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Journal articles on the topic 'Endogenous ROS'

Author: Grafiati

Published: 6 September 2023

Last updated: 31 July 2025

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1

Supruniuk, Elżbieta, Jan Górski, and Adrian Chabowski. "Endogenous and Exogenous Antioxidants in Skeletal Muscle Fatigue Development during Exercise." Antioxidants 12, no. 2 (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 oth

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2

Lu, Qing-Bin. "Reaction Cycles of Halogen Species in the Immune Defense: Implications for Human Health and Diseases and the Pathology and Treatment of COVID-19." Cells 9, no. 6 (2020): 1461. http://dx.doi.org/10.3390/cells9061461.

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There is no vaccine or specific antiviral treatment for COVID-19, which is causing a global pandemic. One current focus is drug repurposing research, but those drugs have limited therapeutic efficacies and known adverse effects. The pathology of COVID-19 is essentially unknown. Without this understanding, it is challenging to discover a successful treatment to be approved for clinical use. This paper addresses several key biological processes of reactive oxygen, halogen and nitrogen species (ROS, RHS and RNS) that play crucial physiological roles in organisms from plants to humans. These inclu

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Sharma, Ajay Kumar, Harshit Singh, and Harinath Chakrapani. "Photocontrolled endogenous reactive oxygen species (ROS) generation." Chemical Communications 55, no. 36 (2019): 5259–62. http://dx.doi.org/10.1039/c9cc01747j.

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4

Pan, Zhixiang, Jun Zhang, Kaili Ji, Vayou Chittavong, Xingyue Ji, and Binghe Wang. "Organic CO Prodrugs Activated by Endogenous ROS." Organic Letters 20, no. 1 (2017): 8–11. http://dx.doi.org/10.1021/acs.orglett.7b02775.

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5

Hole, Paul S., Lorna Pearn, Amanda J. Tonks, et al. "Ras-induced reactive oxygen species promote growth factor–independent proliferation in human CD34+ hematopoietic progenitor cells." Blood 115, no. 6 (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

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6

Federico, Cacciapuoti. "Oxidative Stress as "Mother" of Many Human Diseases at Strong Clinical Impact." Journal of Cardiovascular Medicine and Cardiology 3, no. 1 (2016): 001–6. https://doi.org/10.17352/2455-2976.000020.

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Likewise the 1991 Gulf War, known as a “mother of all battles”, oxidative stress (OS) can be considered as a “mother” of many human diseases life threatening. OS is a condition in which oxidation exceeds the anti-oxidant reactions, causing an imbalance between oxidative and anti-oxidant systems, with prevalence of reactive oxygen species ROS [1-5]. These include: peroxide, superoxide, hydroxyl radical, singlet oxygen and others. Under normal conditions ROS are maintained at physiological levels by several endogenous antioxidant systems, as superoxide dismutase, catalase

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7

HALVEY, Patrick J., Walter H. WATSON, Jason M. HANSEN, Young-Mi GO, Afshin SAMALI, and Dean P. JONES. "Compartmental oxidation of thiol–disulphide redox couples during epidermal growth factor signalling." Biochemical Journal 386, no. 2 (2005): 215–19. http://dx.doi.org/10.1042/bj20041829.

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Exogenously added ROS (reactive oxygen species) cause generalized oxidation of cellular components, whereas endogenously generated ROS induced by physiological stimuli activate discrete signal transduction pathways. Compartmentation is an important aspect of such pathways, but little is known about its role in redox signalling. We measured the redox states of cytosolic and nuclear Trx1 (thioredoxin-1) and mitochondrial Trx2 (thioredoxin-2) using redox Western blot methodologies during endogenous ROS production induced by EGF (epidermal growth factor) signalling. The glutathione redox state was

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Koval, M., S. T. Geist, E. M. Westphale, et al. "Transfected connexin45 alters gap junction permeability in cells expressing endogenous connexin43." Journal of Cell Biology 130, no. 4 (1995): 987–95. http://dx.doi.org/10.1083/jcb.130.4.987.

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Many cells express multiple connexins, the gap junction proteins that interconnect the cytosol of adjacent cells. Connexin43 (Cx43) channels allow intercellular transfer of Lucifer Yellow (LY, MW = 443 D), while connexin45 (Cx45) channels do not. We transfected full-length or truncated chicken Cx45 into a rat osteosarcoma cell line ROS-17/2.8, which expresses endogenous Cx43. Both forms of Cx45 were expressed at high levels and colocalized with Cx43 at plasma membrane junctions. Cells transfected with full-length Cx45 (ROS/Cx45) and cells transfected with Cx45 missing the 37 carboxyl-terminal

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9

Sarniak, Agata, Joanna Lipińska, Karol Tytman, and Stanisława Lipińska. "Endogenous mechanisms of reactive oxygen species (ROS) generation." Postępy Higieny i Medycyny Doświadczalnej 70 (November 14, 2016): 1150–65. http://dx.doi.org/10.5604/17322693.1224259.

