Dual Character of Reactive Oxygen, Nitrogen, and Halogen Species: Endogenous Sources, Interconversions and Neutralization

Moldogazieva, N. T.; Mokhosoev, Innokenty M.; Melnikova, Tatiana I; Zavadskiy, S. P.; Kuzmenko, A. N.; Terentiev, A. A.

doi:10.1134/s0006297920140047

Cited by 24 publications

(19 citation statements)

References 228 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, higher concentrations of ROS production lead to “adaptive stress” responses by the cell (via master switches, such as Nrf2/Keap1 (nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1) or NF- κ B (nuclear factor-kappa B)). Furthermore, in the event of an excessive load of oxidative stress production, called “oxidative distress,” it can lead to oxidative damage of the cells and provoke metabolic failure, compromising cell viability by inactivating enzymes of glycolysis, the Krebs cycle, and the ETC [ 12 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

“…Environmental sources include cigarette smoke, pollutants (such as ozone and nitrogen dioxide), ultraviolet light, ionizing radiation, and xenobiotics [ 7 , 16 ]. Major endogenous sources include the NOX family of NADPH oxidases, complexes I and III of the mitochondrial ETC, the cytochrome P450-containing monooxygenase system, nitric oxide synthases (NOS), xanthine oxidoreductase, and myeloperoxidases [ 15 ]. In particular, NADPH oxidases are transmembrane proteins that transfer electrons from cytoplasmic NADPH across a biological membrane to molecular oxygen (O 2 ) at the outer side of the membrane.…”

Section: Introductionmentioning

confidence: 99%

“…Oxidation of nuclear or mitochondrial DNA can result in strand breaks, aberrant cross-linking, and DNA adducts (covalent bonding of DNA elements to chemical mutagens/carcinogens). Proteins (including crucial enzymes) may sustain oxidative damage at a variety of weak sites and be rendered biologically inert at high ROS concentrations [ 23 ], but, as stated above describing oxidative eustress, through the regulatory functions of low ROS concentrations, proteins may undergo oxidative modification of redox-sensitive residues, and this can cause changes in their activity and underlie alterations in their regulatory functions with no damage in structures and functions of the proteins and the cells [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Papachristoforou

Lambadiari

Maratou

et al. 2020

Journal of Diabetes Research

246

177

View full text Add to dashboard Cite

Oxidative stress (OS) is defined as a disturbance in the prooxidant-antioxidant balance of the cell, in favor of the former, which results in the antioxidant capacity of the cell to be overpowered. Excess reactive oxygen species (ROS) production is very harmful to cell constituents, especially proteins, lipids, and DNA, thus causing damage to the cell. Oxidative stress has been associated with a variety of pathologic conditions, including diabetes mellitus (DM), cancer, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and accelerated aging. Regarding DM specifically, previous experimental and clinical studies have pointed to the fact that oxidative stress probably plays a major role in the pathogenesis and development of diabetic complications. It is postulated that hyperglycemia induces free radicals and impairs endogenous antioxidant defense systems through several different mechanisms. In particular, hyperglycemia promotes the creation of advanced glycation end-products (AGEs), the activation of protein kinase C (PKC), and the hyperactivity of hexosamine and sorbitol pathways, leading to the development of insulin resistance, impaired insulin secretion, and endothelial dysfunction, by inducing excessive ROS production and OS. Furthermore, glucose variability has been associated with OS as well, and recent evidence suggests that also hypoglycemia may be playing an important role in favoring diabetic vascular complications through OS, inflammation, prothrombotic events, and endothelial dysfunction. The association of these diabetic parameters (i.e., hyperglycemia, glucose variability, and hypoglycemia) with oxidative stress will be reviewed here.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Papachristoforou

Lambadiari

Maratou

et al. 2020

Journal of Diabetes Research

246

177

View full text Add to dashboard Cite

show abstract

“…ROS are produced by multiple biochemical reactions in several cellular systems localized on the plasma membrane, membranes of mitochondria and endoplasmic reticulum, and in the cytosol and peroxisomes [ 32 , 33 ]. The mitochondrial electron transport chain is considered as the predominant source of ROS precursors [ 34 ], while NADPH oxidases (NOXs) in the plasma membrane also represent one of the major endogenous sources of ROS [ 35 , 36 , 37 ]. Interestingly, there is a substantial interplay between these two sources: NOXs could increase mitochondrial ROS, which further activates the cytoplasmic NOXs and promotes cellular superoxide production [ 38 , 39 ].…”

