的兰尼碱受体通道以及SR中的肌浆网 - 内质网钙释放ATP酶等蛋白质的调节作用来实现的。NO是一种氧化剂,尽管NO对效应蛋白的作用可与直接氧化反应区分开来。众所周知,宰后肉中的氧化过程会产生与酸败相关的异味、变色和不良风味。宰后即刻的氧化过程似乎会抑制成熟过程中的嫩化,这可能是由于氧化对钙蛋白酶的抑制作用。在气调包装过程中,由于氧气的存在而发生的肌肉组织氧化,也可能对零售展示前肉类储存期间的嫩度发展产生有害影响。总之,有人提出宰后肉的嫩化受宰前骨骼肌释放的NO以及宰后蛋白酶氧化的影响。这一观点与现有的嫩度模型相符,有望有助于提高肉嫩度预测的准确性。文中还讨论了未来的研究方向。