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Reactive oxygen species (ROS) metabolism. A. ROS generation: Cellular ROS is generated by 5 pathways. 1) Superoxide generation: O 2 •-is derived from oxygen (O 2 ) after receiving an electron from various oxidases or from mitochondrial electron transport chain (ETC). 2) Reactive nitrogen species generation: O 2 •-reacts with nitric oxide (NO • ) to form peroxynitrite (ONOO − ). At physiological pH (pKa = 6.8), ONOO − is in equilibrium with peroxynitrous acid (ONOOH). In the aqueous phase, ONOO − rapidly reacts with carbon dioxide (CO 2 ) to generate carbonate radical anion (CO 3 •-) and nitrogen dioxide (NO 2 •
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Accumulated evidence strongly indicates that oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and antioxidants in favor of oxidants, plays an important role in disease pathogenesis. However, ROS can act as signaling molecules and fulfill essential physiological functions at basal levels. Each ROS woul...
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... and OH • generated in RNS pathway (Fig. 1). By its own, it can selectively react with few molecules including CO 2 , thiols, selenium compounds and metal centers. Reaction with CO 2 results in the generation of more toxic free-radicals CO ...
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... NO 2 • ( Fig. 1) which account for the most oxidative and nitrative effect of ONOO − . Reaction with thiols results in the generation of the corresponding disulfide. In contrast, its derivatives CO ...
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... 2 can result in modifications within key cellular targets including guanine for nucleic acids, unsaturated lipids, and targeted amino acids, which would be implicated in various diseases [56,57]. Most recently, 1 O 2 also can regulate vascular tone via the tryptophan-derived hydroperoxide as a signaling molecule inducing arterial relaxation [58]. (Fig. 1 can be reduced by glutathione peroxidase (GPX) or Peroxiredoxin (PRDX)1/4/6 isoforms into H 2 O using GSH as the electron donor. Oxidized GSSG will be reduced back to GSH by glutathione reductase (GSR) after receiving a H from NADPH. GPX can also reduce LOOH to become LOH. Ⅳ) Thioredoxin redox cycle: H 2 O 2 can also be reduced by ...
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... family), uncoupled NOS, xanthine oxidase (XO) and complex I/II/ III/IV of mitochondria (Fig. 1, pathway ...
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... in pathological conditions [52]. In a biological system, ONOO − is in equilibrium with its neutral form peroxynitrous acid (ONOOH) which has a pKa = 6.8 [61]. At physiological pH (7.4 (Fig. 1, pathway 3). OH • generation -OH • can be generated from homolysis fission of ONOOH ( Fig. 1, pathway 2). Most OH • is generated from H 2 O 2 and O ...
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... in pathological conditions [52]. In a biological system, ONOO − is in equilibrium with its neutral form peroxynitrous acid (ONOOH) which has a pKa = 6.8 [61]. At physiological pH (7.4 (Fig. 1, pathway 3). OH • generation -OH • can be generated from homolysis fission of ONOOH ( Fig. 1, pathway 2). Most OH • is generated from H 2 O 2 and O ...
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... a metal ion (iron or copper) catalyzed by Habor-Weiss reaction (Fig. 1, pathway 4) (Fig. 1, pathway 4). L • /LOO • generation -When lipid is attacked by OH • , a hydrogen atom will be abstracted and a carbon-centered lipid radical (L • ) will be formed. L • can react rapidly with O 2 to generate lipid peroxyl radical (LOO • ), which is a moderate oxidant capable of abstracting the H from nearby lipid to generate ...
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... a metal ion (iron or copper) catalyzed by Habor-Weiss reaction (Fig. 1, pathway 4) (Fig. 1, pathway 4). L • /LOO • generation -When lipid is attacked by OH • , a hydrogen atom will be abstracted and a carbon-centered lipid radical (L • ) will be formed. L • can react rapidly with O 2 to generate lipid peroxyl radical (LOO • ), which is a moderate oxidant capable of abstracting the H from nearby lipid to generate lipid hydroperoxide ...
