Bacillus cereus spores pose a potential threat to various food products, including meat, grain, vegetables, and dairy products, due to their remarkable resistance to environmental stress. Ohmic heating (OH) is an emerging alternative technology for inactivating spores. This study aimed to investigate the effects of OH on B. cereus spores, specifically examining its impact on heat resistance, leakage of intracellular substances, integrity of the cortex and membrane, and structural changes, in order to elucidate the potential inactivation mechanism of OH. The results demonstrated the efficacy of OH in inactivating B. cereus spores in various liquid food products while maintaining product quality. The wet heat resistance of spores decreased after OH treatments at low-temperatures (60–70 ℃), potentially promoting subsequent inactivation. Conversely, resistance increased following OH treatments at higher temperatures and oil bath heating (OB) treatments. Similar inactivation effects were observed between OB and OH when the temperature reached 80 and 98 ℃. Both OH and OB treatments damaged spore structures, resulting in leakage of intracellular substances and disruption of homeostasis. However, OH treatment at 10 V/cm and 50 Hz resulted in less leakage of dipicolinic acid, protein, nucleic acids within the spores, and appeared to have additional effects on the structures within the inner membrane. These findings could facilitate the development of OH as a promising technology for effective spore control in food.

Ohmic heating (OH) is a novel rapid heating technology that effectively control Staphylococcus aureus (S. aureus) survival. However, OH-induced sublethal injury to S. aureus pose risks to food safety and public health. Numerous studies have highlighted the importance of membrane repair for bacterial survival. Lipids are the main membranes components, however, their metabolic mechanisms after injured and repair are still unclear. In this study, we compared the lipid compositions of S. aureus in untreated, OH-injured, and end-repair states by non-targeted lipidomics and measured malondialdehyde (MDA) content changes, a lipid injury marker. Then, transcriptomic and parallel reaction monitoring analysis were conducted to examine the expression of lipid metabolism-related genes and key enzymes, respectively. The results revealed that OH treatment caused 53 differentially abundant lipids (DALs) increase, including CL, PG, PE, and Cer, while 83 DALs decreased. In the end-repair stage (repair for 5 h), 71 DALs decreased, while only 21 DALs increased. This phenomenon was also reflected in MDA concentration alternations, suggesting that OH-induced lipid homeostasis disruption and oxidative damage were alleviated upon repair. The overall changes trends of lipid biosynthesis enzyme were consistent with lipidomics. Notably, the general changes of lipids metabolism-related genes exhibited an opposite trend: decreased by OH treatment while partially restored after repair. These findings enhanced our understanding of lipid homeostasis in injured bacteria, provided theoretical support for inhibiting injured S. aureus repair in food, and promoting OH application in the food industry.

Apoptosis in postmortem muscle is a potential factor affecting meat quality. This study aimed to investigate the changes in apoptotic genes and proteins, reactive oxygen species (ROS), caspase-3 activity and their underlying relationship with meat tenderization. As postmortem time extended, there was a significant increase in myofibril fragmentation index (MFI) and destruction of muscle fibers. Oxidative stress deepened alongside the onset of apoptosis. Mitochondrial membrane potential (MMP) decreased, and caspase-3 activity increased during the first 24 h postmortem. Forty apoptotic genes displayed significant differences, involving DNA damage, autophagy, the death receptor pathway, the mitochondrial pathway, the Bcl-2 family, and the caspases family. The expression of most apoptotic genes was abundant in the early postmortem stage, enhancing the potential for early apoptosis. Apoptotic proteins of apoptosis-inducing factor, mitochondrion-associated 1 (AIFM1) and endonuclease G (ENDOG) showed the damage of apoptosis to DNA. Also, the decreasing expression of Bcl2 and increasing expression of Bak1 with time demonstrated the effects of mitochondrial apoptosis on postmortem muscle. These findings suggest that postmortem muscle apoptosis is a physiological process co-regulated by multiple genes, and potentially contributes to meat tenderization and quality.