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10

Wu, Jiaye, Yue Zhang, Ruizhi Hao, Yuan Cao, Xiaoyi Shan, and Yanping Jing. "Nitric Oxide Enhances Cytotoxicity of Lead by Modulating the Generation of Reactive Oxygen Species and Is Involved in the Regulation of Pb2+ and Ca2+ Fluxes in Tobacco BY-2 Cells." Plants 8, no. 10 (2019): 403. http://dx.doi.org/10.3390/plants8100403.

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Lead is a heavy metal known to be toxic to both animals and plants. Nitric oxide (NO) was reported to participate in plant responses to different heavy metal stresses. In this study, we analyzed the function of exogenous and endogenous NO in Pb-induced toxicity in tobacco BY-2 cells, focusing on the role of NO in the generation of reactive oxygen species (ROS) as well as Pb2+ and Ca2+ fluxes using non-invasive micro-test technology (NMT). Pb treatment induced BY-2 cell death and rapid NO and ROS generation, while NO burst occurred earlier than ROS accumulation. The elimination of NO by 2-4-car

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11

Fitzgerald, Phillip, Daniel Beury, and Suzanne Ostrand-Rosenberg. "Glutathione S-transferases as regulators of tumor-induced myeloid-derived suppressor cell survival (66.38)." Journal of Immunology 186, no. 1_Supplement (2011): 66.38. http://dx.doi.org/10.4049/jimmunol.186.supp.66.38.

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Abstract Tumor-induced myeloid-derived suppressor cells (MDSC) are a major barrier to tumor immunotherapy because they inhibit T-cell anti-tumor immunity through various mechanisms, including cystine sequestration and production of reactive oxygen species (ROS). MDSC accumulation, suppressive potency, and survival are driven by inflammation, which also increases MDSC production of ROS. Surprisingly, ROS do not adversely affect MDSC, suggesting that MDSC neutralize endogenous ROS. Because MDSC survival is likely to be controlled by the mechanisms that protect them against endogenous ROS, we are

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Kobayashi, Daisuke, Kei Kondo, Nobuyuki Uehara, et al. "Endogenous Reactive Oxygen Species Is an Important Mediator of Miconazole Antifungal Effect." Antimicrobial Agents and Chemotherapy 46, no. 10 (2002): 3113–17. http://dx.doi.org/10.1128/aac.46.10.3113-3117.2002.

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ABSTRACT We investigated the significance of endogenous reactive oxygen species (ROS) produced by fungi treated with miconazole. ROS production in Candida albicans was measured by a real-time fluorogenic assay. The level of ROS production was increased by miconazole at the MIC (0.125 μg/ml) and was enhanced further in a dose-dependent manner, with a fourfold increase detected when miconazole was used at 12.5 μg/ml. This increase in the level of ROS production was completely inhibited by pyrrolidinedithiocarbamate (PDTC), an antioxidant, at 10 μM. In a colony formation assay, the decrease in ce

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13

Leuti, Alessandro, Mauro Maccarrone, and Valerio Chiurchiù. "Proresolving Lipid Mediators: Endogenous Modulators of Oxidative Stress." Oxidative Medicine and Cellular Longevity 2019 (June 18, 2019): 1–12. http://dx.doi.org/10.1155/2019/8107265.

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Specialized proresolving mediators (SPMs) are a novel class of endogenous lipids, derived byω-6 andω-3 essential polyunsaturated fatty acids such as arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) that trigger and orchestrate the resolution of inflammation, which is the series of cellular and molecular events that leads to spontaneous regression of inflammatory processes and restoring of tissue homeostasis. These lipids are emerging as highly effective therapeutic agents that exert their immunoregulatory activity by activating the proresolving pathway, as rep

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Chen, Billy T., Marat V. Avshalumov, and Margaret E. Rice. "H2O2 Is a Novel, Endogenous Modulator of Synaptic Dopamine Release." Journal of Neurophysiology 85, no. 6 (2001): 2468–76. http://dx.doi.org/10.1152/jn.2001.85.6.2468.

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Recent evidence suggests that reactive oxygen species (ROS) might act as modulators of neuronal processes, including synaptic transmission. Here we report that synaptic dopamine (DA) release can be modulated by an endogenous ROS, H2O2. Electrically stimulated DA release was monitored in guinea pig striatal slices using carbon-fiber microelectrodes with fast-scan cyclic voltammetry. Exogenously applied H2O2reversibly inhibited evoked release in the presence of 1.5 mM Ca2+. The effectiveness of exogenous H2O2, however, was abolished or decreased by conditions that enhance Ca2+ entry, including i

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15

Xu, Jin-Wei, Chen-Chung Liao, Ke-Chang Hung, Zhong-Yao Wang, Yu-Tang Tung, and Jyh-Horng Wu. "Proteomics Reveals Octyl Gallate as an Environmentally Friendly Wood Preservative Leading to Reactive Oxygen Species-Driven Metabolic Inflexibility and Growth Inhibition in White-Rot Fungi (Lenzites betulina and Trametes versicolor)." Journal of Fungi 7, no. 2 (2021): 145. http://dx.doi.org/10.3390/jof7020145.

