Статті в журналах: "Production de ROS"

1

Brand, M. "Mitochondrial ROS production." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 146, no. 4 (April 2007): S56—S57. http://dx.doi.org/10.1016/j.cbpa.2007.01.044.

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2

Hole, Paul S., Lorna Pearn, Amanda J. Tonks, Philip E. James, Alan K. Burnett, Richard L. Darley, and Alex Tonks. "Ras-induced reactive oxygen species promote growth factor–independent proliferation in human CD34+ hematopoietic progenitor cells." Blood 115, no. 6 (February 11, 2010): 1238–46. http://dx.doi.org/10.1182/blood-2009-06-222869.

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Abstract Excessive production of reactive oxygen species (ROS) is a feature of human malignancy and is often triggered by activation of oncogenes such as activated Ras. ROS act as second messengers and can influence a variety of cellular process including growth factor responses and cell survival. We have examined the contribution of ROS production to the effects of N-RasG12D and H-RasG12V on normal human CD34+ progenitor cells. Activated Ras strongly up-regulated the production of both superoxide and hydrogen peroxide through the stimulation of NADPH oxidase (NOX) activity, without affecting the expression of endogenous antioxidants or the production of mitochondrially derived ROS. Activated Ras also promoted both the survival and the growth factor–independent proliferation of CD34+ cells. Using oxidase inhibitors and antioxidants, we found that excessive ROS production by these cells did not contribute to their enhanced survival; rather, ROS promoted their growth factor–independent proliferation. Although Ras-induced ROS production specifically activated the p38MAPK oxidative stress response, this failed to induce expression of the cell-cycle inhibitor, p16INK4A; instead, ROS promoted the expression of D cyclins. These data are the first to show that excessive ROS production in the context of oncogene activation can promote proliferative responses in normal human hematopoietic progenitor cells.

3

Kobayashi, Y., X. Qi, and G. Chen. "MK2 Regulates Ras Oncogenesis through Stimulating ROS Production." Genes & Cancer 3, no. 7-8 (July 1, 2012): 521–30. http://dx.doi.org/10.1177/1947601912462718.

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4

Jia, Rui. "Probing the Production of Intracellular Vesicles Containing Reactive Oxygen and Nitrogen Species by Electrochemical Resistive-pulse Sensing." Electrochemical Society Interface 31, no. 4 (December 1, 2022): 43–44. http://dx.doi.org/10.1149/2.f07224if.

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Reactive oxygen and nitrogen species (ROS/RNS) are known to play an essential role in cell signaling, disease development and progression. The production of ROS/RNS in living cells can be induced by diacylglycerol-lactone (DAG-lactone) through activation of protein kinase C, an important therapeutic target for cancer and other diseases. In a previous report, nano-electrochemistry was performed to evaluate the production of ROS/RNS inside a human breast cell (MCF-10A) treated with DAG-lactone. Simultaneously, the formation of large intracellular vacuoles was observed using a microscope. These results suggest a possibility that the ROS/RNS were stored in the intracellular vacuoles. The experiments carried out during this summer were aimed to elucidate the relationship between the intracellular production of vesicles and ROS/RNS.

5

Pino, José A., Nelson Osses, Daniela Oyarzún, Jorge G. Farías, Ricardo D. Moreno, and Juan G. Reyes. "Differential effects of temperature on reactive oxygen/nitrogen species production in rat pachytene spermatocytes and round spermatids." REPRODUCTION 145, no. 2 (February 2013): 203–12. http://dx.doi.org/10.1530/rep-12-0330.

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) like superoxide and nitric oxide are produced by testis and spermatogenic cells in response to heat stress. However, the magnitude and mechanisms of this production in spermatogenic cells have not been described. In this work, we evaluated ROS/RNS production, its pharmacology, mitochondrial oxidative metabolism, membrane potential and antioxidant capacity at different temperatures in isolated rat pachytene spermatocytes and round spermatids. Our results showed an increment in ROS/RNS production by pachytene spermatocytes when increasing the temperature to 40 °C. Instead, ROS/RNS production by round spermatids did not change at temperatures higher than 33 °C. ROS/RNS production was sensitive to NADPH oxidase inhibitor diphenylene iodonium or the mitochondrial complex I inhibitor rotenone. No additive effects were observed for these two compounds. Our results suggest an important mitochondrial ROS/RNS production in spermatogenic cells. Oligomycin-insensitive oxygen consumption (uncoupled oxygen consumption) increased with temperature and was significantly larger in round spermatids than pachytene spermatocytes, indicating a likely round spermatid mitochondrial uncoupling at high temperatures. A similar conclusion can be reached by measuring the mitochondrial membrane potential using rhodamine 123 fluorescence in permeabilized cells or JC-1 fluorescence in intact cells. The antioxidant capacity was higher in round spermatids than pachytene spermatocytes at 40 °C. Our results strongly suggest that at high temperatures (40 °C) pachytene spermatocytes are more susceptible to oxidative stress, but round spermatids are more protected because of a temperature-induced mitochondrial uncoupling together with a larger antioxidant capacity.

6

N. Agbedanu, Prince, Troy B. Puga, Joshua Schafer, Pearce Harris, Gary Branum, and Nora Strasser. "Investigation of Reactive Oxygen Species production in Human Hepatocytes." Gastroenterology Pancreatology and Hepatobilary Disorders 6, no. 2 (January 12, 2022): 01–06. http://dx.doi.org/10.31579/2641-5194/058.

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1. Aim/Background: Reactive oxygen species (ROS) have been identified as compounds responsible for producing cellular damage. The purpose of this research is to examine if there is production of reactive oxygen species through free radical intermediates within human hepatocytes treated with morphine, bilirubin, or furosemide. The investigation examines the early stages of biotransformation by measuring the levels of reactive oxygen species produced inside of the treated hepatocytes within the first and second hours of treatment. The experiment was designed upon a case of a jaundiced (elevated bilirubin) infant who received morphine and furosemide and later died through unknown mechanisms. The experiment looks to examine if these drug compounds could contribute to cellular damage. This can help to further understand the potential interactions and complications of free radical intermediates produced during the phases of biotransformation. 2. Method: Previously cultured human hepatocytes were washed by centrifugation and re-suspended in 1x supplemental buffer to a concentration of 1x106 cells/mL and seeded in a dark clear bottom 96-well microplate at 100,000 stained cells/well. The cells were treated with either furosemide, morphine, bilirubin, a Tert-Butyl hydro peroxide (TBHP) positive control, or left as a background. Reactive oxygen generated in the presence of these agents were quantified by fluorescence excitation/emission measurement at 495nm/529nm. Fluorescence was measured at one and two hours. ROS generated convert 2',7'-dichlorodihydrofluorescein diacetate to 2',7'-dichlorodihydrofluorescein within the cells, which fluoresces. The fluorescence intensity detected is equivalent to the level of ROS generated. Wells that were untreated were used as blanks and subtracted from background and TBPH. 3. Results: Furosemide and Morphine did not produce statistically significant levels of ROS (p >0.05) above the background in both hours 1 and 2 of biotransformation and ROS measurement (Figure 1). Although Bilirubin did not produce statistically significant (p >0.05) levels of ROS above the background (Figure 2) during the first hour, it did produce statistically significant levels in the second hour of biotransformation. Each compound’s level of ROS was reduced during the second hour, signaling the removal of intermediate ROS metabolites (Figure 2). The production of ROS in each compound signifies that there is biotransformation to an intermediate that produces ROS. 4. Conclusion: The production of ROS above the background by each of the compounds shows there is an intermediate free radical compound that is produced during the biotransformation of each compound [21]. In this study, although furosemide and morphine did not produce statistically significant levels of ROS in both hours of biotransformation, bilirubin did produce significant levels of ROS in the second hour of biotransformation. This finding is in line with previous studies that shows morphine to offer protective effects against ROS production [16, 17]; and bilirubin demonstrating deleterious production of ROS at high doses [18]. Further work must be done to examine the correlation between the levels of ROS and extent of hepatocellular damage.

