scholarly journals Sensitivity to Low-Dose/Low-LET Ionizing Radiation in Mammalian Cells Harboring Mutations in Succinate Dehydrogenase Subunit C is Governed by Mitochondria-Derived Reactive Oxygen Species

2011 ◽  
Vol 175 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Nukhet Aykin-Burns ◽  
Benjamin G. Slane ◽  
Annie T. Y. Liu ◽  
Kjerstin M. Owens ◽  
Malinda S. O'Malley ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ionizing Radiation ◽  
Succinate Dehydrogenase ◽  
Mammalian Cells ◽  
Low Dose ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Subunit C

scholarly journals Surface-bound reactive oxygen species generating nanozymes for selective antibacterial action

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Feng Gao ◽  
Tianyi Shao ◽  
Yunpeng Yu ◽  
Yujie Xiong ◽  
Lihua Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Mammalian Cells ◽  
Bacterial Resistance ◽  
Reactive Oxygen ◽  
Resistant Bacteria ◽  
Oxygen Species ◽  
Antibiotic Resistant ◽  
Generate Surface ◽  
Inert Substrate ◽  
Silver Palladium

AbstractActing by producing reactive oxygen species (ROS) in situ, nanozymes are promising as antimicrobials. ROS’ intrinsic inability to distinguish bacteria from mammalian cells, however, deprives nanozymes of the selectivity necessary for an ideal antimicrobial. Here we report that nanozymes that generate surface-bound ROS selectively kill bacteria over mammalian cells. This result is robust across three distinct nanozymes that universally generate surface-bound ROS, with an oxidase-like silver-palladium bimetallic alloy nanocage, AgPd0.38, being the lead model. The selectivity is attributable to both the surface-bound nature of ROS these nanozymes generate and an unexpected antidote role of endocytosis. Though surface-bound, the ROS on AgPd0.38 efficiently eliminated antibiotic-resistant bacteria and effectively delayed the onset of bacterial resistance emergence. When used as coating additives, AgPd0.38 enabled an inert substrate to inhibit biofilm formation and suppress infection-related immune responses in mouse models. This work opens an avenue toward biocompatible nanozymes and may have implication in our fight against antimicrobial resistance.

Mutagenicity of PFOA in Mammalian Cells: Role of Mitochondria-Dependent Reactive Oxygen Species

2011 ◽  
Vol 45 (4) ◽  
pp. 1638-1644 ◽  
Author(s):  
Guoping Zhao ◽  
Jun Wang ◽  
Xiaofei Wang ◽  
Shaopeng Chen ◽  
Ye Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mammalian Cells ◽  
Reactive Oxygen ◽  
Oxygen Species

Activation of the JAK-STAT pathway by reactive oxygen species

1998 ◽  
Vol 275 (6) ◽  
pp. C1640-C1652 ◽  
Author(s):  
Amy R. Simon ◽  
Usha Rai ◽  
Barry L. Fanburg ◽  
Brent H. Cochran
Keyword(s):  
Reactive Oxygen Species ◽  
Mammalian Cells ◽  
Reactive Oxygen ◽  
Buthionine Sulfoximine ◽  
Early Response ◽  
Carcinoma Cells ◽  
Oxygen Species ◽  
Intracellular Ros ◽  
Diphenylene Iodonium ◽  
Stat Pathway

Reactive oxygen species (ROS) play an important role in the pathogenesis of many human diseases, including the acute respiratory distress syndrome, Parkinson’s disease, pulmonary fibrosis, and Alzheimer’s disease. In mammalian cells, several genes known to be induced during the immediate early response to growth factors, including the protooncogenes c- fos and c- myc, have also been shown to be induced by ROS. We show that members of the STAT family of transcription factors, including STAT1 and STAT3, are activated in fibroblasts and A-431 carcinoma cells in response to H2O2. This activation occurs within 5 min, can be inhibited by antioxidants, and does not require protein synthesis. STAT activation in these cell lines is oxidant specific and does not occur in response to superoxide- or nitric oxide-generating stimuli. Buthionine sulfoximine, which depletes intracellular glutathione, also activates the STAT pathway. Moreover, H2O2stimulates the activity of the known STAT kinases JAK2 and TYK2. Activation of STATs by platelet-derived growth factor (PDGF) is significantly inhibited by N-acetyl-l-cysteine and diphenylene iodonium, indicating that ROS production contributes to STAT activation in response to PDGF. These findings indicate that the JAK-STAT pathway responds to intracellular ROS and that PDGF uses ROS as a second messenger to regulate STAT activation.