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The most commonly applied wood preservatives are based on creosote, pentachlorophenol, and waterborne chromate copper arsenate, which negatively affect the environment. Thus, environmentally friendly wood preservatives are required. This study investigated the antifungal activity and mechanism of several long-chain alkyl gallates (3,4,5-trihydroxybenzoates) against white-rot fungi, Lenzites betulina and Trametes versicolor. The results revealed that octyl gallate (OG) had the best antifungal activity. Additionally, OG may have a mechanism of action similar to surfactants and inhibit ATPase act

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16

Berdiaki, Aikaterini, Monica Neagu, Ioanna Spyridaki, Andrey Kuskov, Serge Perez, and Dragana Nikitovic. "Hyaluronan and Reactive Oxygen Species Signaling—Novel Cues from the Matrix?" Antioxidants 12, no. 4 (2023): 824. http://dx.doi.org/10.3390/antiox12040824.

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Hyaluronan (HA) is a naturally occurring non-sulfated glycosaminoglycan (GAG) localized to the cell surface and the tissue extracellular matrix (ECM). It is composed of disaccharides containing glucuronic acid and N-acetylglucosamine, is synthesized by the HA synthase (HAS) enzymes and is degraded by hyaluronidase (HYAL) or reactive oxygen and nitrogen species (ROS/RNS) actions. HA is deposited as a high molecular weight (HMW) polymer and degraded to low molecular weight (LMW) fragments and oligosaccharides. HA affects biological functions by interacting with HA-binding proteins (hyaladherins)

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17

Reid, Michael B. "Invited Review: Redox modulation of skeletal muscle contraction: what we know and what we don't." Journal of Applied Physiology 90, no. 2 (2001): 724–31. http://dx.doi.org/10.1152/jappl.2001.90.2.724.

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Over the past decade, reactive oxygen species (ROS) and nitric oxide (NO) derivatives have been established as physiological modulators of skeletal muscle function. This mini-review addresses the roles of these molecules as endogenous regulators of muscle contraction. The article is organized in two parts. First, established concepts are briefly outlined. This section provides an overview of ROS production by muscle, antioxidant buffers that oppose ROS effects, enzymatic synthesis of NO in muscle, the effects of endogenous ROS on contractile function, and NO as a contractile modulator. Second,

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18

Katiyar, Sanjay, Mathew C. Casimiro, Luis Dettin, et al. "C-junInhibits Mammary Apoptosis In Vivo." Molecular Biology of the Cell 21, no. 23 (2010): 4264–74. http://dx.doi.org/10.1091/mbc.e10-08-0705.

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c-jun, which is overexpressed in a number of human cancers encodes a critical component of the AP-1 complex. c-jun has been shown to either induce or inhibit cellular apoptosis. Germ line deletion of both c-jun alleles is embryonically lethal. To determine the role of the endogenous c-jun gene in apoptosis, we performed mammary epithelial cell–targeted somatic deletion using floxed c-jun (c-junf/f) conditional knockout mice. Laser capture microdissection demonstrated endogenous c-jun inhibits expression of apoptosis inducing genes and reactive oxygen species (ROS)-reducing genes (MnSOD, catala

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19

Uchikura, Keiichiro, Tatehiko Wada, Sumito Hoshino, et al. "Lipopolysaccharides induced increases in Fas ligand expression by Kupffer cells via mechanisms dependent on reactive oxygen species." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 3 (2004): G620—G626. http://dx.doi.org/10.1152/ajpgi.00314.2003.

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Fas-Fas ligand (FasL)-dependent pathways exert a suppressive effect on inflammatory responses in immune-privileged organs. FasL expression in hepatic Kupffer cells (KC) has been implicated in hepatic immunoregulation. In this study, modulation of FasL expression of KC by endogenous gut-derived bacterial LPS and the role of reactive oxygen species (ROS) as potential mediators of FasL expression in KC were investigated. LPS stimulation of KC resulted in upstream ROS generation and, subsequently, increased FasL expression and consequent Jurkat cell (Fas-positive) apoptosis. The NADPH oxidase and

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20

Syed, Ismail, Chandrashekara N. Kyathanahalli, and Anjaneyulu Kowluru. "Phagocyte-like NADPH oxidase generates ROS in INS 832/13 cells and rat islets: role of protein prenylation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 3 (2011): R756—R762. http://dx.doi.org/10.1152/ajpregu.00786.2010.