7

Ito, Seigo, Hiroyuki Nakashima, Takuya Ishikiriyama, Masahiro Nakashima, Akira Yamagata, Toshihiko Imakiire, Manabu Kinoshita, Shuhji Seki, Hiroo Kumagai, and Naoki Oshima. "Effects of a CCR2 antagonist on macrophages and Toll-like receptor 9 expression in a mouse model of diabetic nephropathy." American Journal of Physiology-Renal Physiology 321, no. 6 (December 1, 2021): F757—F770. http://dx.doi.org/10.1152/ajprenal.00191.2021.

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We classified kidney macrophages (Mφs) into bone marrow-derived (BM-) macrophages expressing high CD11b and tissue-specific resident (Res-) macrophages expressing low CD11b. In diabetic nephropathy (DN) model mice, TLR9 expression and TNF-α production via TLR9 activation in BM-Mφs and ROS production in Res-Mφs were enhanced. Furthermore, CCR2 antagonist suppressed the kidney infiltration of BM-Mφs and their function and the ROS production by Res-Mφs, with concomitant TLR9 suppression. Our study presents a new therapeutic strategy for DN.

8

Doering, Talisa, Justin Maire, Wing Yan Chan, Alexis Perez-Gonzalez, Luka Meyers, Rumi Sakamoto, Isini Buthgamuwa, Linda L. Blackall, and Madeleine J. H. van Oppen. "Comparing the Role of ROS and RNS in the Thermal Stress Response of Two Cnidarian Models, Exaiptasia diaphana and Galaxea fascicularis." Antioxidants 12, no. 5 (May 6, 2023): 1057. http://dx.doi.org/10.3390/antiox12051057.

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Coral reefs are threatened by climate change, because it causes increasingly frequent and severe summer heatwaves, resulting in mass coral bleaching and mortality. Coral bleaching is believed to be driven by an excess production of reactive oxygen (ROS) and nitrogen species (RNS), yet their relative roles during thermal stress remain understudied. Here, we measured ROS and RNS net production, as well as activities of key enzymes involved in ROS scavenging (superoxide dismutase and catalase) and RNS synthesis (nitric oxide synthase) and linked these metrics to physiological measurements of cnidarian holobiont health during thermal stress. We did this for both an established cnidarian model, the sea anemone Exaiptasia diaphana, and an emerging scleractinian model, the coral Galaxea fascicularis, both from the Great Barrier Reef (GBR). Increased ROS production was observed during thermal stress in both species, but it was more apparent in G. fascicularis, which also showed higher levels of physiological stress. RNS did not change in thermally stressed G. fascicularis and decreased in E. diaphana. Our findings in combination with variable ROS levels in previous studies on GBR-sourced E. diaphana suggest G. fascicularis is a more suitable model to study the cellular mechanisms of coral bleaching.

9

Wojtovich, Andrew P., and Thomas H. Foster. "Optogenetic control of ROS production." Redox Biology 2 (2014): 368–76. http://dx.doi.org/10.1016/j.redox.2014.01.019.

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10

Garama, Daniel J., Tiffany J. Harris, Christine L. White, Fernando J. Rossello, Maher Abdul-Hay, Daniel J. Gough, and David E. Levy. "A Synthetic Lethal Interaction between Glutathione Synthesis and Mitochondrial Reactive Oxygen Species Provides a Tumor-Specific Vulnerability Dependent on STAT3." Molecular and Cellular Biology 35, no. 21 (August 17, 2015): 3646–56. http://dx.doi.org/10.1128/mcb.00541-15.

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Increased production of mitochondrion-derived reactive oxygen species (ROS) is characteristic of a metabolic shift observed during malignant transformation. While the exact sources and roles of ROS in tumorigenesis remain to be defined, it has become clear that maintaining redox balance is critical for cancer cell proliferation and survival and, as such, may represent a vulnerability that can be exploited therapeutically. STAT3, a latent cytosolic transcription factor activated by diverse cytokines and growth factors, has been shown to exhibit an additional, nontranscriptional function in mitochondria, including modulation of electron transport chain activity. In particular, malignant transformation by Ras oncogenes exploits mitochondrial STAT3 functions. We used mass spectrometry-based metabolomics profiling to explore the biochemical basis for the STAT3 dependence of Ras transformation. We identified the gamma-glutamyl cycle, the production of glutathione, and the regulation of ROS as a mitochondrion-STAT3-dependent pathway in Ras-transformed cells. Experimental inhibition of key enzymes in the glutathione cycle resulted in the depletion of glutathione, accumulation of ROS, oxidative DNA damage, and cell death in an oncogenic Ras- and mitochondrial STAT3-dependent manner. These data uncover a synthetic lethal interaction involving glutathione production and mitochondrial ROS regulation in Ras-transformed cells that is governed by mitochondrial STAT3 and might be exploited therapeutically.

11

Günther, Julia K., Aleksandar Nikolajevic, Susanne Ebner, Jakob Troppmair, and Sana Khalid. "Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation." Biology 9, no. 5 (May 15, 2020): 99. http://dx.doi.org/10.3390/biology9050099.

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Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. JNK1/2 are not only regulated by ROS—they in turn can also control ROS production. The prooxidant and cell death function of p66Shc requires phosphorylation by JNK1/2. Here, we provide evidence that establishes p66Shc, an oxidoreductase, as a JNK1/2 effector downstream of Rigosertib-induced ROS production, DNA damage, and cell death. This may provide a common pathway for suppression of tumor cell growth by Rigosertib.

12

Tuet, Wing Y., Yunle Chen, Shierly Fok, Julie A. Champion, and Nga L. Ng. "Inflammatory responses to secondary organic aerosols (SOA) generated from biogenic and anthropogenic precursors." Atmospheric Chemistry and Physics 17, no. 18 (September 26, 2017): 11423–40. http://dx.doi.org/10.5194/acp-17-11423-2017.

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Abstract. Cardiopulmonary health implications resulting from exposure to secondary organic aerosols (SOA), which comprise a significant fraction of ambient particulate matter (PM), have received increasing interest in recent years. In this study, alveolar macrophages were exposed to SOA generated from the photooxidation of biogenic and anthropogenic precursors (isoprene, α-pinene, β-caryophyllene, pentadecane, m-xylene, and naphthalene) under different formation conditions (RO2 + HO2 vs. RO2 + NO dominant, dry vs. humid). Various cellular responses were measured, including reactive oxygen and nitrogen species (ROS/RNS) production and secreted levels of cytokines, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). SOA precursor identity and formation condition affected all measured responses in a hydrocarbon-specific manner. With the exception of naphthalene SOA, cellular responses followed a trend where TNF-α levels reached a plateau with increasing IL-6 levels. ROS/RNS levels were consistent with relative levels of TNF-α and IL-6, due to their respective inflammatory and anti-inflammatory effects. Exposure to naphthalene SOA, whose aromatic-ring-containing products may trigger different cellular pathways, induced higher levels of TNF-α and ROS/RNS than suggested by the trend. Distinct cellular response patterns were identified for hydrocarbons whose photooxidation products shared similar chemical functionalities and structures, which suggests that the chemical structure (carbon chain length and functionalities) of photooxidation products may be important for determining cellular effects. A positive nonlinear correlation was also detected between ROS/RNS levels and previously measured DTT (dithiothreitol) activities for SOA samples. In the context of ambient samples collected during summer and winter in the greater Atlanta area, all laboratory-generated SOA produced similar or higher levels of ROS/RNS and DTT activities. These results suggest that the health effects of SOA are important considerations for understanding the health implications of ambient aerosols.

13

Mijatović, Sanja, Ana Savić-Radojević, Marija Plješa-Ercegovac, Tatjana Simić, Ferdinando Nicoletti, and Danijela Maksimović-Ivanić. "The Double-Faced Role of Nitric Oxide and Reactive Oxygen Species in Solid Tumors." Antioxidants 9, no. 5 (April 30, 2020): 374. http://dx.doi.org/10.3390/antiox9050374.

