Transcriptome-based analysis of early post-mortem formation of pale, soft, and exudative (PSE) pork.

Pale, soft, and exudative (PSE) meat can cause consumer dissatisfaction and economic losses. This study determined meat quality, glycolytic enzyme activity, and differential gene expression in the longissimus lumborum (LL) and semimembranosus (SM) of normal and PSE pork carcasses. The SM did not result in PSE meat. Hexokinase, lactate dehydrogenase, and pyruvate kinase activities were lower in the SM of PSE carcasses than in the normal carcasses. Functional enrichment analysis revealed that immune, inflammatory, and muscle fibre genes were significantly enriched in PSE pork. More specifically, PPP1R3G and MSS51 may be key genes regulating pork quality in the SM. Meanwhile, the differential expression of PLVAB, ADIPOQ, LEP, MYH4, MYH7, MYL3, MYL6B, FOS, ATF3, and HSPA6 may induce PSE formation in the LL. These results may provide insights into PSE pork formation mechanisms and reveal candidate genes for improving meat quality after validation.

Proteomics analysis as an approach to understand the formation of pale, soft, and exudative (PSE) pork.

We investigated ten pale, soft, and exudative (PSE), and ten normal meat samples from pig carcasses. The meat quality at 0, 5, 12, and 24 h post-mortem and the key enzyme activities at 0 and 24 h post-mortem were determined. We selected three PSE and three normal samples for proteomics analysis at 0 h and 24 h post-mortem. No remarkable differences in pyruvate kinase (PK) and lactate dehydrogenase (LDH) activity were observed between samples at 0 h post-mortem; however, creatine kinase (CK) activity was significantly higher in PSE meat. Hexokinase (HK) activity in PSE samples was higher than that in normal samples at 24 h post-mortem. Bioinformatics analysis of the proteome showed that PSE was related to glycolysis, TCA cycle, oxidative phosphorylation, muscle tissue structure, signal transduction, and molecular chaperones. This research found that proteins such as troponin T slow skeletal muscle isoform X, GADPH, L-lactate dehydrogenase A chain, and gamma-enolase isoform X1 might be responsible for PSE.