PARP-1 inhibition induces a late increase in the level of reactive oxygen species in cells after ionizing radiation

2012 ◽  
Vol 732 (1-2) ◽  
pp. 9-15 ◽  
Author(s):  
Artur Cieślar-Pobuda ◽  
Yuriy Saenko ◽  
Joanna Rzeszowska-Wolny
Keyword(s):  
Reactive Oxygen Species ◽  
Ionizing Radiation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Parp 1 ◽  
In Cells

scholarly journals PARP-1 inhibition with or without ionizing radiation confers reactive oxygen species-mediated cytotoxicity preferentially to cancer cells with mutant TP53

Oncogene ◽  
2018 ◽  
Vol 37 (21) ◽  
pp. 2793-2805 ◽  
Author(s):  
Qi Liu ◽  
Liliana Gheorghiu ◽  
Michael Drumm ◽  
Rebecca Clayman ◽  
Alec Eidelman ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Parp 1

Abstract 097: Recombinant Human Erythropoietin Prevents Reactive Oxygen Species - Induced Apoptosis Via Akt and p38 MAPK Pathway During Hypoxia/ Reperfusion Injury

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Asiya Parvin Allaudeen ◽  
Ajay Devendran ◽  
John E Baker ◽  
Anuradha Dhanasekaran
Keyword(s):  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Intact Cell ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Human Erythropoietin ◽  
In Cells

Erythropoietin (EPO) is a cytokine produced primarily in the kidney that is essential for red blood cell production. Apart from playing a role in hematopoiesis, EPO also has a protective role in heart myocytes, ovarian, glial cells brain and retinal diseases. In this study we observed that recombinant human EPO (rhEPO) reduces Hypoxia/ Reperfusion (H/R) injury by virtue of its effect on EPO receptor prosurvival signaling pathway, which ultimately leads to reduced expression of apoptotic proteins and increased survival of cardiomyocytes. H9C2 cells were exposed to H/R with or without pretreatment using 10, 15 and 20 U/ml of rhEPO. We determined viability using MTT, nuclear fragmentation by Hoechst staining, apoptotic nuclei by Acridine orange and Ethidium bromide, Reactive Oxygen Species (ROS) by Dicholorofluoresin Diacetate and activity of late apoptotic protease, Caspase-3 by colorimetric Caspase-3 assay. The expression of mitochondrial superoxide dismutase (MnSOD) by RT-PCR and Western blot, phospho-Akt and p38 MAPK by Confocal microscopy were analyzed. Cell viability is increased in cells pretreated with rhEPO compared to cell exposed to H/R. Cells subjected to H/R showed early apoptotic and late apoptotic cells but showed normal nuclei with intact cell membrane in cells pretreated with rhEPO. Intracellular production of ROS and Caspase-3 activity was decreased in cells pretreated with rhEPO compared to cells exposed to H/R. The expression of MnSOD RNA and protein was up-regulated in response to rhEPO, but not in H/R. The phosphorylative activation of Akt, p38MAPK progressively diminished during H/R but increased in rhEPO pretreated cells. We show that rhEPO prevents apoptosis in cardiomyocytes, subjected to H/R injury via phosphorylation of Akt and p38MAPK. These results it is hoped would help us distinguish the cell signaling pathways involved in cardioprotection and thus would open new avenues in cardiovascular therapy.

scholarly journals cAMP Activates The generation of Reactive Oxygen Species and Inhibits The Secretion of IL-6 in Peripheral Blood Mononuclear Cells from Type 2 Diabetic Patients

2009 ◽  
Vol 2 (5) ◽  
pp. 317-321 ◽  
Author(s):  
Camila Armond Isoni ◽  
Érica Abreu Borges ◽  
Clara Araújo Veloso ◽  
Rafael Teixeira Mattos ◽  
Miriam Martins Chaves ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
In Cells