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Disturbed redox homeostasis represents a hallmark of cancer phenotypes, affecting cellular metabolism and redox signaling. Since reactive oxygen and nitrogen species (ROS/RNS) are involved in regulation of proliferation and apoptosis, they may play a double-faced role in cancer, entailing protumorigenic and tumor-suppressing effects in early and later stages, respectively. In addition, ROS and RNS impact the activity and communication of all tumor constituents, mediating their reprogramming from anti- to protumorigenic phenotypes, and vice versa. An important role in this dichotomic action is played by the variable amounts of O2 in the tumor microenvironment, which dictates the ultimate outcome of the influence of ROS/RNS on carcinogenesis. Moreover, ROS/RNS levels remarkably influence the cancer response to therapy. The relevance of ROS/RNS signaling in solid tumors is witnessed by the emergence of novel targeted treatments of solid tumors with compounds that target ROS/RNS action and production, such as tyrosine kinase inhibitors and monoclonal antibodies, which might contribute to the complexity of redox regulation in cancer. Prospectively, the dual role of ROS/RNS in the different stages of tumorigenesis through different impact on oxidation and nitrosylation may also allow development of tailored diagnostic and therapeutic approaches.

14

Bonini, Marcelo G., and Asrar B. Malik. "Regulating the regulator of ROS production." Cell Research 24, no. 8 (May 20, 2014): 908–9. http://dx.doi.org/10.1038/cr.2014.66.

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15

Wrzaczek, Michael, Mikael Brosché, and Jaakko Kangasjärvi. "ROS signaling loops — production, perception, regulation." Current Opinion in Plant Biology 16, no. 5 (October 2013): 575–82. http://dx.doi.org/10.1016/j.pbi.2013.07.002.

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16

Moreno-Sánchez, R., L. Hernández-Esquivel, N. A. Rivero-Segura, A. Marín-Hernández, S. J. Ralph, and S. Rodríguez-Enríquez. "ROS production by respiratory complex II." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1817 (October 2012): S116. http://dx.doi.org/10.1016/j.bbabio.2012.06.311.

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17

Grivennikova, Vera G., and Andrei D. Vinogradov. "Respiratory complex II catalyzed ROS production." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1857 (August 2016): e77-e78. http://dx.doi.org/10.1016/j.bbabio.2016.04.181.

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18

Supruniuk, Elżbieta, Jan Górski, and Adrian Chabowski. "Endogenous and Exogenous Antioxidants in Skeletal Muscle Fatigue Development during Exercise." Antioxidants 12, no. 2 (February 16, 2023): 501. http://dx.doi.org/10.3390/antiox12020501.

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Muscle fatigue is defined as a decrease in maximal force or power generated in response to contractile activity, and it is a risk factor for the development of musculoskeletal injuries. One of the many stressors imposed on skeletal muscle through exercise is the increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which intensifies as a function of exercise intensity and duration. Exposure to ROS/RNS can affect Na+/K+-ATPase activity, intramyofibrillar calcium turnover and sensitivity, and actin–myosin kinetics to reduce muscle force production. On the other hand, low ROS/RNS concentrations can likely upregulate an array of cellular adaptative responses related to mitochondrial biogenesis, glucose transport and muscle hypertrophy. Consequently, growing evidence suggests that exogenous antioxidant supplementation might hamper exercise-engendering upregulation in the signaling pathways of mitogen-activated protein kinases (MAPKs), peroxisome-proliferator activated co-activator 1α (PGC-1α), or mammalian target of rapamycin (mTOR). Ultimately, both high (exercise-induced) and low (antioxidant intervention) ROS concentrations can trigger beneficial responses as long as they do not override the threshold range for redox balance. The mechanisms underlying the two faces of ROS/RNS in exercise, as well as the role of antioxidants in muscle fatigue, are presented in detail in this review.

19

George, Alex, Sebastian Koochaki, Suvarnamala Pushkaran, Narla Mohandas, Yi Zheng, Clinton H. Joiner та Theodosia A. Kalfa. "Elevated Reactive Oxygen Species Production In Sickle Erythrocytes Is Modulated by a Pathway Involving Endothelin-1, TGFβ1, PKC, and Rac GTPases". Blood 116, № 21 (19 листопада 2010): 1634. http://dx.doi.org/10.1182/blood.v116.21.1634.1634.

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Abstract Abstract 1634 Chronic inflammation has emerged as an important pathogenic mechanism in sickle cell disease. One component of this inflammatory response is oxidant stress mediated by reactive oxygen species (ROS) generated by leukocytes, endothelial cells, plasma enzymes, and sickle erythrocytes. Sickle RBC ROS generation has been attributed to sickle hemoglobin auto-oxidation and Fenton chemistry reactions catalyzed by denatured heme moieties bound to the RBC membrane. The potential role of enzymatic mechanisms in ROS production in RBCs has not been fully explored. One candidate for enzyme-mediated ROS production in SS RBCs is NADPH oxidase, which is activated by the small Rho GTPases Rac1 and Rac2 in a variety of cell types (Hordijk P.L. Circ. Res. 2006; 98:453-462). Using flow cytometry with 5-(and 6-)-chloromethyl-2`,7`-dichlorodihydrofluorescein diacetate, a peroxide-sensitive probe, we determined that ROS generation is elevated in HbSS RBCs by 150–250% relative to that in HbAA RBCs. The NADPH oxidase NOX subunit homologs NOX1 and NOX5 were expressed in erythrocytes, and treatment of SS RBCs with the NADPH oxidase inhibitor diphenyleneiodonium (DPI) reduced ROS generation in a dose-dependent manner. Inhibition of PKC or Rac activity by the small molecule-inhibitors calphostin and NSC23766, respectively, also resulted in decreased ROS production in HbSS-RBCs in a dose-dependent fashion, while PKC activation by phorbol 12-myristate 13-acetate (PMA) increased ROS production. This effect of PMA could be inhibited by parallel treatment with NSC23766, implicating a PKC-Rac axis in erythrocyte ROS production. Enzymatic ROS production in sickle RBCs was dependent on the availability of free intracellular calcium, since it was inhibited by BAPTA-AM, a cell-permeable calcium chelator. Moreover, we found that ROS generation in SS RBCs was modulated by humoral factors. Incubation of AA RBCs in blood type-matched SS patient plasma resulted in increased ROS generation, while the incubation of SS RBCs in AA plasma decreased ROS production. Immunoblotting of AA and SS RBC membranes with specific antibodies revealed receptors for the inflammatory signaling molecules TGFβ1 and Endothelin-1 (ET-1), both of which are present in elevated levels in the plasma of patients with SCD. Incubation of AA RBCs with TGFβ1 or ET-1 resulted in increased Rac activation and increased ROS production in these treated cells. Our results suggest that ROS production in sickle RBCs is mediated by NADPH oxidase through Ca2+-regulated PKC and Rac signals, which in turn are modulated by plasma TGFβ1 and ET-1 via their receptors. ROS-mediated damage to RBC membrane components is known to contribute to erythrocyte deformation and fragility in sickle cell disease. Erythrocyte ROS generation, RBC lysis, vaso-occlusion, and the inflammatory response to tissue damage may therefore act in a positive feedback loop to drive the pathophysiology of sickle cell disease. These data may offer new therapeutic targets to counteract inflammation and RBC fragility and deformation in sickle cell disease. Disclosures: No relevant conflicts of interest to declare.

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Fan, Jinshui, Annahita Sallmyr, Kyu-Te Kim, Kamal Datta, Paul Shapiro, Donald Small, and Feyruz V. Rassool. "Internal Tandem Duplications of FLT3 Induces Increased ROS Production, DNA Damage and Misrepair: Implications for Genomic Instability and Disease Resistance in Myeloid Malignancies." Blood 110, no. 11 (November 16, 2007): 17. http://dx.doi.org/10.1182/blood.v110.11.17.17.

