Bacterial Oxidative Stress Responses and Cellular Damage Caused by Photocatalytic and Photoelectrocatalytic Inactivation

Abstract

This chapter review’s recent research works about the bacterial oxidative stress responses and cellular damage during the photocatalytic (PC) and photoelectrocatalytic (PEC) bacterial inactivation processes. In the PC or PEC systems, high levels of reactive oxygen species (ROSs) would be generated, causing oxidative stress to bacterial cells. Bacterial anti-oxidative responses regulated by oxyR and soxRS can be induced by elevated ROS level. However, the oxidative stress responses, producing catalase and superoxide dismutase (SOD), failed to occur during PEC inactivation process, indicating that the ROS levels increased too sharply and overwhelmed the bacterial tolerance. Nevertheless, both catalase and SOD were proved to contribute greatly to the bacterial resistance to PEC inactivation, demonstrated by the different inactivation performance of parental E. coli BW25113 and its katG or sodA single-gene knockout mutants. More proofs were supplied by the growing bacterial catalase level together with their tolerance to PEC treatment as the bacteria were preincubated by low concentrations of hydrogen peroxide. Another aspect to understand the disinfection mechanism is the bacterial oxidative damage, especially the lethal disruption step of PC or PEC inactivation, which is essential for the development of mechanism-based PC or PEC disinfection kinetic models. Recent reports revealed that the oxidative damage of bacterial membrane structure (lipid bilayers), which is commonly recognized as the most important attack target of ROSs, however, was probably not the mortal injury to cells during PEC treatment because it happened later as compared with the inactivation behavior. It was the disruption of adenosine triphosphate (ATP) generation potential that directly causes bacterial death, because relative ATP generation rate and bacterial survival ratio coincided with each other, and ATP metabolism is crucial for cellular survival. The membrane structure destruction, represented by the oxidative damage of unsaturated fatty acids, was supposed to cause increasing membrane permeability and exposure of ATP metabolism complex to ROSs, thus promoted the bacterial inactivation.