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... be formed. L • can react rapidly with O 2 to generate lipid peroxyl radical (LOO • ), which is a moderate oxidant capable of abstracting the H from nearby lipid to generate lipid hydroperoxide (LOOH) and a new L • . The reaction propagates until the lipid radicals react with scavenging antioxidants or other free-radicals to form a covalent bond (Fig. 1, pathway 5). In addition, L • /LOO • can exist during a reaction process in which lipoxygenases catalyze the addition of dioxygen to polyunsaturated fatty acids to form hydroperoxides ...
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... Clearance: In order to maintain the ROS at a steady state, there are five major ROS clearance pathways ( Fig. 1 1-5 using reduced Thioredoxin (TrxR) as the electron donor; Ⅴ) Xenobiotic detoxification by glutathione transferase (GST). (Table 2) ROS metabolic clearance is involved with antioxidants. The aerobic organisms evolved an efficient antioxidant system which can be classified into two categories: enzymatic antioxidants and non-enzymatic ...
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... (Fig. 1, clearance pathway I). In human, there are three isoforms of SOD: SOD1 (Cu/Zn), SOD2 (Mn) and SOD3 (Cu/Zn) [66]. All three isoforms rely on their containing metals for their dismutation activity. SOD1 is widely distributed in all tissues and cells. It is the major isoform for clearance of O ...
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... -CAT is an iron-containing peroxidase to catalyze two H 2 O 2 into two H 2 O and one O 2 (Fig. 1, clearance pathway II). The second order rate constant of reaction with peroxide is 8 × 10 6 M −1 s −1 [68]. In mammals, it is predominately expressed in liver and erythrocytes [69] [70]. In the glutathione redox cycle, GPX reduces H 2 O 2 or ROOH and become oxidized (GPX O ) and inactive. GPX O can be converted back to its reduced form (GPX R ) by GSH. GSH ...
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... [69] [70]. In the glutathione redox cycle, GPX reduces H 2 O 2 or ROOH and become oxidized (GPX O ) and inactive. GPX O can be converted back to its reduced form (GPX R ) by GSH. GSH becomes glutathione disulfide (GSSG), which is reduced back to GSH after a hydride (H-) is transferred from NADPH catalyzed by glutathione reductase (GSR) (Fig. 1, clearance pathway III). Unlike CAT, GPX senses small elevation of H 2 O 2 . In human, eight isoforms of GPX (GPX1-8) have been identified, which vary by distribution, ROS targets and biological functions [71,72] (Table 2). GPX1 is the most abundant isoform and ubiquitously expressed in most tissue, mostly found in the cytosol and mitochondrial matrix, and ...
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... and nucleus, and targets peroxidized lipid (ROOH). GPX5 is specifically expressed in the epididymis, critical for protecting spermatozoa against lipid peroxidation. GPX6 is restricted to in embryo and olfactory epithelium and mainly targeting on H 2 O 2 . GPX7 is found in Leydig cell, hepatocyte, and adrenal gland. GPX7 is involved in de (Fig. 1, clearance pathway Ⅳ). In mammals, six isoforms (PRDX1-6) have been identified [74]. All isoforms contain a conserved cysteine residue (C P ), which can be oxidized by H 2 O 2 or ROOH into sulfenic acid (C P -SOH). C P -SOH then reacts with another semi-conserved Cys residue (C R ) to form a disulfide bond. Based on the location or absence of the C R , PRDX ...
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... highest concentration in the liver. It is the major antioxidant maintaining the whole body's redox status and often referred to as the body's master antioxidant. It is a tripeptide composed of three amino acids: Cys, glycine, and glutamate. The sulfhydryl (SH) group on Cys residue accounts for its strong e−donating feature. As described above in Fig. 1, GSH can be used as the reductant of GPX O (clearance pathway III) or used by glutathione S-transferases (GST) for detoxification of xenobiotics (clearance pathway Ⅴ). In addition, GSH serves as a reductant of a variety of oxidized antioxidants-such as vitamin C and Vitamin ...
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... expression of the protective protein GTP cyclohydrolase in ECs [87]. (Table 3) Mitochondrial ETC -ROS detected in mitochondria can be generated by the Mitochondrial-localized oxidases [22]. The vast majority of Mitochondrial ROS is generated from the mitochondrial electric transport chain (ETC), especially from complex I (Com I) and Com III (Fig. 2, pathway 1a). Their relative contribution to overall mitochondrial O ...
