Enhanced production of reactive oxygen species by gadolinium oxide nanoparticles under core–inner-shell excitation by proton or monochromatic X-ray irradiation: implication of the contribution from the interatomic de-excitation-mediated nanoradiator effect to dose enhancement

Conventional photodynamic therapy (PDT) is limited by its penetration depth due to the photosensitizer and light source. In this study, we developed X-ray induced photodynamic therapy that applied X-ray as the light source to activate Ce-doped CaCO3 (CaCO3:Ce) to generate an intracellular reactive oxygen species (ROS) for killing cancer cells. The A549 cell line was used as the in vitro and in vivo model to evaluate the efficacy of X-ray-induced CaCO3:Ce. The cell viability significantly decreased and cell cytotoxicity obviously increased with CaCO3:Ce exposure under X-ray irradiation, which is less harmful than radiotherapy in tumor treatment. CaCO3:Ce produced significant ROS under X-ray irradiation and promoted A549 cancer cell death. CaCO3:Ce can enhance the efficacy of X-ray induced PDT, and tumor growth was inhibited in vivo. The blood analysis and hematoxylin and eosin stain (H&E) stain fully supported the safety of the treatment. The mechanisms underlying ROS and CO2 generation by CaCO3:Ce activated by X-ray irradiation to induce cell toxicity, thereby inhibiting tumor growth, is discussed. These findings and advances are of great importance in providing a novel therapeutic approach as an alternative tumor treatment.

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Phototransformation of zinc oxide nanoparticles and coexisting pollutant: Role of reactive oxygen species

The Science of The Total Environment ◽

10.1016/j.scitotenv.2020.138335 ◽

2020 ◽

Vol 728 ◽

pp. 138335

Author(s):

Meng-ru Li ◽

Fei-fei Liu ◽

Su-chun Wang ◽

Xin Cheng ◽

Huan Zhang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Zinc Oxide ◽

Zinc Oxide Nanoparticles ◽

Reactive Oxygen ◽

Oxide Nanoparticles ◽

Oxygen Species

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Involvement of reactive oxygen species in ionizing radiation–induced upregulation of cell surface Toll-like receptor 2 and 4 expression in human monocytic cells

Journal of Radiation Research ◽

10.1093/jrr/rrx011 ◽

2017 ◽

Vol 58 (5) ◽

pp. 626-635 ◽

Cited By ~ 8

Author(s):

Hironori Yoshino ◽

Ikuo Kashiwakura

Keyword(s):

Reactive Oxygen Species ◽

Protein Synthesis ◽

Ionizing Radiation ◽

Cell Surface ◽

Reactive Oxygen ◽

Mitogen Activated Protein Kinase ◽

Protein Synthesis Inhibitor ◽

Oxygen Species ◽

X Ray ◽

Radiation Induced

Abstract Toll-like receptors (TLRs) are pattern recognition receptors that recognize pathogen-associated molecular patterns and are indispensable for antibacterial and antiviral immunity. Our previous report showed that ionizing radiation increases the cell surface expressions of TLR2 and TLR4 and enhances their responses to agonists in human monocytic THP1 cells. The present study investigated how ionizing radiation increases the cell surface expressions of TLR2 and TLR4 in THP1 cells. The THP1 cells treated or not treated with pharmaceutical agents such as cycloheximide and N-acetyl-L-cysteine (NAC) were exposed to X-ray irradiation, following which the expressions of TLRs and mitogen-activated protein kinase were analyzed. X-ray irradiation increased the mRNA expressions of TLR2 and TLR4, and treatment with a protein synthesis inhibitor cycloheximide abolished the radiation-induced upregulation of their cell surface expressions. These results indicate that radiation increased those receptors through de novo protein synthesis. Furthermore, treatment with an antioxidant NAC suppressed not only the radiation-induced upregulation of cell surface expressions of TLR2 and TLR4, but also the radiation-induced activation of the c-Jun N-terminal kinase (JNK) pathway. Since it has been shown that the inhibitor for JNK can suppress the radiation-induced upregulation of TLR expression, the present results suggest that ionizing radiation increased the cell surface expressions of TLR2 and TLR4 through reactive oxygen species–mediated JNK activation.

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