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Recent evidence suggests that an acute increase in the generation of phagocyte-like NADPH-oxidase (Nox)-mediated reactive oxygen species (ROS) may be necessary for glucose-stimulated insulin secretion. Using rat islets and INS 832/13 cells, we tested the hypothesis that activation of specific G proteins is necessary for nutrient-mediated intracellular generation of ROS. Stimulation of β-cells with glucose or a mixture of mitochondrial fuels (mono-methylsuccinate plus α-ketoisocaproic acid) markedly elevated intracellular accumulation of ROS, which was attenuated by selective inhibitors of Nox

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21

Yan, Ying, Fei Tong, and Jianer Chen. "Endogenous BMP-4/ROS/COX-2 Mediated IPC and Resveratrol Alleviated Brain Damage." Current Pharmaceutical Design 25, no. 9 (2019): 1030–39. http://dx.doi.org/10.2174/1381612825666190506120611.

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The objective of the study was to examine the therapeutic role of combined ischemic preconditioning (IPC) and resveratrol (RES) on brain ischemia/reperfusion injury (BI/RI) by modulating endogenous bone morphogenetic protein-4 (BMP-4)/reactive oxygen species (ROS)/cyclooxygenase-2 (COX-2) in rats. Sprague Dawley (SD) rats were pretreated with 20 mg/kg RES (20 mg/kg RES was administered once a day via intraperitoneal injection 7 days prior to the I/R procedure) and IPC (equal volumes of saline were administered once a day by intraperitoneal injection over 7 days, and the bilateral common caroti

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Shohami, Esther, Elie Beit-Yannai, Michal Horowitz, and Ron Kohen. "Oxidative Stress in Closed-Head Injury: Brain Antioxidant Capacity as an Indicator of Functional Outcome." Journal of Cerebral Blood Flow & Metabolism 17, no. 10 (1997): 1007–19. http://dx.doi.org/10.1097/00004647-199710000-00002.

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It has been suggested that reactive oxygen species (ROS) play a role in the pathophysiology of brain damage. A number of therapeutic approaches, based on scavenging these radicals, have been attempted both in experimental models and in the clinical setting. In an experimental rat and mouse model of closed-head injury (CHI), we have studied the total tissue nonenzymatic antioxidant capacity to combat ROS. A major mechanism for neutralizing ROS uses endogenous low-molecular weight antioxidants (LMWA). This review deals with the source and nature of ROS in the brain, along with the endogenous def

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Olla, Stefania, Chiara Siguri, Antonella Fais, Benedetta Era, Massimo Claudio Fantini, and Amalia Di Petrillo. "Inhibitory Effect of Quercetin on Oxidative Endogen Enzymes: A Focus on Putative Binding Modes." International Journal of Molecular Sciences 24, no. 20 (2023): 15391. http://dx.doi.org/10.3390/ijms242015391.

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Oxidative stress is defined as an imbalance between the production of free radicals and reactive oxygen species (ROS) and the ability of the body to neutralize them by anti-oxidant defense systems. Cells can produce ROS during physiological processes, but excessive ROS can lead to non-specific and irreversible damage to biological molecules, such as DNA, lipids, and proteins. Mitochondria mainly produce endogenous ROS during both physiological and pathological conditions. Enzymes like nicotinamide adenine dinucleotide phosphate oxidase (NOX), xanthine oxidase (XO), lipoxygenase (LOX), myeloper

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Hamitouche, Fella, Jean Armengaud, Luc Dedieu, and Catherine Duport. "Cysteine Proteome Reveals Response to Endogenous Oxidative Stress in Bacillus cereus." International Journal of Molecular Sciences 22, no. 14 (2021): 7550. http://dx.doi.org/10.3390/ijms22147550.

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At the end of exponential growth, aerobic bacteria have to cope with the accumulation of endogenous reactive oxygen species (ROS). One of the main targets of these ROS is cysteine residues in proteins. This study uses liquid chromatography coupled to high-resolution tandem mass spectrometry to detect significant changes in protein abundance and thiol status for cysteine-containing proteins from Bacillus cereus during aerobic exponential growth. The proteomic profiles of cultures at early-, middle-, and late-exponential growth phases reveals that (i) enrichment in proteins dedicated to fighting

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Berndt, Carsten, Christopher Horst Lillig, and Arne Holmgren. "Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: implications for diseases in the cardiovascular system." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 3 (2007): H1227—H1236. http://dx.doi.org/10.1152/ajpheart.01162.2006.