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... [133] (Fig. 2, pathway 1a). Mitochondria-ROS generation can be prevented by blocking the NOX1/2 or mitochondrial K ATP [134], or by inhibiting NOX1/2 or PKCɛ activity [135]. Mitochondria-ROS can also be produced by NOX4 in mitochondrial intermembrane in certain cell types such as CM and EC which can be activated by AngII/Gαq signaling [136] (Fig. 2, pathway 1b). ...
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... [133] (Fig. 2, pathway 1a). Mitochondria-ROS generation can be prevented by blocking the NOX1/2 or mitochondrial K ATP [134], or by inhibiting NOX1/2 or PKCɛ activity [135]. Mitochondria-ROS can also be produced by NOX4 in mitochondrial intermembrane in certain cell types such as CM and EC which can be activated by AngII/Gαq signaling [136] (Fig. 2, pathway 1b). In addition, NOX-ROS can be generated by stimulation of advanced glycation end-products, lipopolysaccharide or cytokines, and results in Mitochondria-ROS production in rat renal cells [137] or glioma cells respectively ...
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Microglia express constitutively a Nox2 enzyme that is involved in neuroinflammation by the generation of reactive oxygen species (ROS). Amyloid β (Aβ) plays a crucial role in Alzheimer’s disease. However, the mechanism of Aβ-induced microglial dysfunction and redox-regulation of microgliosis in aging remains unclear. In this study, we examined Nox...
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... It occurs because of an imbalance between the production of reactive oxygen species (ROS) and antioxidant activity [4]. Reactive nitrogen species (RNS), which are ROS with nitrogen instead of oxygen, also cause oxidative stress [5]. ...
Oxidative stress plays a central role in most chronic liver diseases and, in particular, in metabolic dysfunction-associated fatty liver disease (MAFLD), the new definition of an old condition known as non-alcoholic fatty liver disease (NAFLD). The mechanisms leading to hepatocellular fat accumulation in genetically predisposed individuals who adopt a sedentary lifestyle and consume an obesogenic diet progress through mitochondrial and endoplasmic reticulum dysfunction, which amplifies reactive oxygen species (ROS) production, lipid peroxidation, malondialdehyde (MDA) formation, and influence the release of chronic inflammation and liver damage biomarkers, such as pro-inflammatory cytokines. This close pathogenetic link has been a key stimulus in the search for therapeutic approaches targeting oxidative stress to treat steatosis, and a number of clinical trials have been conducted to date on subjects with NAFLD using drugs as well as supplements or nutraceutical products. Vitamin E, Vitamin D, and Silybin are the most studied substances, but several non-pharmacological approaches have also been explored, especially lifestyle and diet modifications. Among the dietary approaches, the Mediterranean Diet (MD) seems to be the most reliable for affecting liver steatosis, probably with the added value of the presence of extra virgin olive oil (EVOO), a healthy food with a high content of monounsaturated fatty acids, especially oleic acid, and variable concentrations of phenols (oleocanthal) and phenolic alcohols, such as hydroxytyrosol (HT) and tyrosol (Tyr). In this review, we focus on non-pharmacological interventions in MAFLD treatment that target oxidative stress and, in particular, on the role of EVOO as one of the main antioxidant components of the MD.
... Cellular function is disrupted and a number of clinical illnesses result from oxidative stress, which occurs when the equilibrium between ROS production and antioxidant defense is disturbed [18]. ROS are involved in a number of human disorders, including cardiovascular disease, since they can damage or destroy cells by attacking proteins, carbohydrates, nucleic acids, and polyunsaturated fatty acids [19]. Free radicals possess the capacity to selectively attack and harm the peptide backbone as well as the amino acid side chains of proteins, leading to the creation of diverse radical protein derivatives [20]. ...
