Journal articles: 'Oxidative stress factors'

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Borodin, E. A. "OXIDATIVE STRESS AND BRONCHIAL HYPERSENSITIVITY TO LOW TEMPERATURE AND OSMOTIC FACTORS." Amur Medical Journal, no. 3 (2017): 17–19. http://dx.doi.org/10.22448/amj.2017.3.17-19.

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Dorszewska, Jolanta, Marta Kowalska, Michał Prendecki, Thomas Piekut, Joanna Kozłowska, and Wojciech Kozubski. "Oxidative stress factors in Parkinson’s disease." Neural Regeneration Research 16, no. 7 (2021): 1383. http://dx.doi.org/10.4103/1673-5374.300980.

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Brini, Faiçal, and Walid Saibi. "Oxidative stress and antioxidant defense in Brassicaceae plants under abiotic stresses." SDRP Journal of Plant Science 5, no. 1 (2021): 232–44. http://dx.doi.org/10.25177/jps.5.1.ra.10694.

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Brassicaceae plants, as an important source of primary and secondary metabolites, are becoming a research model in plant science. Plants have developed different ways to ward off environmental stress factors. This is lead to the activation of various defense mechanisms resulting in a qualitative and/or quantitative change in plant metabolite production. Reactive oxygen species (ROS) is being continuously produced in cell during normal cellular processes. Under stress conditions, there are excessive production of ROS causing progressive oxidative damage and ultimately cell death. Despite their destructive activity, ROS are considered as important secondary messengers of signaling pathway that control metabolic fluxes and a variety of cellular processes. Plant response to environmental stress depends on the delicate equilibrium between ROS production, and their scavenging. This balance of ROS level is required for performing its dual role of acting as a defensive molecule in signaling pathway or a destructive molecule. Efficient scavenging of ROS produced during various environmental stresses requires the action of several non-enzymatic as well as enzymatic antioxidants present in the tissues. In this review, we describe the ROS production and its turnover and the role of ROS as messenger molecules as well as inducers of oxidative damage in Brassicaceae plants. Further, the antioxidant defense mechanisms comprising of enzymatic and non-enzymatic antioxidants have been discussed. Keywords: Abiotic stress, Antioxidant defence, Brassicaceae, Oxidative stress, ROS

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Hao, Yue, Mingjie Xing, and Xianhong Gu. "Research Progress on Oxidative Stress and Its Nutritional Regulation Strategies in Pigs." Animals 11, no. 5 (May 13, 2021): 1384. http://dx.doi.org/10.3390/ani11051384.

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Oxidative stress refers to the dramatic increase in the production of free radicals in human and animal bodies or the decrease in the ability to scavenging free radicals, thus breaking the antioxidation–oxidation balance. Various factors can induce oxidative stress in pig production. Oxidative stress has an important effect on pig performance and healthy growth, and has become one of the important factors restricting pig production. Based on the overview of the generation of oxidative stress, its effects on pigs, and signal transduction pathways, this paper discussed the nutritional measures to alleviate oxidative stress in pigs, in order to provide ideas for the nutritional research of anti-oxidative stress in pigs.

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Lozano-Picazo, Carmen María, and Francisco Fernández-Belda. "Especies reactivas de oxígeno y su implicación en Biomedicina." Anales de Veterinaria de Murcia 34 (December 16, 2020): 17–26. http://dx.doi.org/10.6018/analesvet.332621.