Diagnostic Range Ionizing Radiation and Reactive Oxygen Species Production: an Initial Experience

2021 ◽  
Vol 11 (5) ◽  
Author(s):  
Sirohi Shikha ◽  
Tandon Prof. Anupama ◽  
Banerjee Prof. B.D. ◽  
Kumar Ranjeet
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Ionizing Radiation ◽  
Venous Blood ◽  
Radiation Detection ◽  
Control Sample ◽  
Reactive Oxygen ◽  
P Value ◽  
Oxygen Species ◽  
Mdct Examination

Radiation is a common occurrence in our daily lives that comes from both natural and man-made sources. Ionizing Radiation (IR) causes damage either directly or indirectly through the generation of reactive oxygen species (ROS). Oxidative damage to DNA, lipids, proteins, and many metabolites occurs through a complex series of processes that are enhanced by endogenous signalling which is activated by free radicals. Though literature is abundant on ROS and antioxidants at high doses, no study to the best of our knowledge has assessed the ROS levels after Multi Detector Computed Tomography (MDCT) examination (i.e. in diagnostic range radiation). The aim of the present study was to assess the production of ROS after diagnostic level radiation by MDCT examination and at 24 hour follow up. The study involved fifty patients posted for clinically indicated MDCT which were recruited. The average radiation dose was 2-9 mGy. Three blood samples were drawn, one prior to CT (control sample), within half an hour of CT (post CT) and 24 hrs after CT. 3 ml venous blood was withdrawn in aseptic conditions and immediately serum was isolated for ROS assessment. The blood examination results were compared in immediate and post 24 hour after MDCT and both were compared with control values and correlated with radiation parameters. Our results have shown a significant increase in ROS level in immediate post CT samples compared to prior CT scan samples (control) (p value <0.0001). The ROS levels reduced at 24 hours compared to immediate post CT, however they were still higher than control values. Our findings reflect that there is a rapid increase in free radicals production in the mitochondria after diagnostic level radiation. Detection of higher ROS levels at 24 hours suggests incomplete repair with the presence of some residual oxidative species at 24 hours.

Flavonoids, the Family of Plant-derived Antioxidants making inroads into Novel Therapeutic Design against IR-induced Oxidative Stress in Parkinson’s Disease

2021 ◽  
Vol 19 ◽  
Author(s):  
Tapan Behl ◽  
Gagandeep Kaur ◽  
Aayush Sehgal ◽  
Gokhan Zengin ◽  
Sukhbir Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ionizing Radiation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Radiation Induced ◽  
Novel Therapeutic

Background: Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various pieces of evidences assembled during preceding years reveal the pertinent role of ionizing radiation-induced oxidative stress in the progression of neurodegenerative insults such as Parkinson’s disease, which have been contributing to increased proliferation and generation of reactive oxygen species. Objective: This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson’s disease and proposes novel therapeutic interventions of flavonoid family offering effective management and slowing down the progression of Parkinson’s disease. Method: Published papers were searched via MEDLINE, PubMed, etc. published to date for in-depth database collection. Results: The potential of oxidative damage may harm the non-targeted cells. It can also modulate the functions of central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerates the progression of Parkinson’s disease at the molecular, cellular, or tissue levels. In Parkinson’s disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms. Conclusion: Rising interest has extensively engrossed on the clinical trial designs based on the plant derived family of antioxidants. They are known to exert multifarious impact either way in neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.

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

2017 ◽  
Vol 58 (5) ◽  
pp. 626-635 ◽  
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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