Effects of apoptosis on quality changes of Larimichthys crocea postmortem storage with emphasis on cytochrome c-mediated lipid deterioration.

Apoptosis in fish muscle postmortem has been confirmed. Based on the apoptosis is associated with quality deterioration in fish during storage. This study aims to investigate the impact of apoptosis on the quality of Larimichthys crocea at 4 °C storage, particularly the lipid deterioration mediated by cytochrome c (cyt-c). The results indicated that the apoptosis inhibitor cyclosporin A (CsA) mitigated the decline in glycogen and ATP levels during 6-12 h, reduced the extent of mitochondrial damage during 12-72 h, especially inhibiting mitochondrial permeability transition pore (MPTP) opening, delayed the release of mitochondrial cyt-c into the cytoplasm, inhibiting apoptosis. Furthermore, inhibition of apoptosis reduced the activity of endogenous proteases (caspase-3, calpain, cathepsin B, and cathepsin L), which significantly reduced myofibrillar protein degradation over 72-120 h. Notably, inhibition of apoptosis led to a particularly evident reduction in lipid oxidation and plasmalogen levels during the pre-storage period (12-72 h), in which cyt-c attributed to an important role. This study establishes a novel mechanistic link between cyt-c-mediated apoptotic and lipid oxidation coupled with plasmalogen degradation in fish postmortem storage.