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Las especies reactivas de oxígeno (ROS) actúan como regulador intracelular cuando se generan de forma controlada en puntos concretos de la célula. Modifican la función de proteínas mediante la oxidación reversible de cisteínas. Hay quinasas y fosfatasas de proteínas, factores de transcripción y canales iónicos que están regulados por ROS. Estrés oxidativo y daño celular aparecen cuando los mecanismos antioxidantes de protección son incapaces de mantener bajo el nivel intracelular de ROS. En estas condiciones, ROS inducen pérdida de viabilidad celular en patologías degenerativas de corazón y cerebro y promueven proliferación celular ilimitada en procesos tumorales. La alteración de la función mitocondrial juega un papel clave en la generación del estrés oxidativo y por tanto es una diana terapéutica preferente para evitar o aminorar los daños oxidativos producidos por ROS. Reactive oxygen species (ROS) act as intracellular regulator when they are generated under control in specific cell spots. They modify proteins function by cysteine reversible oxidation. There are protein kinases and phosphatases, transcription factors and ionic channels that are regulated by ROS. Oxidative stress and cell damage arise when the protection antioxidant mechanisms are unable to keep low the intracellular ROS level. Under these conditions, ROS induce cell viability loss in heart and brain degenerative pathologies and promote unlimited cell proliferation in tumor processes. Alteration of the mitochondrial function is a key player in the oxidative stress generation and therefore it is preferential therapeutic target for prevention or attenuation of the ROS-induced oxidative damage.

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Li, Jinjin, Yuan Zhang, Jingyun Zhang, Rongna Dong, Juanjuan Guo, and Qiumei Zhang. "Oxidative Stress and Its Related Factors in Latent Autoimmune Diabetes in Adults." BioMed Research International 2021 (September 13, 2021): 1–6. http://dx.doi.org/10.1155/2021/5676363.

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Aims. Few research was reported to explore oxidative stress in individuals with latent autoimmune diabetes in adults (LADA). Therefore, our goal is to study oxidative stress and related factors in LADA patients. Methods. In this study, 250 Chinese inpatients were diagnosed with LADA ( n = 110 ) and type 2 diabetes mellitus ( n = 140 ) and 140 healthy volunteers were recruited. Moreover, individuals with LADA were followed for 6 months to evaluate whether short-term glycemic control during hospitalization can improve oxidative stress. Clinical and laboratory measurements of height, weight, blood pressure, glycosylated hemoglobin (HbA1c), blood lipids, 8-isoprostaglandin F2α (8-iso-PGF2α), and superoxide dismutase (SOD) were performed. Stepwise multiple regression analyses were used to assess factors that related to oxidative stress in individuals with LADA. Results. Compared with patients with type 2 diabetes, individuals with LADA have better oxidative stress and worse oxidative stress than healthy volunteers. After multiple regression analyses, systolic blood pressure, HbA1c, duration of diabetes, and diabetic retinopathy were associated with 8-iso-PGF2α and HbA1c. Diabetic retinopathy and diabetic ketosis were associated with SOD in individuals with LADA. Our results also revealed that, after 6 months of follow-up, oxidative stress was improved to some extent in persons with LADA. Conclusions. Our results show that compared with type 2 diabetes, LADA means less oxidative stress, and compared with healthy volunteers, it means more oxidative stress. Systolic blood pressure, HbA1c, duration of diabetes, diabetic retinopathy, and ketosis were associated with oxidative stress in individuals with LADA. Furthermore, short-term glycemic control can improve oxidative stress to some extent in individuals with LADA.

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Ryan, Sarah M., Kaitie Wildman, Briseida Oceguera-Perez, Scott Barbee, Nathan T. Mortimer, and Alysia D. Vrailas-Mortimer. "Evolutionarily conserved transcription factors drive the oxidative stress response in Drosophila." Journal of Experimental Biology 223, no. 14 (June 12, 2020): jeb221622. http://dx.doi.org/10.1242/jeb.221622.