Peripheral blood mononuclear cells (PBMNC) from patients with type 2 diabetes (DM2) have generated higher levels of reactive oxygen species (ROS) that were higher than those in cells from healthy individuals. In the presence of a cAMP-elevating agent, ROS production was significantly activated in PBMNC from DM2 patients but it was inhibited in cells from healthy subjects. Higher levels of IL-6 has been detected in the supernatant of PBMNC cultures from DM2 patients in comparison with healthy controls. When cells were cultured in the presence of a cAMP-elevating agent, the level of IL-6 decreased has by 46% in the supernatant of PBMNC from DM2 patients but it remained unaltered in controls. No correlations between ROS and IL-6 levels in PBMNC from DM2 patients or controls have been observed. Secretions of IL-4 or IFN by PBMNC from patients or controls have not been affected by the elevation of cAMP. cAMP elevating agents have activated the production of harmful reactive oxidant down modulated IL-6 secretion by these cells from DM2 patients, suggesting an alteration in the metabolic response possibly due to hyperglicemia. The results suggest that cAMP may play an important role in the pathogenesis of diabetes.

scholarly journals Caffeic Acid - Potential Antioxidant in Cultured Human Retinal Pigment Epithelial Cells

1970 ◽  
Vol 66 (2) ◽  
Author(s):  
Dumitriţa RUGINǍ ◽  
Adela PINTEA ◽  
Raluca PÂRLOG ◽  
Andreea VARGA
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Caffeic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Defence ◽  
Rpe Cells ◽  
In Cells

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.

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.

Increased Generation of Vascular Reactive Oxygen Species by Ang II Is Mediated Via Src-Dependent Pathways in Essential Hypertension.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 685-685
Author(s):  
Rhian M Touyz ◽  
Ernesto L Schiffrin
Keyword(s):  
Reactive Oxygen Species ◽  
Essential Hypertension ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Leucine Incorporation ◽  
Oxygen Species ◽  
Ang Ii ◽  
Growth Responses ◽  
Hypertensive Patients ◽  
In Cells

42 We tested the hypothesis that augmented Ang II-induced vascular smooth muscle cell (VSMC) growth in human hypertension is mediated via Src-dependent pathways that generate reactive oxygen species (ROS). VSMCs from arteries of normotensive and hypertensive subjects were studied. Production of ROS was measured by fluorescence digital imaging using dichlorofluorescin diacetate (6 μM). The roles of Src and NADH/NADPH oxidase were assessed with the specific inhibitors, PP2 (10 μM) and diphenylene iodinium (DPI) (10 μM) respectively. c-Src phosphorylation was determined by western blot and kinase activity was assessed by measuring enolase phosphorylation. Ang II increased DCFDA fluorescence. This effect was inhibited by catalase, indicating that the signal was derived predominantly from H 2 O 2 . Ang II increased H 2 O 2 production within 40 minutes. Responses were greater (p<0.05) in cells from hypertensive patients (E max =82±nM) than normotensive subjects (E max = 67±nM). DPI and PP2, but not PP3 (inactive analogue) attenuated (p<0.05) Ang II-induced H 2 O 2 production. PP2 effects were greater in cells from hypertensive patients (delta H 2 O 2 , 28±5nM) vs controls (delta H 2 O 2 , 16±2nM). Ang II increased c-Src phosphorylation and activity, with responses 3-4 fold higher in hypertensives. DPI and PP2 (p<0.01) attenuated Ang II-induced DNA and protein synthesis, as measured by 3 H-thymidine and 3 H-leucine incorporation respectively. Growth responses in hypertensive patients were normalized by PP2. In VSMCs from hypertensive patients, Ang II-induced generation of ROS and growth are augmented. These effects are mediated, in part, by Src-dependent, NADH/NADPH oxidase-dependent cascades. Thus increased Src activity may be an upstream modulator of redox-sensitive pathways that regulate vascular growth and remodeling in essential hypertension.

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.

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