A myocardial infarction (MI), is the irreversible death (necrosis) of heart muscle commonly known as a heart attack. Acute myocardial infarction (AMI) occurs when blood flow decreases or stops to the coronary artery of the heart, causing damage to the heart muscle. MI is associated with an intelligible imbalance in oxidative stress. After myocardial injury, many cardiac biomarkers become detectable in venous circulation such as cardiac enzymes. The study's main goals were to evaluate the clinical significant change in cardiac enzymes and investigate the positive and negative correlation with some serum oxidative stress markers total oxidative state (TOS), free amine and total antioxidant capacity (TAC) in patient and control groups. This study contained 120 subjects who were divided evenly into patients and control groups for the period between July and September 2022. The serum levels of oxidative stress markers were measured manually using spectrophotometer (model, Cecil, CE10N / England). The activity of cardiac enzymes and lipid profile were also determined by using Spectrophotometric kits supplied from Biolabo, France. The study showed that TOS had a significantly positive correlation with CK (r = 0.269*, p= 0.038) and ALT (r = 0.259*, p= 0.046), also for free amine, TnI (r = 0.287*, p= 0.026). Moreover, cardiac Troponin had highly positive correlation with oxidants and enzymes of the cardiomyocyte.
... Several enzymes can keep ROS levels stable. Among them, we can mention SOD and CAT, and their regulation is important for the treatment of NAFLD [67,68]. Chen et al. [12] showed that a HF diet can decrease the levels of SOD, GPx, and GSH, which are major antioxidant markers, and data that corroborate our work show SOD downregulation in the HF group. ...
Obesity is a complex chronic disease characterized by excess body fat (adipose) that is harmful to health and has been a major global health problem. It may be associated with several diseases, such as nonalcoholic fatty liver disease (NAFLD). Polyunsaturated fatty acids (PUFA) are lipid mediators that have anti-inflammatory characteristics and can be found in animals and plants, with capybara oil (CO) being a promising source. So, we intend to evaluate the hepatic pathophysiological alterations in C57Bl/6 mice with NAFLD, caused by obesity, and the possible beneficial effects of OC in the treatment of this disease. Eighteen 3-month-old male C57Bl/6 mice received a control or high-fat diet for 18 weeks. From the 15th to the 18th week, the animals received treatment—through orogastric gavage—with placebo or free capybara oil (5 g/kg). Parameters inherent to body mass, glucose tolerance, evaluation of liver enzymes, percentage of hepatic steatosis, oxidative stress, the process of cell death with the apoptotic biomarkers (Bax, Bcl2, and Cytochrome C), and the ultrastructure of hepatocytes were analyzed. Even though the treatment with CO was not able to disassemble the effects on the physiological parameters, it proved to be beneficial in reversing the morphological and ultrastructural damage present in the hepatocytes. Thus, demonstrating that CO has beneficial effects in reducing steatosis and the apoptotic pathway, it is a promising treatment for NAFLD.
... Crucially, the ROS generated by PSs exhibit a short lifespan (10 −9 -10 −4 s) and a limited diffusion range (5-300 nm), [24] restricting the localization of PS-generated ROS to a confined region to exert cytotoxicity. Therefore, effective PS NPs must overcome at least five biological obstacles, encompassing blood circulation, tumor accumulation, penetration, cell uptake, and PS release to reach all cancer cells for efficient antitumor effect. ...
Fluorescence imaging‐guided photodynamic therapy (FIG‐PDT) holds promise for cancer treatment, yet challenges persist in poor imaging quality, phototoxicity, and insufficient anti‐tumor effect. Herein, a novel nanoplatform, LipoHPM, designed to address these challenges, is reported. This approach employs an acid‐sensitive amine linker to connect a biotin‐modified hydrophilic polymer (BiotinPEG) with a new hydrophobic photosensitizer (MBA), forming OFF‐state BiotinPEG‐MBA (PM) micelles via an aggregation‐caused quenching (ACQ) effect. These micelles are then co‐loaded with the tumor penetration enhancer hydralazine (HDZ) into pH‐sensitive liposomes (LipoHPM). Leveraging the ACQ effect, LipoHPM is silent in both fluorescence and reactive oxygen species (ROS) generation during blood circulation but restores both properties upon disassembly. Following intravenous injection in tumor‐bearing mice, LipoHPM actively targets tumor cells overexpressing biotin‐receptors, contributing to enhanced tumor accumulation. Upon cellular internalization, LipoHPM disassembles within lysosomes, releasing HDZ to enhance tumor penetration and inhibit tumor metastasis. Concurrently, the micelles activate fluorescence for tumor imaging and boost the production of both type‐I and type‐II ROS for tumor eradication. Therefore, the smart LipoHPM synergistically integrates near‐infrared emission, activatable tumor imaging, robust ROS generation, efficient anti‐tumor and anti‐metastasis activity, successfully overcoming limitations of conventional photosensitizers and establishing itself as a promising nanoplatform for potent FIG‐PDT applications.