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Reactive oxygen species (ROS) and the cellular thiol redox state are crucial mediators of multiple cell processes like growth, differentiation, and apoptosis. Excessive ROS production or oxidative stress is associated with several diseases, including cardiovascular disorders like ischemia-reperfusion. To prevent ROS-induced disorders, the heart is equipped with effective antioxidant systems. Key players in defense against oxidative stress are members of the thioredoxin-fold family of proteins. Of these, thioredoxins and glutaredoxins maintain a reduced intracellular redox state in mammalian ce

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Paladino, Simona, Andrea Conte, Rocco Caggiano, Giovanna Maria Pierantoni, and Raffaella Faraonio. "Nrf2 Pathway in Age-Related Neurological Disorders: Insights into MicroRNAs." Cellular Physiology and Biochemistry 47, no. 5 (2018): 1951–76. http://dx.doi.org/10.1159/000491465.

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A general hallmark of neurological diseases is the loss of redox homeostasis that triggers oxidative damages to biomolecules compromising neuronal function. Under physiological conditions the steady-state concentrations of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are finely regulated for proper cellular functions. Reduced surveillance of endogenous antioxidant defenses and/or increased ROS/RNS production leads to oxidative stress with consequent alteration of physiological processes. Neuronal cells are particularly susceptible to ROS/RNS due to their biochemical compos

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Laurent, Alexis, Carole Nicco, Christiane Chéreau, et al. "Controlling Tumor Growth by Modulating Endogenous Production of Reactive Oxygen Species." Cancer Research 65, no. 3 (2005): 948–56. http://dx.doi.org/10.1158/0008-5472.948.65.3.

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Abstract Paradoxically, reactive oxygen species (ROS) can promote normal cellular proliferation and carcinogenesis, and can also induce apoptosis of tumor cells. In this report, we study the contribution of ROS to various cellular signals depending on the nature and the level of ROS produced. In nontransformed NIH 3T3 cells, ROS are at low levels and originate from NADPH oxidase. Hydrogen peroxide (H2O2), controlled by the glutathione system, is pivotal for the modulation of normal cell proliferation. In CT26 (colon) and Hepa 1-6 (liver) tumor cells, high levels of ROS, close to the threshold

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Stieg, David C., Yifang Wang, Ling-Zhi Liu, and Bing-Hua Jiang. "ROS and miRNA Dysregulation in Ovarian Cancer Development, Angiogenesis and Therapeutic Resistance." International Journal of Molecular Sciences 23, no. 12 (2022): 6702. http://dx.doi.org/10.3390/ijms23126702.

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The diverse repertoires of cellular mechanisms that progress certain cancer types are being uncovered by recent research and leading to more effective treatment options. Ovarian cancer (OC) is among the most difficult cancers to treat. OC has limited treatment options, especially for patients diagnosed with late-stage OC. The dysregulation of miRNAs in OC plays a significant role in tumorigenesis through the alteration of a multitude of molecular processes. The development of OC can also be due to the utilization of endogenously derived reactive oxygen species (ROS) by activating signaling pat

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Tang, Chunchao, Yuqi Gao, Tingting Liu, et al. "Bioluminescent probe for detecting endogenous hypochlorite in living mice." Organic & Biomolecular Chemistry 16, no. 4 (2018): 645–51. http://dx.doi.org/10.1039/c7ob02842c.

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Hörandl, Elvira, and Dave Speijer. "How oxygen gave rise to eukaryotic sex." Proceedings of the Royal Society B: Biological Sciences 285, no. 1872 (2018): 20172706. http://dx.doi.org/10.1098/rspb.2017.2706.

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How did full meiotic eukaryotic sex evolve and what was the immediate advantage allowing it to develop? We propose that the crucial determinant can be found in internal reactive oxygen species (ROS) formation at the start of eukaryotic evolution approximately 2 × 10 9 years ago. The large amount of ROS coming from a bacterial endosymbiont gave rise to DNA damage and vast increases in host genome mutation rates. Eukaryogenesis and chromosome evolution represent adaptations to oxidative stress. The host, an archaeon, most probably already had repair mechanisms based on DNA pairing and recombinat

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Satrialdi, Cellina Pratiwi, Ryan Novia Khaeranny, and Diky Mudhakir. "The development of mitochondria-targeted quercetin for rescuing Sertoli cells from oxidative stress." Research in Pharmaceutical Sciences 20, no. 1 (2025): 109–20. https://doi.org/10.4103/rps.rps_226_23.

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Background and purpose: The imbalance between reactive oxygen species (ROS) production and endogenous antioxidant capacity leads to oxidative stress, which may damage several cellular functions, particularly spermatogenesis. This condition is a leading cause of male infertility, so controlling ROS levels is crucial. The ROS level can be controlled by supporting the endogenous antioxidant system through antioxidant therapy. Mitochondria are the prime target for antioxidant therapy due to the majority of endogenous ROS produced in mitochondria and their critical role in providing energy during f

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Garlid, Anders O., Martin Jaburek, Jeremy P. Jacobs, and Keith D. Garlid. "Mitochondrial reactive oxygen species: which ROS signals cardioprotection?" American Journal of Physiology-Heart and Circulatory Physiology 305, no. 7 (2013): H960—H968. http://dx.doi.org/10.1152/ajpheart.00858.2012.