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Abstract The FMS-like tyrosine kinase (FLT3), which belongs to the class III receptor tyrosine kinase family, is primarily expressed by hematopoietic cells and plays an important role in hematopoiesis. Activating mutations of FLT3 occur in approximately 30% of myeloid malignancies and, at least for the internal tandem duplications (ITDs) of the juxtamembrane region, are an independent predictor of poor clinical outcome. FLT3 signaling in leukemia includes activation of RAS, PI3 kinase/AKT pathways, and signal transducer and activator of transcription-5 (STAT5), leading to increased cellular proliferation and survival. We have previously shown that N-RAS activation can initiate a cycle of genomic instability whereby increased reactive oxygen species (ROS) leads to double strand breaks (DSB) and error-prone repair in myeloid malignancies. Virtually nothing is known about the role of FLT3 mutations in genomic instability. Here we report that FLT3/ITD signaling can lead to genomic instability that may be driven by increased ROS production. We find that mouse myeloid progenitor cells (32D) stably expressing FLT3/ITD (32D/ITD), demonstrate significantly increased ROS production compared with isogenic controls, as measured by flow cytometric analysis of the fuorescent probe, 2’,7’-dichlorofluoresecein (H2DCHF-DA) which is oxidized in the presence of ROS. FLT3/ITD cells treated with small molecule tyrosine kinase inhibitors (TKI) of FLT3 significantly reduced ROS levels. Intriguingly, we find that phosphorylated STAT5 (pSTAT5), which is greatly stimulated by mutant FLT3 signaling, binds RAC1-GTP, an essential component of ROS-producing NADPH oxidase. This novel finding suggests that STAT5 may have unique non-genomic functions involved in regulating RAC1 activation and ROS generation. FLT3 mutant cells treated with siRNA to down-regulate STAT5, show significantly reduced ROS. Inhibition of RAC1 and NADPH oxidase in FLT3 mutant cells also leads to reduced ROS levels, providing further evidence for the involvement of RAC1 in ROS production. While RAC1 activity is unchanged by FLT3 inhibition, significantly less RAC1 binds NADPH oxidase protein GP91phox in the cell membrane. Therefore pSTAT5 binding to RAC1-GTP may be necessary for NADPH oxidase activity and ROS production. Importantly, human leukemia cell lines (MOLM-14 & MV-4-11) and primary samples (N=3) with naturally occurring FLT3/ITD also show significantly decreased ROS in a dose- and time-dependent manner, following treatment with FLT3 TKI, confirming the mouse cell line data. Blocking ROS production by inhibition of FLT3 in AML cells significantly decreased γH2AX foci formation, suggesting reduced DSB. An in vitro DSB repair assay based on plasmid rejoining in nuclear extracts was used to assess repair efficiency and fidelity. Higher repair efficiency and fidelity was observed following inhibition of the FLT3-mediated endogenous ROS production in FLT3/ITD-positive human AML cells. Our data serve as a model system to further study the role of FLT3-mediated increased ROS in propagating genomic instability and for therapeutic targeting in an effort to stabilize the genome and reduce the accumulation of additional mutations in these cases of AML.

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Thurlow, Lance, and Anthony Richardson. "Aberrant insulin signaling results in mTOR suppression and immune dysfunction during diabetic infections. (INM7P.427)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 123.5. http://dx.doi.org/10.4049/jimmunol.192.supp.123.5.

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Abstract Diabetics have defects in several aspects of immunity that result in increased infection rates; however, the underlying mechanisms of immune dysfunction are not well defined. Previous studies in this area concluded that infections in diabetics are hyper-inflamed as indicated by increased cytokine production. Conversely, despite high levels of pro-inflammatory cytokines, our research shows that innate immune cells from diabetics cannot produce inflammatory effectors such as reactive oxygen species (ROS) and nitric oxide (NO). ROS/RNS generation by immune cells is essential for killing bacteria and requires cells to undergo a metabolic shift reminiscent of Warburg metabolism. This shift is required for NADPH production, the sole reductant needed for ROS/RNS generation. Using murine infection models and cell culture, we show that Toll-like receptor signaling induces Warburg metabolism through activation of the mammalian target of rapamycin (mTOR). Moreover, we show that mTOR signaling is suppressed in diabetics and results in decreased ROS/RNS generation and worse infection outcomes. Finally, we demonstrate that mTOR inhibition in diabetes is caused by the activation of AMP-activated protein kinase (AMPK) as a result of deficient insulin signaling. Thus, diabetic infections are not hyper-inflamed. Instead, immune dysfunction in diabetic infections is caused by aberrant insulin signaling resulting in mTOR suppression and diminished antimicrobial effector production.

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Abou-Rjeileh, Ursula, and G. Andres Contreras. "Redox Regulation of Lipid Mobilization in Adipose Tissues." Antioxidants 10, no. 7 (July 7, 2021): 1090. http://dx.doi.org/10.3390/antiox10071090.

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Lipid mobilization in adipose tissues, which includes lipogenesis and lipolysis, is a paramount process in regulating systemic energy metabolism. Reactive oxygen and nitrogen species (ROS and RNS) are byproducts of cellular metabolism that exert signaling functions in several cellular processes, including lipolysis and lipogenesis. During lipolysis, the adipose tissue generates ROS and RNS and thus requires a robust antioxidant response to maintain tight regulation of redox signaling. This review will discuss the production of ROS and RNS within the adipose tissue, their role in regulating lipolysis and lipogenesis, and the implications of antioxidants on lipid mobilization.

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Lindgren, Helena, Stephan Stenmark, Wangxue Chen, Arne Tärnvik, and Anders Sjöstedt. "Distinct Roles of Reactive Nitrogen and Oxygen Species To Control Infection with the Facultative Intracellular Bacterium Francisella tularensis." Infection and Immunity 72, no. 12 (December 2004): 7172–82. http://dx.doi.org/10.1128/iai.72.12.7172-7182.2004.

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ABSTRACT Reactive nitrogen species (RNS) and reactive oxygen species (ROS) are important mediators of the bactericidal host response. We investigated the contribution of these two mediators to the control of infection with the facultative intracellular bacterium Francisella tularensis. When intradermally infected with the live vaccine strain F. tularensis LVS, mice deficient in production of RNS (iNOS−/− mice) or in production of ROS by the phagocyte oxidase (p47 phox−/− mice) showed compromised resistance to infection. The 50% lethal dose (LD50) for iNOS−/− mice was <20 CFU, and the LD50 for p47 phox−/− mice was 4,400 CFU, compared to an LD50 of >500,000 CFU for wild-type mice. The iNOS−/− mice survived for 26.4 ± 1.8 days, and the p47 phox−/− mice survived for 10.1 ± 1.3 days. During the course of infection, the serum levels of gamma interferon (IFN-γ) and interleukin-6 were higher in iNOS−/− and p47 phox−/− mice than in wild-type mice. Histological examination of livers of iNOS−/− mice revealed severe liver pathology. Splenocytes obtained 5 weeks after primary infection from antibiotic-treated iNOS−/− mice showed an in vitro recall response that was similar in magnitude and greater secretion of IFN-γ compared to cells obtained from wild-type mice. In summary, mice lacking expression of RNS or ROS showed extreme susceptibility to infection with F. tularensis LVS. The roles of RNS and ROS seemed to be distinct since mice deficient in production of ROS showed dissemination of infection and died during the early phase of infection, whereas RNS deficiency led to severe liver pathology and a contracted course of infection.

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BECKETT, Richard Peter, Farida V. MINIBAYEVA, and Zsanett LAUFER. "Extracellular reactive oxygen species production by lichens." Lichenologist 37, no. 5 (September 2005): 397–407. http://dx.doi.org/10.1017/s0024282905014921.

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This review discusses the production of reactive oxygen species (ROS) by lichens and their possible roles. All organisms produce ROS, and production is increased by many abiotic and biotic stresses. Intracellular ROS production is generally considered to be harmful, and a variety of enzymic and non-enzymic scavenging systems exist to detoxify them. However, extracellular ROS formation has been suggested to play ‘positive roles’, particularly in the response of organisms to stress. Given their high stress tolerance, it is rather surprising that studies on extracellular ROS production by lichens have just started. Surveys of a wide range of lichens have shown that constitutively high rates of extracellular superoxide production occur in the Suborder Peltigerineae, but production appears to be absent in other groups. In some members of the Peltigerineae ROS production is stimulated by desiccation and wounding. It seems probable that the enzymes that produce the superoxide are laccases, based on first the types of substrates that lichens can break down, and second the dependence of the breakdown of these substrates on pH, temperature and the presence of inhibitors. While much more work is needed, we suggest that physiological roles of extracellular ROS production will be found to include defence against pathogens, melanization, and lignin breakdown.

