Microwave ultrahigh temperature processing offers a promising alternative to conventional heatexchangerbased sterilization for liquid foods, addressing challenges such as fouling, thermal degradation of heatlabile nutrients, and high energy consumption. However, the inactivation mechanisms of microwave UHT against thermophilic bacteria remain inadequately understood. In a study published in ENG. Chem. Eng., researchers at Sichuan University and collaborators investigated the bactericidal efficacy and mechanisms of microwave UHT treatment (2450 MHz) against vegetative cells of Geobacillus stearothermophilus ATCC 7953, a key indicator organism for sterilization validation.
Bacterial suspensions with an initial population of 7.70±0.15 log CFU·mL⁻¹ were subjected to eight powertime combinations achieving 136±1 °C, followed by immediate cooling. The results revealed a striking nonlinear relationship between microwave power and inactivation efficacy. The most effective treatments were observed at 150 W·mL⁻¹ for 40 s and 300 W·mL⁻¹ for 20 s, achieving reductions of 4.99±0.33 and 5.14±0.50 log CFU·mL⁻¹, respectively. Intermediate powers of 200 W·mL⁻¹ for 29 s and 250 W·mL⁻¹ for 24 s yielded substantially lower reductions of 3.08±0.26 and 2.92±0.33 log, respectively. At the extremes, the 100 W·mL⁻¹ treatment for 59 s achieved a reduction of 4.29±0.46 log, while the 400 W·mL⁻¹ treatment for 13 s achieved 4.03±0.35 log. This nonlinear pattern suggests that microwave processing involves mechanistically distinct inactivation pathways whose relative contributions vary with power density and heating rate.
Mechanistic analyses revealed that all microwave treatments significantly compromised cell membrane integrity. The 300 W·mL⁻¹ treatment induced maximal nucleic acid and protein leakage (OD₂₆₀: 0.0760, OD₂₈₀: 0.1017), followed by the 150 W·mL⁻¹ treatment (OD₂₆₀: 0.0643, OD₂₈₀: 0.0790). Intermediate powers showed substantially lower leakage, consistent with their reduced bactericidal efficacy. Metabolic activity, assessed by TTCdehydrogenase reduction, was most profoundly suppressed at 150 W·mL⁻¹ (59.3 % reduction), followed by 400 W·mL⁻¹ (53.8 %) and 300 W·mL⁻¹ (52.7 %). The 200 and 250 W·mL⁻¹ treatments showed only modest reductions (41.8 % and 44.0 %), aligning with their inferior inactivation.
Oxidative stress emerged as a central lethal mechanism. The 300 W·mL⁻¹ treatment generated the highest intracellular reactive oxygen species level (61.1 % increase over control) and the highest malondialdehyde content (2.15 mmol·mL⁻¹, a 6.0fold increase), indicating extensive lipid peroxidation. The 150 W·mL⁻¹ treatment showed moderate but significant ROS elevation (35.4 %). Critically, the 200 and 250 W·mL⁻¹ treatments produced ROS levels not significantly different from control and the lowest MDA accumulation, explaining their reduced efficacy. Scanning electron microscopy confirmed distinct morphological alterations: lowpower extended treatment caused compressiontype damage, optimal conditions induced cell rupture, and highpower short treatment resulted in shrinkage.
These findings demonstrate that microwave UHT inactivation proceeds through two distinct pathways: acute oxidative shock at high power and cumulative thermaloxidative synergy at low power with extended duration. This work provides a scientific foundation for optimizing microwave UHT processing in liquid food applications.

DOI
10.1007/s11705-026-2682-2