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Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa AD, Garlid KD. Am J Physiol Heart Circ Physiol 295, H874–H882, 2008). The ROS responsible for this effect is not known. The present study focuses on superoxide (O2·−), hydrogen peroxide (H2O2), and hydroxyl r

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Feinendegen, L. E. "Reactive oxygen species in cell responses to toxic agents." Human & Experimental Toxicology 21, no. 2 (2002): 85–90. http://dx.doi.org/10.1191/0960327102ht216oa.

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This review first summarizes experimental data on biological effects of different concentrations of ROS in mammalian cells and on their potential role in modifying cell responses to toxic agents. It then attempts to link the role of steadily produced metabolic ROS at various concentrations in mammalian cells to that of environmentally derived ROS bursts from exposure to ionizing radiation. The ROS from both sources are known to both cause biological damage and change cellular signaling, depending on their concentration at a given time. At low concentrations signaling effects of ROS appear to p

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Sharma, Anmol, Pawan Gupta, and Pranav Kumar Prabhakar. "Endogenous Repair System of Oxidative Damage of DNA." Current Chemical Biology 13, no. 2 (2019): 110–19. http://dx.doi.org/10.2174/2212796813666190221152908.

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DNA is one of the most important biomolecules of living cells which carries genetic information from generation to generation. Many endogenous and exogenous agents may disrupt the structure of DNA. Change in the cellular genome can lead to errors in replication, transcription and in protein synthesis. DNA damage occurs naturally or result from a metabolic and hydrolytic process which release some very active chemical entities like free radicals, Reactive Oxygen Species (ROS), Reactive Nitrogen Intermediate (RNI), Reactive Carbonyl Species (RCS), lipid peroxidation products and alkylating agent

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Brynildsen, Mark P., Jonathan A. Winkler, Catherine S. Spina, I. Cody MacDonald, and James J. Collins. "Potentiating antibacterial activity by predictably enhancing endogenous microbial ROS production." Nature Biotechnology 31, no. 2 (2013): 160–65. http://dx.doi.org/10.1038/nbt.2458.

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Das, Laxmidhar, та Manjula Vinayak. "Anti-carcinogenic action of curcumin by activation of antioxidant defence system and inhibition of NF-κB signalling in lymphoma-bearing mice". Bioscience Reports 32, № 2 (2011): 161–70. http://dx.doi.org/10.1042/bsr20110043.

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NF-κB (nuclear factor κB) plays a significant role in inflammation, immunity, cell proliferation, apoptosis and malignancy. ROS (reactive oxygen species) are among the most important regulating factors of NF-κB. Intracellular ROS are mainly regulated by an endogenous antioxidant defence system. Any disruption of redox balance leads to oxidative stress, which causes a number of pathological conditions including inflammation and malignancy. Increased metabolic activity in cancerous cells leads to oxidative stress, which is further enhanced due to depletion of the endogenous antioxidant defence s

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Airik, Merlin, Haley Arbore, Elizabeth Childs, et al. "Mitochondrial ROS Triggers KIN Pathogenesis in FAN1-Deficient Kidneys." Antioxidants 12, no. 4 (2023): 900. http://dx.doi.org/10.3390/antiox12040900.

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Karyomegalic interstitial nephritis (KIN) is a genetic adult-onset chronic kidney disease (CKD) characterized by genomic instability and mitotic abnormalities in the tubular epithelial cells. KIN is caused by recessive mutations in the FAN1 DNA repair enzyme. However, the endogenous source of DNA damage in FAN1/KIN kidneys has not been identified. Here we show, using FAN1-deficient human renal tubular epithelial cells (hRTECs) and FAN1-null mice as a model of KIN, that FAN1 kidney pathophysiology is triggered by hypersensitivity to endogenous reactive oxygen species (ROS), which cause chronic

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Gregnani, Marcos Fernandes, Leonardo Martins, and Wieslawa Agnieszka Fogel. "Mechanistic Insights into the Interaction Between Kinin Receptors and Histamine H2 Receptor Pathways in Oxidative Stress." Receptors 3, no. 4 (2024): 513–37. http://dx.doi.org/10.3390/receptors3040026.