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Wellington, Melanie, Kristy Dolan, and Damian J. Krysan. "Live Candida albicans Suppresses Production of Reactive Oxygen Species in Phagocytes." Infection and Immunity 77, no. 1 (November 3, 2008): 405–13. http://dx.doi.org/10.1128/iai.00860-08.

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ABSTRACT Production of reactive oxygen species (ROS) is an important aspect of phagocyte-mediated host responses. Since phagocytes play a crucial role in the host response to Candida albicans, we examined the ability of Candida to modulate phagocyte ROS production. ROS production was measured in the murine macrophage cell line J774 and in primary phagocytes using luminol-enhanced chemiluminescence. J774 cells, murine polymorphonuclear leukocytes (PMN), human monocytes, and human PMN treated with live C. albicans produced significantly less ROS than phagocytes treated with heat-killed C. albicans. Live C. albicans also suppressed ROS production in murine bone marrow-derived macrophages from C57BL/6 mice, but not from BALB/c mice. Live C. albicans also suppressed ROS in response to external stimuli. C. albicans and Candida glabrata suppressed ROS production by phagocytes, whereas Saccharomyces cerevisiae stimulated ROS production. The cell wall is the initial point of contact between Candida and phagocytes, but isolated cell walls from both heat-killed and live C. albicans stimulated ROS production. Heat-killed C. albicans has increased surface exposure of 1,3-β-glucan, a cell wall component that can stimulate phagocytes. To determine whether surface 1,3-β-glucan exposure accounted for the difference in ROS production, live C. albicans cells were treated with a sublethal dose of caspofungin to increase surface 1,3-β-glucan exposure. Caspofungin-treated C. albicans was fully able to suppress ROS production, indicating that suppression of ROS overrides stimulatory signals from 1,3-β-glucan. These studies indicate that live C. albicans actively suppresses ROS production in phagocytes in vitro, which may represent an important immune evasion mechanism.

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Kaludercic, Nina, and Valentina Giorgio. "The Dual Function of Reactive Oxygen/Nitrogen Species in Bioenergetics and Cell Death: The Role of ATP Synthase." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–17. http://dx.doi.org/10.1155/2016/3869610.

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) targeting mitochondria are major causative factors in disease pathogenesis. The mitochondrial permeability transition pore (PTP) is a mega-channel modulated by calcium and ROS/RNS modifications and it has been described to play a crucial role in many pathophysiological events since prolonged channel opening causes cell death. The recent identification that dimers of ATP synthase form the PTP and the fact that posttranslational modifications caused by ROS/RNS also affect cellular bioenergetics through the modulation of ATP synthase catalysis reveal a dual function of these modifications in the cells. Here, we describe mitochondria as a major site of production and as a target of ROS/RNS and discuss the pathophysiological conditions in which oxidative and nitrosative modifications modulate the catalytic and pore-forming activities of ATP synthase.

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Zinkevich, Natalya S., and David D. Gutterman. "ROS-induced ROS release in vascular biology: redox-redox signaling." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 2011): H647—H653. http://dx.doi.org/10.1152/ajpheart.01271.2010.

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The involvement of reactive oxygen species (ROS) in regulating vascular function both in normal vessels and as part of an adaptive response during disease has been intensively studied. From the recognition that ROS serve as important signaling molecules has emerged multiple lines of evidence that there is a functional connectivity between intracellular sites of ROS production. This cross talk has been termed ROS-induced ROS release (RIRR) and is supported by a variety of observations showing that RIRR is a common mechanism for ROS amplification and regional ROS generation. The compartmentalization of ROS production within a cell is critical to its signaling function and is facilitated by microlocalization of specific scavengers. This review will provide descriptions and examples of important mechanisms of RIRR.

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James, Lloyd R. A., Ron Sluyter, Carolyn T. Dillon, and Stephen F. Ralph. "Effects of Gold Nanoparticles and Gold Anti-Arthritic Compounds on Inflammation Marker Expression in Macrophages." Australian Journal of Chemistry 70, no. 9 (2017): 1057. http://dx.doi.org/10.1071/ch17062.

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The ability of aurothiomalate and auranofin to alter the production of several cellular mediators of inflammation by RAW264.7 macrophages, was compared with each other and that of gold nanoparticles (Au NPs). Addition of auranofin was found to have a pronounced ability to lower the production of reactive nitrogen and oxygen species (RNS and ROS respectively), as well as interleukin-10 (IL-10) and tumour necrosis factor (TNF), by macrophages that were subsequently treated with lipopolysaccharide (LPS) to stimulate production of the mediators. In contrast, prior treatment of the cells with either aurothiomalate or Au NPs had either little or no significant effect on production of RNS and ROS. Treatment of the macrophages with Au NPs had a small effect on production of TNF by cells that were subsequently stimulated with LPS; however, the effect was much smaller than that elicited by auranofin. Similarly, aurothiomalate had a small but significant effect on production of IL-10. Varying the size of the Au NPs or the identity of the protective sheath surrounding the nanoparticles did not have a significant effect on the production of RNS or ROS by LPS-stimulated macrophages. The results of some of these investigations are discussed in the light of other studies reported in the literature. In addition, results obtained by scanning electron microscopy and energy-dispersive X-ray spectroscopy are presented that provide evidence for the accumulation of gold within macrophages exposed to Au NPs.

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Hansel, Colleen M., and Julia M. Diaz. "Production of Extracellular Reactive Oxygen Species by Marine Biota." Annual Review of Marine Science 13, no. 1 (January 3, 2021): 177–200. http://dx.doi.org/10.1146/annurev-marine-041320-102550.

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Reactive oxygen species (ROS) are produced ubiquitously across the tree of life. Far from being synonymous with toxicity and harm, biological ROS production is increasingly recognized for its essential functions in signaling, growth, biological interactions, and physiochemical defense systems in a diversity of organisms, spanning microbes to mammals. Part of this shift in thinking can be attributed to the wide phylogenetic distribution of specialized mechanisms for ROS production, such as NADPH oxidases, which decouple intracellular and extracellular ROS pools by directly catalyzing the reduction of oxygen in the surrounding aqueous environment. Furthermore, biological ROS production contributes substantially to natural fluxes of ROS in the ocean, thereby influencing the fate of carbon, metals, oxygen, and climate-relevant gases. Here, we review the taxonomic diversity, mechanisms, and roles of extracellular ROS production in marine bacteria, phytoplankton, seaweeds, and corals, highlighting the ecological and biogeochemical influences of this fundamental and remarkably widespread process.

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Comhair, Suzy A. A., and Serpil C. Erzurum. "Antioxidant responses to oxidant-mediated lung diseases." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 2 (August 1, 2002): L246—L255. http://dx.doi.org/10.1152/ajplung.00491.2001.

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated throughout the human body. Enzymatic and nonenzymatic antioxidants detoxify ROS and RNS and minimize damage to biomolecules. An imbalance between the production of ROS and RNS and antioxidant capacity leads to a state of “oxidative stress” that contributes to the pathogenesis of a number of human diseases by damaging lipids, protein, and DNA. In general, lung diseases are related to inflammatory processes that generate increased ROS and RNS. The susceptibility of the lung to oxidative injury depends largely on its ability to upregulate protective ROS and RNS scavenging systems. Unfortunately, the primary intracellular antioxidants are expressed at low levels in the human lung and are not acutely induced when exposed to oxidative stresses such as cigarette smoke and hyperoxia. However, the response of extracellular antioxidant enzymes, the critical primary defense against exogenous oxidative stress, increases rapidly and in proportion to oxidative stress. In this paper, we review how antioxidants in the lung respond to oxidative stress in several lung diseases and focus on the mechanisms that upregulate extracellular glutathione peroxidase.

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Wal, Agnieszka, Pawel Staszek, Barbara Pakula, Magdalena Paradowska, and Urszula Krasuska. "ROS and RNS Alterations in the Digestive Fluid of Nepenthes × ventrata Trap at Different Developmental Stages." Plants 11, no. 23 (November 29, 2022): 3304. http://dx.doi.org/10.3390/plants11233304.

