Abstract

Transport stress (TS) prior to slaughter can accelerate the deterioration of flesh quality. Currently, the information necessary to understand the TS behavior and the molecular mechanisms during the postmortem muscle is still lacking. Therefore, the present study investigated the physicochemical and microbiological quality, microstructure, endogenous enzymes, apoptosis and related signaling pathways of refrigerated fish muscle. Results showed that TS accelerated the deterioration of flesh quality, characterized by pH fluctuations, increased drip loss, total volatile basic nitrogen (TVB-N) content, and total bacterial count. Histological observations showed that TS had more profound effects on muscle damage and fiber disorganization compared to the control group. Meanwhile, the activities of cathepsin B, calpain, and collagenase were significantly elevated, which further supported the increased degradation of muscle fiber structure. At the molecular level, TS increased caspase-3, −8, and − 9 activities, indicating the activation of mitochondrial and death receptor pathways. Transcriptional levels showed that activated apoptosis was regulated by pro-apoptotic factors (Bax and Apaf-1) and anti-apoptotic factors (Bcl-2, Mcl-1 and IAP), which were regulated by p38 MAPK signaling pathway. Thus, TS is suggested to accelerate flesh quality deterioration in fish muscle via apoptosis regulation.