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Reactive oxygen species (ROS) encompass various molecular oxygen derivatives naturally produced during aerobic metabolism, including superoxide anions, hydrogen peroxide, and hydroxyl radicals. Excessive ROS production leads to oxidative distress, causing cellular damage and contributing to various pathologies, often alongside inflammation. Endogenous sources of ROS include mitochondrial activity and NADPH oxidases. The antioxidant system, comprising enzymes such as superoxide dismutase, peroxiredoxin, and catalase, mitigates ROS-induced damage. This review explores the regulation of ROS by me

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Aranda-Rivera, Ana Karina, Alfredo Cruz-Gregorio, Yalith Lyzet Arancibia-Hernández, Estefani Yaquelin Hernández-Cruz, and José Pedraza-Chaverri. "RONS and Oxidative Stress: An Overview of Basic Concepts." Oxygen 2, no. 4 (2022): 437–78. http://dx.doi.org/10.3390/oxygen2040030.

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Oxidative stress (OS) has greatly interested the research community in understanding damaging processes occurring in cells. OS is triggered by an imbalance between reactive oxygen species (ROS) production and their elimination by the antioxidant system; however, ROS function as second messengers under physiological conditions. ROS are produced from endogenous and exogenous sources. Endogenous sources involve mitochondria, nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), oxidases (NOXs), endoplasmic reticulum (ER), xanthine oxidases (XO), endothelial nitric oxide synthase (eNOs), a

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Chkadua, Gvanca, Eka Nozadze, Leila Tsakadze, et al. "THE EFFECT OF IONIZING RADIATION ON HIPPOCAMPAL NA,K-ATPASE ACTIVITY." Radiobiology and Radiation Safety 5, no. 6 (2025): 5–13. https://doi.org/10.63465/rrs520258976.

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Ionizing radiation (IR) exposure initiates the rapid generation of reactive oxygen species (ROS), leading to oxidative stress and cellular damage. While ROS serve as critical signaling molecules under physiological conditions, excessive levels can disrupt membrane integrity via lipid peroxidation and impair membrane-bound enzymes such as Na⁺,K⁺-ATPase. In this context, our study investigates the dual effect of IR-induced ROS and endogenous ouabain on Na⁺,K⁺-ATPase activity. We demonstrate that different doses of IR (1 Gy and 5 Gy) initially enhance enzyme activity through reversible redox modi

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Tam, Beatrice M., Orson L. Moritz, Lawrence B. Hurd, and David S. Papermaster. "Identification of an Outer Segment Targeting Signal in the Cooh Terminus of Rhodopsin Using Transgenic Xenopus laevis." Journal of Cell Biology 151, no. 7 (2000): 1369–80. http://dx.doi.org/10.1083/jcb.151.7.1369.

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Mislocalization of the photopigment rhodopsin may be involved in the pathology of certain inherited retinal degenerative diseases. Here, we have elucidated rhodopsin's targeting signal which is responsible for its polarized distribution to the rod outer segment (ROS). Various green fluorescent protein (GFP)/rhodopsin COOH-terminal fusion proteins were expressed specifically in the major red rod photoreceptors of transgenic Xenopus laevis under the control of the Xenopus opsin promoter. The fusion proteins were targeted to membranes via lipid modifications (palmitoylation and myristoylation) as

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Jimenez-Moreno, Natalia, and Jon D. Lane. "Autophagy and Redox Homeostasis in Parkinson’s: A Crucial Balancing Act." Oxidative Medicine and Cellular Longevity 2020 (November 10, 2020): 1–38. http://dx.doi.org/10.1155/2020/8865611.

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated primarily from endogenous biochemical reactions in mitochondria, endoplasmic reticulum (ER), and peroxisomes. Typically, ROS/RNS correlate with oxidative damage and cell death; however, free radicals are also crucial for normal cellular functions, including supporting neuronal homeostasis. ROS/RNS levels influence and are influenced by antioxidant systems, including the catabolic autophagy pathways. Autophagy is an intracellular lysosomal degradation process by which invasive, damaged, or redundant cytoplasmic comp

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Sallmyr, Annahita, Jinshui Fan, Kamal Datta, et al. "Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML." Blood 111, no. 6 (2008): 3173–82. http://dx.doi.org/10.1182/blood-2007-05-092510.

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Abstract Activating mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor occur in approximately 30% of acute myeloid leukemia (AML) patients and, at least for internal tandem duplication (ITD) mutations, are associated with poor prognosis. FLT3 mutations trigger downstream signaling pathways including RAS-MAP/AKT kinases and signal transducer and activator of transcription-5 (STAT5). We find that FLT3/ITD mutations start a cycle of genomic instability whereby increased reactive oxygen species (ROS) production leads to increased DNA double-strand breaks (DSBs) and repair errors that may

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Parfenova, Helena, Charles W. Leffler, Shyamali Basuroy, Jianxiong Liu, and Alexander L. Fedinec. "Antioxidant Roles of Heme Oxygenase, Carbon Monoxide, and Bilirubin in Cerebral Circulation during Seizures." Journal of Cerebral Blood Flow & Metabolism 32, no. 6 (2012): 1024–34. http://dx.doi.org/10.1038/jcbfm.2012.13.