Section: Oxidative Stress and Oxidative Dna Damagementioning

confidence: 99%

Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease

Wang

Carmone

et al. 2021

IJMS

View full text Add to dashboard Cite

Atrial fibrillation (AF) and ischemic heart disease (IHD) represent the two most common clinical cardiac diseases, characterized by angina, arrhythmia, myocardial damage, and cardiac dysfunction, significantly contributing to cardiovascular morbidity and mortality and posing a heavy socio-economic burden on society worldwide. Current treatments of these two diseases are mainly symptomatic and lack efficacy. There is thus an urgent need to develop novel therapies based on the underlying pathophysiological mechanisms. Emerging evidence indicates that oxidative DNA damage might be a major underlying mechanism that promotes a variety of cardiac diseases, including AF and IHD. Antioxidants, nicotinamide adenine dinucleotide (NAD+) boosters, and enzymes involved in oxidative DNA repair processes have been shown to attenuate oxidative damage to DNA, making them potential therapeutic targets for AF and IHD. In this review, we first summarize the main molecular mechanisms responsible for oxidative DNA damage and repair both in nuclei and mitochondria, then describe the effects of oxidative DNA damage on the development of AF and IHD, and finally discuss potential targets for oxidative DNA repair-based therapeutic approaches for these two cardiac diseases.

show abstract

“…Reperfusion, in each phase, is accompanied by the accelerated generation of reactive oxygen (ROS), nitrogen (RNS) and halogen (RHS) species. Their production is incited by inflammatory cues and, in turn, ROS, RNS and RHS perpetuate and exacerbate an ongoing inflammation by upregulating cytokine and chemokine release [ 4 , 5 ]. Halogenated and nitrated derivatives of tyrosine are used as markers of leukocyte-mediated tissue damage.…”

Section: Introductionmentioning

confidence: 99%

Sitagliptin Modulates Oxidative, Nitrative and Halogenative Stress and Inflammatory Response in Rat Model of Hepatic Ischemia-Reperfusion

et al. 2021

View full text Add to dashboard Cite

A possibility of repurposing sitagliptin, a well-established antidiabetic drug, for alleviating injury caused by ischemia-reperfusion (IR) is being researched. The aim of this study was to shed some light on the molecular background of the protective activity of sitagliptin during hepatic IR. The expression and/or concentration of inflammation and oxidative stress-involved factors have been determined in rat liver homogenates using quantitative RT-PCR and Luminex® xMAP® technology and markers of nitrative and halogenative stress were quantified using targeted metabolomics (LC-MS/MS). Animals (n = 36) divided into four groups were treated with sitagliptin (5 mg/kg) (S and SIR) or saline solution (C and IR), and the livers from IR and SIR were subjected to ischemia (60 min) and reperfusion (24 h). The midkine expression (by 2.2-fold) and the free 3-nitrotyrosine (by 2.5-fold) and IL-10 (by 2-fold) concentration were significantly higher and the Nox4 expression was lower (by 9.4-fold) in the IR than the C animals. As compared to IR, the SIR animals had a lower expression of interleukin-6 (by 4.2-fold) and midkine (by 2-fold), a lower concentration of 3-nitrotyrosine (by 2.5-fold) and a higher Nox4 (by 2.9-fold) and 3-bromotyrosine (by 1.4-fold). In conclusion, IR disturbs the oxidative, nitrative and halogenative balance and aggravates the inflammatory response in the liver, which can be attenuated by low doses of sitagliptin.

show abstract

Dual Character of Reactive Oxygen, Nitrogen, and Halogen Species: Endogenous Sources, Interconversions and Neutralization

Cited by 24 publications

References 228 publications

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease

Sitagliptin Modulates Oxidative, Nitrative and Halogenative Stress and Inflammatory Response in Rat Model of Hepatic Ischemia-Reperfusion

Contact Info

Product

Resources

About