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The carnivorous pitcher plant, Nepenthes × ventrata (Hort. ex Fleming = N. ventricosa Blanco × N. alata Blanco), produces passive traps containing digestive fluid. Although reactive oxygen species (ROS) in the fluid were detected in some pitcher plants, the participation of reactive nitrogen species (RNS) in the digestion process has not yet been examined. The aim of this work was to investigate the production of superoxide anion (O2•−), nitric oxide (NO) and peroxynitrite (ONOO−) levels in the digestive fluid of traps throughout organ development. We revealed the ROS and RNS occurrence in the digestive fluid, linked to the ROS-scavenging capacity and total phenolics content. In digestive fluid from the fed traps, NO emission was higher than in the fluid from the developed unfed pitcher. The concentration of nitrite (NO2−) decreased in the fluid from the fed traps in comparison to the unfed ones, pointing at NO2− as the key source of NO. The enhanced emission of NO was associated with lowered content of ONOO− in the fluid, probably due to lower production of O2•−. At the same time, despite a decline in total phenolics, the maximum ROS scavenging capacity was detected. In addition, ROS and RNS were noted even in closed traps, suggesting their involvement not only in digestion per se but also their action as signaling agents in trap ontogeny.

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Andrukhiv, Anastasia, Alexandre D. Costa, Ian C. West, and Keith D. Garlid. "Opening mitoKATP increases superoxide generation from complex I of the electron transport chain." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 5 (November 2006): H2067—H2074. http://dx.doi.org/10.1152/ajpheart.00272.2006.

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Opening the mitochondrial ATP-sensitive K+ channel (mitoKATP) increases levels of reactive oxygen species (ROS) in cardiomyocytes. This increase in ROS is necessary for cardioprotection against ischemia-reperfusion injury; however, the mechanism of mitoKATP-dependent stimulation of ROS production is unknown. We examined ROS production in suspensions of isolated rat heart and liver mitochondria, using fluorescent probes that are sensitive to hydrogen peroxide. When mitochondria were treated with the KATP channel openers diazoxide or cromakalim, their ROS production increased by 40–50%, and this effect was blocked by 5-hydroxydecanoate. ROS production exhibited a biphasic dependence on valinomycin concentration, with peak production occurring at valinomycin concentrations that catalyze about the same K+ influx as KATP channel openers. ROS production decreased with higher concentrations of valinomycin and with all concentrations of a classical protonophoretic uncoupler. Our studies show that the increase in ROS is due specifically to K+ influx into the matrix and is mediated by the attendant matrix alkalinization. Myxothiazol stimulated mitoKATP-dependent ROS production, whereas rotenone had no effect. This indicates that the superoxide originates in complex I (NADH:ubiquinone oxidoreductase) of the electron transport chain.

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Luo, Zhen, Qin Zhao, Jixiang Liu, Yunting Xi, Ruogu Peng, Jennifer Liao, and Jack Diwu. "Flow Cytometric Analysis of Intracellular ROS and RNS Production and Curcumin Inhibition." Free Radical Biology and Medicine 100 (November 2016): S103—S104. http://dx.doi.org/10.1016/j.freeradbiomed.2016.10.263.

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CURY-BOAVENTURA, Maria F., and Rui CURI. "Regulation of reactive oxygen species (ROS) production by C18 fatty acids in Jurkat and Raji cells." Clinical Science 108, no. 3 (February 18, 2005): 245–53. http://dx.doi.org/10.1042/cs20040281.

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In the present study, the effects of C18 fatty acids with different numbers of double bonds, SA (stearic acid; C18:0), OA (oleic acid; C18:1), LA (linoleic acid; C18:2) and γ-LNA (γ-linolenic acid; C18:3), on ROS (reactive oxygen species) production by Jurkat (a human T-lymphocyte-derived cell line) and Raji (a human B-lymphocyte-derived cell line) cells were investigated. ROS production was determined by NBT (Nitro Blue Tetrazolium) reduction (intracellular and extracellular ROS production) and by dihydroethidium oxidation using flow cytometry (intracellular ROS production). The effectiveness on ROS production was γ-LNA<SA<OA<LA in Jurkat cells and SA<γ-LNA<OA<LA in Raji cells. LA (found in corn, soya bean and sunflower oils) was more potent than OA (found in olive oil) in stimulating ROS production in both Raji and Jurkat cells. The lower ROS production by OA compared with LA may be one of the benefits of olive oil consumption. As SA and γ-LNA acids had little or no effect, further studies on the site of ROS production in these cells were carried out with OA and LA only. Activation of NADPH oxidase via PKC (protein kinase C) was found to be the major mechanism of ROS production induced by OA and LA in Jurkat and Raji cells.

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Aktanova, Alina A., Olga S. Boeva, Margarita Sh Barkovskaya, Ekaterina A. Kovalenko, and Ekaterina A. Pashkina. "Influence of Cucurbiturils on the Production of Reactive Oxygen Species by T- and B-Lymphocytes, Platelets and Red Blood Cells." International Journal of Molecular Sciences 24, no. 2 (January 11, 2023): 1441. http://dx.doi.org/10.3390/ijms24021441.

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Reactive oxygen species (ROS) are highly reactive chemical molecules containing oxygen. ROS play an important role in signaling and cell homeostasis at low and moderate concentrations. ROS could be a cause of damage to proteins, nucleic acids, lipids, membranes and organelles at high concentrations. There are a lot of cells that can produce ROS to maintain functional activity. It is known that metal nanoparticles can increase production of ROS in cells. However, the effect of cucurbiturils on ROS production is still unknown. In our study, we evaluated production of ROS by the immune (T-, B-lymphocytes, NK-cells) and non-immune cells (red blood cells, platelets), as well as tumor cells line (1301, K562) after treatment with cucurbiturils in vitro. Assessment of reactive oxide species (ROS) were provided by using dihydrorhodamine 123 (DHR 123). Fluorescence intensity and percentage DHR123 were measured by flow cytometry. Platelets, erythrocytes and activated T-helpers were changed the level of ROS production in response to stimulation with cucurbiturils. It was found that the percentage of these ROS-producing cells was reduced by cucurbiturils. Thus, cucurbiturils may affect the production of ROS by cells, but further research is needed in this area.

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Wang, Jong-Shyan, Tan Lee, and Shu-Er Chow. "Role of exercise intensities in oxidized low-density lipoprotein-mediated redox status of monocyte in men." Journal of Applied Physiology 101, no. 3 (September 2006): 740–44. http://dx.doi.org/10.1152/japplphysiol.00144.2006.

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Exercise significantly influences the progression of atherosclerosis. Oxidized LDL (ox-LDL), as a stimulator of oxidative stress, facilitates monocyte-related atherogenesis. This study investigates how exercise intensity impacts ox-LDL-mediated redox status of monocytes. Twenty-five sedentary healthy men exercised mildly, moderately, and heavily (i.e., 40, 60, and 80% maximal oxygen consumption, respectively) on a bicycle ergometer. Reactive oxygen species (ROS) production, cytosolic and mitochondrial superoxide dismutase (c-SOD and m-SOD, respectively) activities, and total and reduced-form γ-glutamylcysteinyl glycine (t-GSH and r-GSH, respectively) contents in monocytes mediated by ox-LDL were measured. This experiment obtained the following findings: 1) ox-LDL increased monocyte ROS production and was accompanied by decreased c-SOD and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium (DPI) (a NADPH oxidase inhibitor) or rotenone/2-thenoyltrifluoroacetone (TTFA) (mitochondrial complex I/II inhibitors) hindered ox-LDL-induced monocyte ROS production; 2) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise; and 3) heavy exercise augmented the inhibition of ox-LDL-induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA-mediated monocyte ROS productions were unchanged in response to mild and moderate exercise. We conclude that heavy exercise increases ox-LDL-induced monocyte ROS production, possibly by decreasing m-SOD activity and r-GSH content in monocytes. However, mild and moderate exercise likely protects individuals against suppression of anti-oxidative capacity of monocyte by ox-LDL.