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Postictal cerebrovascular dysfunction is an adverse effect of seizures in newborn piglets. The brain heme oxygenase (HO) provides protection against cerebrovascular dysfunction. We investigated the contribution of reactive oxygen species (ROS) to seizure-induced vascular damage and the mechanism of HO vasoprotection. In a bicuculline model of seizures, we addressed the hypotheses: (1) seizures increase brain ROS; (2) ROS contribute to cerebral vascular dysfunction; (3) ROS initiate a vasoprotective mechanisms by activating endogenous HO; and (4) HO products have antioxidant properties. As asse

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Hikmah, Febrial. "The Role of Reactive Oxygen Species (ROS) in Cancer Stem Cells." Jurnal Kedokteran YARSI 29, no. 3 (2022): 120–34. http://dx.doi.org/10.33476/jky.v29i3.1270.

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Reactive Oxygen Species (ROS) are aerobic metabolic byproducts, mainly produced by mitochondria. Most types of cancer contain high amounts of ROS. An increase in endogenous ROS triggers adaptive changes, induces oxidative stress and cytotoxic. Oxidative stress can lead to cancer. But on the other hand, the radiotherapy treatment method induces the formation of ROS in the process of cell death. Resistance therapy in cancer cells is associated with high antioxidant enzymes that neutralize ROS in cancer cells. In addition, therapeutic resistance and recurrence are also associated with the presenc

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Castelli, Serena, Pamela De Falco, Fabio Ciccarone, Enrico Desideri, and Maria Rosa Ciriolo. "Lipid Catabolism and ROS in Cancer: A Bidirectional Liaison." Cancers 13, no. 21 (2021): 5484. http://dx.doi.org/10.3390/cancers13215484.

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Although cancer cell metabolism was mainly considered to rely on glycolysis, with the concomitant impairment of mitochondrial metabolism, it has recently been demonstrated that several tumor types are sustained by oxidative phosphorylation (OXPHOS). In this context, endogenous fatty acids (FAs) deriving from lipolysis or lipophagy are oxidised into the mitochondrion, and are used as a source of energy through OXPHOS. Because the electron transport chain is the main source of ROS, cancer cells relying on fatty acid oxidation (FAO) need to be equipped with antioxidant systems that maintain the R

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Korge, Paavo, and James N. Weiss. "Redox regulation of endogenous substrate oxidation by cardiac mitochondria." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 3 (2006): H1436—H1445. http://dx.doi.org/10.1152/ajpheart.01292.2005.

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Reactive oxygen species (ROS) play important roles in regulating mitochondrial function, as well as in ischemia-reperfusion injury and cardioprotection. Here we show that, in the absence of exogenous substrates, cardiac mitochondria have a surprisingly large capacity to phosphorylate ADP by oxidizing endogenous substrates, provided that H2O2 is removed from the extramitochondrial environment and a reduced environment is maintained in the matrix. In isolated mitochondria without exogenous substrates, addition of catalase and the membrane-permeant reducing agent N-acetylcysteine (Nac) or the ROS

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Arazi, Hamid, Ehsan Eghbali, and Katsuhiko Suzuki. "Creatine Supplementation, Physical Exercise and Oxidative Stress Markers: A Review of the Mechanisms and Effectiveness." Nutrients 13, no. 3 (2021): 869. http://dx.doi.org/10.3390/nu13030869.

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Oxidative stress is the result of an imbalance between the generation of reactive oxygen species (ROS) and their elimination by antioxidant mechanisms. ROS degrade biogenic substances such as deoxyribonucleic acid, lipids, and proteins, which in turn may lead to oxidative tissue damage. One of the physiological conditions currently associated with enhanced oxidative stress is exercise. Although a period of intense training may cause oxidative damage to muscle fibers, regular exercise helps increase the cells’ ability to reduce the ROS over-accumulation. Regular moderate-intensity exercise has

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Zhao, Fan, Jiayu Yao, Yu Tong, et al. "H₂O₂-replenishable and GSH-depletive ROS ‘bomb’ for self-enhanced chemodynamic therapy." Materials Advances 3, no. 2 (2022): 1191–99. http://dx.doi.org/10.1039/d1ma00646k.

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Sadanandan, Nadia, Blaise Cozene, You Jeong Park, et al. "Pituitary Adenylate Cyclase-Activating Polypeptide: A Potent Therapeutic Agent in Oxidative Stress." Antioxidants 10, no. 3 (2021): 354. http://dx.doi.org/10.3390/antiox10030354.

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Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The pathology behind oxidative stress in stroke is of particular interest due to its detrimental effects on the brain. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body’s endogenous antioxidant system, which le

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