细胞色素c
线粒体
细胞生物学
肌原纤维
细胞凋亡
蛋白质降解
程序性细胞死亡
半胱氨酸蛋白酶3
生物
化学
线粒体凋亡诱导通道
生物化学
分子生物学
作者
Xue Li,Ling Hu,Xinrong Zhu,Xia Guo,Xiaorong Deng,Jian Zhang
出处
期刊:Food Chemistry
[Elsevier]
日期:2021-08-05
卷期号:367: 130767-130767
被引量:27
标识
DOI:10.1016/j.foodchem.2021.130767
摘要
This study aimed to investigate the effect of caspase-3 inhibitor in mitochondrial apoptosis activation on structure protein degradation during postmortem storage. Mitochondrial dysfunction, apoptotic factors, structure protein degradation and the myofibrillar rupture index between the control and caspase-3 inhibitor groups were determined. The results show caspase-3 inhibitor repressed the mitochondrial membrane permeability and mitochondrial swelling, as well as increased mitochondrial membrane potential, causing a decrease in the release of cytochrome c from mitochondria to cytoplasm and caspase-9/3 activities (P < 0.05). Subsequently, small myofibrillar proteins (desmin and troponin-T) were susceptible to degradation, initiating texture deterioration. By contrast, giant structure proteins (titin and nebulin) were degraded during later postmortem storage, predominantly contributing to fish softening. The results further suggest that caspase-3 is involved in degradation of structure proteins during postmortem through mitochondrial apoptosis pathways.
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