... Every fraction of the tetramer GPx contains a selenium atom [35]. This enzyme has eight isoforms distributed across different tissues (GPX1-GPX8) [77][78][79]. These isoforms are shown in Table 2. ...
Age-related macular degeneration (AMD) is a chronic disease that usually develops in older people. Pathogenetic changes in this disease include anatomical and functional complexes. Harmful factors damage the retina and macula. These changes may lead to partial or total loss of vision. The disease can occur in two clinical forms: dry (the progression is slow and gentle) and exudative (wet—progression is acute and severe), which usually starts in the dry form; however, the coexistence of both forms is possible. The etiology of AMD is not fully understood, and the precise mechanisms of the development of this illness are still unknown. Extensive genetic studies have shown that AMD is a multi-factorial disease and that genetic determinants, along with external and internal environmental and metabolic-functional factors, are important risk factors. This article reviews the role of glutathione (GSH) enzymes engaged in maintaining the reduced form and polymorphism in glutathione S-transferase theta-1 (GSTT1) and glutathione S-transferase mu-1 (GSTM1) in the development of AMD. We only chose papers that confirmed the influence of the parameters on the development of AMD. Because GSH is the most important antioxidant in the eye, it is important to know the influence of the enzymes and genetic background to ensure an optimal level of glutathione concentration. Numerous studies have been conducted on how the glutathione system works till today. This paper presents the current state of knowledge about the changes in GSH, GST, GR, and GPx in AMD. GST studies clearly show increased activity in ill people, but for GPx, the results relating to activity are not so clear. Depending on the research, the results also suggest higher and lower GPx activity in patients with AMD. The analysis of polymorphisms in GST genes confirmed that mutations lead to weaker antioxidant barriers and may contribute to the development of AMD; unfortunately, a meta-analysis and some research did not confirm that connection. Unspecific results of many of the parameters that make up the glutathione system show many unknowns. It is so important to conduct further research to understand the exact mechanism of defense functions of glutathione against oxidative stress in the human eye.
... Cellular function is disrupted and a number of clinical illnesses result from oxidative stress, which occurs when the equilibrium between ROS production and antioxidant defense is disturbed [18]. ROS are involved in a number of human disorders, including cardiovascular disease, since they can damage or destroy cells by attacking proteins, carbohydrates, nucleic acids, and polyunsaturated fatty acids [19]. Free radicals possess the capacity to selectively attack and harm the peptide backbone as well as the amino acid side chains of proteins, leading to the creation of diverse radical protein derivatives [20]. ...
A myocardial infarction (MI), is the irreversible death (necrosis) of heart muscle commonly known as a heart attack. Acute myocardial infarction (AMI) occurs when blood flow decreases or stops to the coronary artery of the heart, causing damage to the heart muscle. MI is associated with an intelligible imbalance in oxidative stress. After myocardial injury, many cardiac biomarkers become detectable in venous circulation such as cardiac enzymes. The study's main goals were to evaluate the clinical significant change in cardiac enzymes and investigate the positive and negative correlation with some serum oxidative stress markers total oxidative state (TOS), free amine and total antioxidant capacity (TAC) in patient and control groups. This study contained 120 subjects who were divided evenly into patients and control groups for the period between July and September 2022. The serum levels of oxidative stress markers were measured manually using spectrophotometer (model, Cecil, CE10N / England). The activity of cardiac enzymes and lipid profile were also determined by using Spectrophotometric kits supplied from Biolabo, France. The study showed that TOS had a significantly positive correlation with CK (r = 0.269*, p= 0.038) and ALT (r = 0.259*, p= 0.046), also for free amine, TnI (r = 0.287*, p= 0.026). Moreover, cardiac Troponin had highly positive correlation with oxidants and enzymes of the cardiomyocyte.