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Panda, Poojarani, Henu Kumar Verma, Saikrishna Lakkakula, Neha Merchant, Fairrul Kadir, Shamsur Rahman, Mohammad Saffree Jeffree, Bhaskar V. K. S. Lakkakula, and Pasupuleti Visweswara Rao. "Biomarkers of Oxidative Stress Tethered to Cardiovascular Diseases." Oxidative Medicine and Cellular Longevity 2022 (June 24, 2022): 1–15. http://dx.doi.org/10.1155/2022/9154295.

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Cardiovascular disease (CVD) is a broad term that incorporated a group of conditions that affect the blood vessels and the heart. CVD is a foremost cause of fatalities around the world. Multiple pathophysiological mechanisms are involved in CVD; however, oxidative stress plays a vital role in generating reactive oxygen species (ROS). Oxidative stress occurs when the concentration of oxidants exceeds the potency of antioxidants within the body while producing reactive nitrogen species (RNS). ROS generated by oxidative stress disrupts cell signaling, DNA damage, lipids, and proteins, thereby resulting in inflammation and apoptosis. Mitochondria is the primary source of ROS production within cells. Increased ROS production reduces nitric oxide (NO) bioavailability, which elevates vasoconstriction within the arteries and contributes to the development of hypertension. ROS production has also been linked to the development of atherosclerotic plaque. Antioxidants can decrease oxidative stress in the body; however, various therapeutic drugs have been designed to treat oxidative stress damage due to CVD. The present review provides a detailed narrative of the oxidative stress and ROS generation with a primary focus on the oxidative stress biomarker and its association with CVD. We have also discussed the complex relationship between inflammation and endothelial dysfunction in CVD as well as oxidative stress-induced obesity in CVD. Finally, we discussed the role of antioxidants in reducing oxidative stress in CVD.

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Diaz, Julia M., Colleen M. Hansel, Bettina M. Voelker, Chantal M. Mendes, Peter F. Andeer, and Tong Zhang. "Widespread Production of Extracellular Superoxide by Heterotrophic Bacteria." Science 340, no. 6137 (May 2, 2013): 1223–26. http://dx.doi.org/10.1126/science.1237331.

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Superoxide and other reactive oxygen species (ROS) originate from several natural sources and profoundly influence numerous elemental cycles, including carbon and trace metals. In the deep ocean, the permanent absence of light precludes currently known ROS sources, yet ROS production mysteriously occurs. Here, we show that taxonomically and ecologically diverse heterotrophic bacteria from aquatic and terrestrial environments are a vast, unrecognized, and light-independent source of superoxide, and perhaps other ROS derived from superoxide. Superoxide production by a model bacterium within the ubiquitous Roseobacter clade involves an extracellular oxidoreductase that is stimulated by the reduced form of nicotinamide adenine dinucleotide (NADH), suggesting a surprising homology with eukaryotic organisms. The consequences of ROS cycling in immense aphotic zones representing key sites of nutrient regeneration and carbon export must now be considered, including potential control of carbon remineralization and metal bioavailability.

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Odyniec, Maria L., Adam C. Sedgwick, Alexander H. Swan, Maria Weber, T. M. Simon Tang, Jordan E. Gardiner, Miao Zhang, et al. "‘AND’-based fluorescence scaffold for the detection of ROS/RNS and a second analyte." Chemical Communications 54, no. 61 (2018): 8466–69. http://dx.doi.org/10.1039/c8cc04316g.

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Jin, Shi, Ramesh M. Ray та Leonard R. Johnson. "TNF-α/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive oxygen species". American Journal of Physiology-Gastrointestinal and Liver Physiology 294, № 4 (квітень 2008): G928—G937. http://dx.doi.org/10.1152/ajpgi.00219.2007.

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Previously we have shown that both Rac1 and c-Jun NH2-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-α/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. The present studies tested the hypothesis that Rac1-mediated ROS production is involved in TNF-α-induced apoptosis. In this study, we showed that TNF-α/CHX-induced ROS production and hydrogen peroxide (H2O2)-induced oxidative stress increased apoptosis. Inhibition of Rac1 by a specific inhibitor NSC23766 prevented TNF-α-induced ROS production. The antioxidant, N-acetylcysteine (NAC), or rotenone (Rot), the mitochondrial electron transport chain inhibitor, attenuated mitochondrial ROS production and apoptosis. Rot also prevented JNK1/2 activation during apoptosis. Inhibition of Rac1 by expression of dominant negative Rac1 decreased TNF-α-induced mitochondrial ROS production. Moreover, TNF-α-induced cytosolic ROS production was inhibited by Rac1 inhibition, diphenyleneiodonium (DPI, an inhibitor of NADPH oxidase), and NAC. In addition, DPI inhibited TNF-α-induced apoptosis as judged by morphological changes, DNA fragmentation, and JNK1/2 activation. Mitochondrial membrane potential change is Rac1 or cytosolic ROS dependent. Lastly, all ROS inhibitors inhibited caspase-3 activity. Thus these results indicate that TNF-α-induced apoptosis requires Rac1-dependent ROS production in intestinal epithelial cells.

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Wu, Winnie, Oleksandr Platoshyn, Amy L. Firth, and Jason X. J. Yuan. "Hypoxia divergently regulates production of reactive oxygen species in human pulmonary and coronary artery smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 4 (October 2007): L952—L959. http://dx.doi.org/10.1152/ajplung.00203.2007.

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Acute hypoxia causes pulmonary vasoconstriction and coronary vasodilation. The divergent effects of hypoxia on pulmonary and coronary vascular smooth muscle cells suggest that the mechanisms involved in oxygen sensing and downstream effectors are different in these two types of cells. Since production of reactive oxygen species (ROS) is regulated by oxygen tension, ROS have been hypothesized to be a signaling mechanism in hypoxia-induced pulmonary vasoconstriction and vascular remodeling. Furthermore, an increased ROS production is also implicated in arteriosclerosis. In this study, we determined and compared the effects of hypoxia on ROS levels in human pulmonary arterial smooth muscle cells (PASMC) and coronary arterial smooth muscle cells (CASMC). Our results indicated that acute exposure to hypoxia (Po2 = 25–30 mmHg for 5–10 min) significantly and rapidly decreased ROS levels in both PASMC and CASMC. However, chronic exposure to hypoxia (Po2 = 30 mmHg for 48 h) markedly increased ROS levels in PASMC, but decreased ROS production in CASMC. Furthermore, chronic treatment with endothelin-1, a potent vasoconstrictor and mitogen, caused a significant increase in ROS production in both PASMC and CASMC. The inhibitory effect of acute hypoxia on ROS production in PASMC was also accelerated in cells chronically treated with endothelin-1. While the decreased ROS in PASMC and CASMC after acute exposure to hypoxia may reflect the lower level of oxygen substrate available for ROS production, the increased ROS production in PASMC during chronic hypoxia may reflect a pathophysiological response unique to the pulmonary vasculature that contributes to the development of pulmonary vascular remodeling in patients with hypoxia-associated pulmonary hypertension.

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Islam, Md Moshiul, Wenxiu Ye, Fahmida Akter, Mohammad Saidur Rhaman, Daiki Matsushima, Shintaro Munemasa, Eiji Okuma, et al. "Reactive Carbonyl Species Mediate Methyl Jasmonate-Induced Stomatal Closure." Plant and Cell Physiology 61, no. 10 (August 18, 2020): 1788–97. http://dx.doi.org/10.1093/pcp/pcaa107.

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Abstract Production of reactive oxygen species (ROS) is a key signal event for methyl jasmonate (MeJA)- and abscisic acid (ABA)-induced stomatal closure. We recently showed that reactive carbonyl species (RCS) stimulates stomatal closure as an intermediate downstream of hydrogen peroxide (H2O2) production in the ABA signaling pathway in guard cells of Nicotiana tabacum and Arabidopsis thaliana. In this study, we examined whether RCS functions as an intermediate downstream of H2O2 production in MeJA signaling in guard cells using transgenic tobacco plants overexpressing A. thaliana 2-alkenal reductase (n-alkanal + NAD(P)+ ⇌ 2-alkenal + NAD(P)H + H+) (AER-OE tobacco) and Arabidopsis plants. The stomatal closure induced by MeJA was impaired in the AER-OE tobacco and was inhibited by RCS scavengers, carnosine and pyridoxamine, in the wild-type (WT) tobacco plants and Arabidopsis plants. Application of MeJA significantly induced the accumulation of RCS, including acrolein and 4-hydroxy-(E)-2-nonenal, in the WT tobacco but not in the AER-OE plants. Application of MeJA induced H2O2 production in the WT tobacco and the AER-OE plants and the H2O2 production was not inhibited by the RCS scavengers. These results suggest that RCS functions as an intermediate downstream of ROS production in MeJA signaling and in ABA signaling in guard cells.

