This review focuses on the antibacterial activities of visible light-responsive titanium dioxide (TiO₂) photocatalysts. These photocatalysts have a range of applications including disinfection, air and water cleaning, deodorization, and pollution and environmental control. Titanium dioxide is a chemically stable and inert material, and can continuously exert antimicrobial effects when illuminated. The energy source could be solar light; therefore, TiO₂ photocatalysts are also useful in remote areas where electricity is insufficient. However, because of its large band gap for excitation, only biohazardous ultraviolet (UV) light irradiation can excite TiO₂, which limits its application in the living environment. To extend its application, impurity doping, through metal coating and controlled calcination, has successfully modified the substrates of TiO₂ to expand its absorption wavelengths to the visible light region. Previous studies have investigated the antibacterial abilities of visible light-responsive photocatalysts using the model bacteria Escherichia coli and human pathogens. The modified TiO₂ photocatalysts significantly reduced the numbers of surviving bacterial cells in response to visible light illumination. They also significantly reduced the activity of bacterial endospores; reducing their toxicity while retaining their germinating abilities. It is suggested that the photocatalytic killing mechanism initially damages the surfaces weak points of the bacterial cells, before totally breakage of the cell membranes. The internal bacterial components then leak from the cells through the damaged sites. Finally, the photocatalytic reaction oxidizes the cell debris. In summary, visible light-responsive TiO₂ photocatalysts are more convenient than the traditional UV light-responsive TiO₂ photocatalysts because they do not require harmful UV light irradiation to function. These photocatalysts, thus, provide a promising and feasible approach for disinfection of pathogenic bacteria; facilitating the prevention of infectious diseases.

The antibacterial activity of photocatalytic titanium dioxide (TiO ₂ ) substrates is induced primarily by UV light irradiation. Recently, nitrogen- and carbon-doped TiO ₂ substrates were shown to exhibit photocatalytic activities under visible-light illumination. Their antibacterial activity, however, remains to be quantified. In this study, we demonstrated that nitrogen-doped TiO ₂ substrates have superior visible-light-induced bactericidal activity against Escherichia coli compared to pure TiO ₂ and carbon-doped TiO ₂ substrates. We also found that protein- and light-absorbing contaminants partially reduce the bactericidal activity of nitrogen-doped TiO ₂ substrates due to their light-shielding effects. In the pathogen-killing experiment, a significantly higher proportion of all tested pathogens, including Shigella flexneri , Listeria monocytogenes , Vibrio parahaemolyticus , Staphylococcus aureus , Streptococcus pyogenes , and Acinetobacter baumannii , were killed by visible-light-illuminated nitrogen-doped TiO ₂ substrates than by pure TiO ₂ substrates. These findings suggest that nitrogen-doped TiO ₂ has potential application in the development of alternative disinfectants for environmental and medical usages.

Bactericidal activity of traditional titanium dioxide (TiO₂) photocatalyst is effective only upon irradiation by ultraviolet light, which restricts the potential applications of TiO₂ for use in our living environments. Recently carbon-containing TiO₂ was found to be photoactive at visible-light illumination that affords the potential to overcome this problem; although, the bactericidal activity of these photocatalysts is relatively lower than conventional disinfectants. Evidenced from scanning electron microscopy and confocal Raman spectral mapping analysis, we found the interaction with bacteria was significantly enhanced in these anatase/rutile mixed-phase carbon-containing TiO₂. Bacteria-killing experiments indicate that a significantly higher proportion of all tested pathogens including Staphylococcus aureus, Shigella flexneri and Acinetobacter baumannii, were eliminated by the new nanoparticle with higher bacterial interaction property. These findings suggest the created materials with high bacterial interaction ability might be a useful strategy to improve the antimicrobial activity of visible-light-activated TiO₂.

Both protein kinase C (PKC) and reactive oxygen species (ROS) are well-known signaling messengers cross-talking with each other to activate mitogen-activated protein kinases (MAPKs) for progression of hepatocellular carcinoma (HCC). However, the underlying mechanisms are not well elucidated. Especially, whether mitochondrial ROS (mtROS) is involved and how it triggers MAPK signaling are intriguing. In this study, we found mtROS generation and phosphorylation of MAPKs were mediated by PKCδ in HCCs treated with the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Heat shock protein 60 (HSP60), one of the chaperones in mitochondria was the major protein oxidized in TPA-treated HCCs. Moreover, depletion of HSP60 or expression of HSP60 cysteine mutant prevented TPA-induced phosphorylation of MAPKs. To delineate how HSP60 mediated MAPK activation, the role of Raf kinase inhibitor protein (RKIP), a negative regulator of MAPK, was investigated. TPA dissociated RKIP from HSP60 in both mitochondria and cytosol, concurrently with translocation of HSP60 and MAPK from mitochondria to cytosol, which was associated with robust phosphorylation of MAPKs in the cytosol. Moreover, TPA induced opposite phenotypical changes of HCCs, G1 cell cycle arrest, and cell migration, which were prevented by mtROS scavengers and depletion of PKCδ and HSP60. Consistently, TPA increased the migration-related genes, hydrogen peroxide inducible clone5, matrix metalloproteinase-1/3, lamininγ2, and suppressed the cell cycle regulator cyclin E1 (CCNE1) via PKCδ/mtROS/HSP60/MAPK-axis. Finally, c-jun and c-fos were required for TPA-induced expression of the migration-related genes and a novel microRNA, miR-6134, was responsible for TPA-induced suppression of CCNE1. In conclusion, PKCδ cross-talked with mtROS to trigger HSP60 oxidation for release of RKIP to activate MAPK, regulating gene expression for migration, and G1 cell cycle arrest in HCC. Targeted therapy aiming at key players like PKCδ, RKIP, and HSP60 is promising for preventing HCC progression.