... •− ), hydroxyl radical (OH • ), carbonate radical anion (CO 3 •− ), nitrogen dioxide (NO 2 • ), alkoxyl/alkyl peroxyl (RO • /ROO • ), etc., and non-radicals lacking unpaired electrons and characterized as two-electron oxidants, including hydrogen peroxide (H 2 O 2 ), nitric oxide (NO), hypochlorous acid (HOCl), etc. [1,2]. With an intensive oxidative capacity, ROS can attack nucleic acids, proteins, and lipids, resulting in DNA damage, lipid peroxidation [3], and altering protein post-translational modification, represented by redox modification [4] and phosphorylation [5]. ...
Oxidative stress refers to the imbalance between the production of reactive oxygen species (ROS) and the endogenous antioxidant defense system. Its involvement in cell senescence, apoptosis, and series diseases has been demonstrated. Advances in carcinogenic research have revealed oxidative stress as a pivotal pathophysiological pathway in tumorigenesis and to be involved in lung cancer, glioma, hepatocellular carcinoma, leukemia, and so on. This review combs the effects of oxidative stress on tumorigenesis on each phase and cell fate determination, and three features are discussed. Oxidative stress takes part in the processes ranging from tumorigenesis to tumor death via series pathways and processes like mitochondrial stress, endoplasmic reticulum stress, and ferroptosis. It can affect cell fate by engaging in the complex relationships between senescence, death, and cancer. The influence of oxidative stress on tumorigenesis and progression is a multi-stage interlaced process that includes two aspects of promotion and inhibition, with mitochondria as the core of regulation. A deeper and more comprehensive understanding of the effects of oxidative stress on tumorigenesis is conducive to exploring more tumor therapies.
... The terms ROS and RNS refer to different molecules with variable reactivity including free radicals and non-radical species (reviewed in [18,94,[96][97][98]). The generation of ROS occurs during aerobic metabolism by the mitochondrial electron transport chain (ETC), or from specific enzymatic reactions as well as through the non-enzymatic Fenton reactions that in the presence of free iron or copper directly produce ROS (reviewed in [98][99][100]) ( Figure 2). ...
... The terms ROS and RNS refer to different molecules with variable reactivity including free radicals and non-radical species (reviewed in [18,94,[96][97][98]). The generation of ROS occurs during aerobic metabolism by the mitochondrial electron transport chain (ETC), or from specific enzymatic reactions as well as through the non-enzymatic Fenton reactions that in the presence of free iron or copper directly produce ROS (reviewed in [98][99][100]) ( Figure 2). Examples of ROS are the non-radical hydrogen peroxide (H 2 O 2 ) and various oxygen-centered radicals like the superoxide anion (O 2 ...
... The most relevant RNS comprise the intercellular messenger nitric oxide (NO • ) generated by different NOS enzymes from the oxidation of L-arginine (the amino acid), the nitrogen dioxide (NO 2 • ) radical and the peroxynitrite anion, a powerful oxidant [18,98,99,102,123,124] (Figure 2). The NO • molecule rapidly reacts with superoxide anion generating ONOO − ; therefore, NO • is often considered to be a toxic species, albeit it is also able to terminate lipid peroxidation propagation reactions (as discussed below) [125]. ...
Ferroptosis is a type of programmed cell death that differs from apoptosis, autophagy, and necrosis and is related to several physio-pathological processes, including tumorigenesis, neu-rodegeneration, senescence, blood diseases, kidney disorders, and ischemia-reperfusion injuries. Ferroptosis is linked to iron accumulation, eliciting dysfunction of antioxidant systems, which favor the production of lipid peroxides, cell membrane damage, and ultimately, cell death. Thus, signaling pathways evoking ferroptosis are strongly associated with those protecting cells against iron excess and/or lipid-derived ROS. Here, we discuss the interaction between the metabolic pathways of ferroptosis and antioxidant systems, with a particular focus on transcription factors implicated in the regulation of ferroptosis, either as triggers of lipid peroxidation or as ferroptosis antioxidant defense pathways.
