肌原纤维
钙蛋白酶抑制剂
蛋白质水解
化学
卡尔帕因
组织蛋白酶
肌膜
蛋白酵素
蛋白质降解
肌浆
生物化学
细胞生物学
肌节
酶
生物
心肌细胞
内质网
膜
作者
Christine Delbarre‐Ladrat,Romuald Chéret,Richard G. Taylor,Véronique Verrez‐Bagnis
标识
DOI:10.1080/10408390591000929
摘要
Postmortem tenderization is caused by enzymatic degradation of key structural proteins in myofibrils as well as in extracellular matrix, and of proteins involved in intermyofibrillar linkages and linkages between myofibrils and the sarcolemma. The function of these proteins is to maintain the structural integrity of myofibrils. Current data indicate that calpains and cathepsins may be responsible for degradation of these proteins. Other phenomena occurring in cells postmortem (pH drop, sarcoplasmic Ca2+ increase, osmotic pressure rise, oxidative processes) may act in synergy with proteases. Our understanding of the underlying mechanisms of muscle degradation should be improved for an accurate evaluation of the postmortem muscle changes and consequently of the fish quality.
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