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Do, Yen Thi, Seungmee Lee, Changmin Shin, Hyewon Chung, Jin Young Kim, Eunyoung Ha, Sojin Shin, and Ji Hae Seo. "Abstract 7155: Dichloroacetate reverses cisplatin resistance in ovarian cancer through promoting ROS production." Cancer Research 84, no. 6_Supplement (March 22, 2024): 7155. http://dx.doi.org/10.1158/1538-7445.am2024-7155.

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Abstract Chemotherapy resistance and the high rate of ovarian cancer relapse pose major challenges in the treatment of ovarian cancer. The development of chemoresistance contributes to poor overall prognosis associated with ovarian cancer and high cancer-related mortality in women worldwide. Herein, we found that Dichloroacetate (DCA), a pan-pyruvate dehydrogenase kinase (PDK) inhibitor, is a potent agent to overcome Cisplatin (CP) resistance in ovarian cancer treatment. Firstly, we elucidated that phosphorylation of pyruvate dehydrogenase (pPDH) was elevated in CP-resistant ovarian cancer cells. Then, blockage of pPDH by DCA treatment significantly inhibited cell migratory and invasive capacity in CP-resistant ovarian cancer cells through the transition of motile mesenchymal phenotypes into epithelial characteristics. DCA markedly decreased the number of sphere formations and attenuated the stem cell-like properties in CP-resistant ovarian cancer cells. In combination with CP treatment, DCA effectively inhibited cell proliferation in chemoresistant ovarian cancer cells by triggering apoptosis. Collectively, we suggested that DCA is a promising drug to reverse CP resistance for ovarian cancer treatment. We further tested the underlying mechanisms of DCA to restore CP sensitivity in ovarian cancer. We found that CP treatment promoted reactive oxygen species (ROS) production to induce cell death in CP-sensitive ovarian cancer. However, CP-resistant ovarian cancer cells exhibited higher basal levels of ROS compared with sensitive cancer cells, and CP treatment failed to generate ROS production. That means ovarian cancer cells steadily adapted to elevated ROS levels, then becoming ROS-adapted ovarian cancer cells to survive. Interestingly, DCA treatment results in the buildup of ROS production, causing cell death in CP-resistant ovarian cancer. Therefore, our study suggests that ROS production can be an attractive target in DCA treatment to restore CP sensitivity in ovarian cancer. Citation Format: Yen Thi Do, Seungmee Lee, Changmin Shin, Hyewon Chung, Jin Young Kim, Eunyoung Ha, Sojin Shin, Ji Hae Seo. Dichloroacetate reverses cisplatin resistance in ovarian cancer through promoting ROS production [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7155.

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Oh, Jin-Mi, Yun-Kyoung Ryu, Jong-Seok Lim, and Eun-Yi Moon. "Hypoxia Induces Paclitaxel-Resistance through ROS Production." Biomolecules and Therapeutics 18, no. 2 (April 30, 2010): 145–51. http://dx.doi.org/10.4062/biomolther.2010.18.2.145.

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45

Schluterman, Marie K., Shelby L. Chapman, Grzegorz Korpanty, Hiromi Yanagisawa, and Rolf A. Brekken. "Fibulin-5 inhibits integrin-induced ROS production." Matrix Biology 27 (December 2008): 11. http://dx.doi.org/10.1016/j.matbio.2008.09.224.

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46

Conti, L., E. O Donnel, J. Price, A. Love, P. Dominy, and A. Sadanandom. "SUMO proteases regulate ROS production in Arabidopsis." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 146, no. 4 (April 2007): S260. http://dx.doi.org/10.1016/j.cbpa.2007.01.656.

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47

Hoffmann, Sheila, Marta Orlando, Ewa Andrzejak, Christine Bruns, Thorsten Trimbuch, Christian Rosenmund, Craig C. Garner, and Frauke Ackermann. "Light-Activated ROS Production Induces Synaptic Autophagy." Journal of Neuroscience 39, no. 12 (January 17, 2019): 2163–83. http://dx.doi.org/10.1523/jneurosci.1317-18.2019.

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48

Medvedev, Roman Y., Daniel G. P. Turner, Brock W. Thompson, and Alexey V. Glukhov. "Sphingomyelinase-induced ROS production suppresses cardiac performance." Biophysical Journal 123, no. 3 (February 2024): 386a. http://dx.doi.org/10.1016/j.bpj.2023.11.2348.

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49

Bashan, Nava, Julia Kovsan, Ilana Kachko, Hilla Ovadia, and Assaf Rudich. "Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species." Physiological Reviews 89, no. 1 (January 2009): 27–71. http://dx.doi.org/10.1152/physrev.00014.2008.

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Regulated production of reactive oxygen species (ROS)/reactive nitrogen species (RNS) adequately balanced by antioxidant systems is a prerequisite for the participation of these active substances in physiological processes, including insulin action. Yet, increasing evidence implicates ROS and RNS as negative regulators of insulin signaling, rendering them putative mediators in the development of insulin resistance, a common endocrine abnormality that accompanies obesity and is a risk factor of type 2 diabetes. This review deals with this dual, seemingly contradictory, function of ROS and RNS in regulating insulin action: the major processes for ROS and RNS generation and detoxification are presented, and a critical review of the evidence that they participate in the positive and negative regulation of insulin action is provided. The cellular and molecular mechanisms by which ROS and RNS are thought to participate in normal insulin action and in the induction of insulin resistance are then described. Finally, we explore the potential usefulness and the challenges in modulating the oxidant-antioxidant balance as a potentially promising, but currently disappointing, means of improving insulin action in insulin resistance-associated conditions, leading causes of human morbidity and mortality of our era.

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Feagins, Linda A., Hui Ying Zhang, Xi Zhang, Kathy Hormi-Carver, Tojo Thomas, Lance S. Terada, Stuart J. Spechler, and Rhonda F. Souza. "Mechanisms of oxidant production in esophageal squamous cell and Barrett's cell lines." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (February 2008): G411—G417. http://dx.doi.org/10.1152/ajpgi.00373.2007.

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We hypothesized that differences among individuals in reflux-induced oxidant production by esophageal squamous epithelial cells might contribute to the development of Barrett's esophagus. We studied the effects of acid and bile acids on the production of reactive oxygen species (ROS) in esophageal squamous cell lines derived from gastroesophageal reflux disease patients with (NES-B3T) and without (NES-G2T) Barrett's esophagus and in a Barrett's epithelial cell line (BAR-T). Cells were incubated with an ROS-sensitive probe and exposed to acidic medium, neutral bile acid medium, or acidic bile acid medium. ROS were quantified in the presence and absence of diphenyleneiodonium chloride (DPI, an NADPH oxidase inhibitor), NG-monomethyl-l-arginine (l-NMMA, a nitric oxide synthase inhibitor), and rotenone (a mitochondrial electron transport chain inhibitor). Acidic bile acid medium induced ROS production in both squamous cell lines; however, only DPI blocked ROS production by NES-B3T cells, whereas both DPI and l-NMMA blocked ROS production by NES-G2T cells. In BAR-T cells, acidic medium and acidic bile acid medium induced the production of ROS; l-NMMA prevented ROS production after exposure to acidic medium, whereas ROS production induced by acidic bile acid medium was blocked by DPI. These studies demonstrate that there are differences between esophageal squamous cells and Barrett's epithelial cells and between esophageal squamous cells from gastroesophageal reflux disease patients with and without Barrett's esophagus in the mechanisms of oxidant production induced by exposure to acid and bile acids.

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