Additionally, bacteria often have negative potential on their outer walls, ranging from five to thirty mV. Since the DT-entrapped Brij micelle shares similar negative surface charge, micellized DT gets repelled by the bacterial cells. Thus, preventing its entry into the cells and resulting in no growth reduction at pH 7. However, at a low pH (<2), the increased protonation augments ionic firmness across the double layer formation of the micelle by eliminating surface charge. This compaction, driven by increased Van der Waal's affinity force, compromises the stability and development of the micelle arrangement. Consequently, at pH 1.5, a significant inhibition (reflected in decreased viable CFU counts) was observed for both strains, indicating the sustained release of DT from the micelle. This release also suggests enhanced mobility for liberated DT across the bacterial cell membrane/wall due to reduced steric hindrance. The reduction in viable cell numbers in B. subtilis was slightly greater than that in E. coli, indicating that B. subtilis is more vulnerable to DT . Comparatively, Brij 58 micellized DT exhibited a 9-11% greater potential for viable cell reduction than Brij S20 micellized DT, attributed to DT's superior stability within the Brij 58 micelle. Furthermore, two-way ANOVA analysis demonstrated that the suppression of bacterial growth resulting from DT liberation from Brij micelles is highly reliant on Brij concentration and system pH (p<0.05 in both cases). At low pH, protonated DT becomes more reactive toward the bacterial protein/enzyme thiol groups that are nucleophilic in nature. Thus, it increases the reactivity despite the enhanced stability of DT at low pH .