... A well-known antioxidant defense system for maintaining redox homeostasis is the NF-E2-related factor 2-Kelch-like ECH-associated protein 1 (Nrf2-Keap1) system [32]. Under oxidizing conditions, Keap1 releases Nrf2, which undergoes nuclear translocation to upregulate antioxidant response elements (AREs) such as glutathione peroxidases, thioredoxins, peroxiredoxins, and superoxide dismutase [32,33]. ...
Bladder cancer (BCa) is the most common genitourinary malignancy, with a high global incidence and recurrence rate that is paired with an increasing caregiver burden and higher financial cost, in addition to increasing morbidity and mortality worldwide. Histologically, BCa is categorized into non-muscle invasive, muscle invasive, and metastatic BCa, on the basis of which the therapeutic strategy is determined. Despite all innovations and recent advances in BCa research, conventional therapies such as chemotherapy, immunotherapy, radiotherapy, and surgery fall short in the complete management of this important malignancy. Besides this worrying trend, the molecular basis of BCa development also remains poorly understood. Burgeoning evidence from experimental and clinical studies suggests that oxidative stress resulting from an imbalance between reactive oxygen species (ROS) generation and the body’s antioxidant production plays an integral role in BCa development and progression. Hence, ROS-induced oxidative stress-related pathways are currently under investigation as potential therapeutic targets of BCa. This review focuses on our current understanding regarding ROS-associated pathways in BCa pathogenesis and progression, as well as on antioxidants as potential adjuvants to conventional BCa therapy.
... And non-radical substances such as H2O2, ONOO-, ONOOH, HOCl, O2. These substances are not always harmful; in some cases, they can be protective [2]. This is the case of the NO radical. ...
... It can react with lipid free radicals LO. (Lipid oxy) and LOO. (peroxy radical) terminating the lipid peroxidation reaction [2]. This would mean that free radicals are not fundamentally pathological but rather constitute signalling molecules and it would be pathological when it accumulates in the organism and interact with lipids, proteins, nucleic acids and could cause damages at the neurological or psychological level or on other biological systems [3]. ...
Guiera senegalensis is a plant of the Combretaceae family, found in West Africa and Central Africa. It has many properties such as antibacterial, antifungal, anticancer, antioxidants, which are the subject of this study. The objective of this study was to realize a qualitative and quantitative phytochemical screening, evaluation of the antioxidant activity of the plant leaf extracts. Plant extractions was done in accordance with the methods described by Fonmboh and collaborators on the leaves of the plant; a qualitative phytochemical screening according to the methods described by Shaik and al quantitative phytochemical screening consisting of colorimetric dosage and finally the antioxidant activity was explored in-vitro by the Folin-Ciocalteu method and by the phosphomolybdenum method. This study revealed the presence of primary metabolites such as carbohydrates and proteins but also secondary metabolites such as alkaloids, flavonoids and coumarins. Quantification analysis demonstrated a significant concentration of these metabolites depending on the extract. Carbohydrates, proteins and polyphenols had a higher concentration in the hydro-ehtanolic extract with concentrations of 45,38 ± 1,88, 1172,31 ± 17,59, 310,27 ± 11,83 µg/ml respectively. Flavonoids, flavonols and alkaloids in the Aqueous maceration extract with concentrations of 145,84 ± 8,34, 169,52 ± 10,13, 320,56 ± 67,52 µg/ml. and Tannins in decoction extract with a concentration of 338,55 ± 12,25 µg/ml. The in-vitro antioxidant activity demonstrated an inhibition percentage of the order of 70.96 ± 0.58% in the extract obtained by hydro-ethanolic maceration. This study confirms the use of the plant in category 1 traditional medicine, and results show a promising potential for developing a category 2 phytomedicine. Future studies should explore the use of phytochemical compounds involved in this antioxidant activity as well as its mechanism.