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ABSTRACTAs organisms are constantly exposed to the damaging effects of oxidative stress through both environmental exposure and internal metabolic processes, they have evolved a variety of mechanisms to cope with this stress. One such mechanism is the highly conserved p38 MAPK (p38K) pathway, which is known to be post-translationally activated in response to oxidative stress, resulting in the activation of downstream antioxidant targets. However, little is known about the role of p38K transcriptional regulation in response to oxidative stress. Therefore, we analyzed the p38K gene family across the genus Drosophila to identify conserved regulatory elements. We found that oxidative stress exposure results in increased p38K protein levels in multiple Drosophila species and is associated with increased oxidative stress resistance. We also found that the p38Kb genomic locus includes conserved AP-1 and lola-PT transcription factor consensus binding sites. Accordingly, over-expression of these transcription factors in D. melanogaster is sufficient to induce transcription of p38Kb and enhances resistance to oxidative stress. We further found that the presence of a putative lola-PT binding site in the p38Kb locus of a given species is predictive of the species' survival in response to oxidative stress. Through our comparative genomics approach, we have identified biologically relevant putative transcription factor binding sites that regulate the expression of p38Kb and are associated with resistance to oxidative stress. These findings reveal a novel mode of regulation for p38K genes and suggest that transcription may play as important a role in p38K-mediated stress responses as post-translational modifications.

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H., Yeldu M., and Arinola O. G. "Oxidative stress factors in Nigerians with rheumatoid arthritis." International Journal of Research in Medical Sciences 5, no. 5 (April 26, 2017): 1948. http://dx.doi.org/10.18203/2320-6012.ijrms20171823.

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Background: Rheumatoid arthritis (RA) is a chronic progressive inflammatory autoimmune disorder characterized by symmetric erosive synovitis and sometimes with multi-system involvement. But the exact mechanism of the disease is not fully understood. In the light of above explanation, the present study measured the plasma levels of total peroxide potential (TPP), total antioxidant potential (TAP), malondialdehyde (MDA), oxidative stress index (OSI) and nitric oxide (NO) in relation to the titer of rheumatoid factor among RA patients compared with controls.Methods: This study included 28 rheumatoid arthritis patients and 28 apparently healthy subjects as controls who were matched for age (50-60 years), sex, and socioeconomic status. Rheumatoid factor was estimated using latex method as described by manufacturer. Anthropometric parameters and plasma levels of TPP, TAP, OSI, MDA and NO were determined using standard techniques.Results: The result indicated that with the exception of mean body weight which was significantly (p<0.001) higher among RA patients (90.61±2.02 years) as compared with controls (77.91±2.51 years), mean age, height and body mass index of RA patients (55.68±1.05kg, 1.65±0.01m and 33.40±0.83 kg/m2 respectively) were not significantly different compared with controls (54.07±1.04kg, 1.61±0.02m and 30.44±1.28 kg/m2 respectively). Plasma TPP, NO, OSI and MDA were significantly (p<0.01; p<0.001) higher while, plasma TAP is significantly lower among RA patients compared with controls. Plasma MDA was positively correlated with titer of rheumatoid factor in the RA patients.Conclusions: Our findings therefore may raise the concept that there are some yet unknown key events in the pathogenesis of RA determination of sex of the skull along with other parameters.

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Block, G. "Factors Associated with Oxidative Stress in Human Populations." American Journal of Epidemiology 156, no. 3 (August 1, 2002): 274–85. http://dx.doi.org/10.1093/aje/kwf029.

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Møller, Peter, Håkan Wallin, and Lisbeth E. Knudsen. "Oxidative stress associated with exercise, psychological stress and life-style factors." Chemico-Biological Interactions 102, no. 1 (September 1996): 17–36. http://dx.doi.org/10.1016/0009-2797(96)03729-5.

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Ilderbayev, Oralbek, Assem Okassova, Saule Rakhyzhanova, Gulzhan Ilderbayeva, and Lashyn Zhazykbayeva. "The levels of oxidative stress in a combination of stress factors." Journal of Medicine and Life 15, no. 8 (August 2022): 927–31. http://dx.doi.org/10.25122/jml-2021-0060.

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We studied the effect of the combined action of ionizing radiation and induced immobilization stress on the lipid peroxidation process and antioxidant protection of organs (mesenteric lymph nodes, spleen, adrenal glands, thymus, and liver) and immune cels - the blood lymphocytes. Results were obtained on the role of free-radical oxidation in combination with exposure to ionizing radiation and immobilization stress at an early stage in the experiment. Gamma radiation in the acute period resulted in significant changes in lipoperoxidation and antioxidant systems. The first period of immobilization stress was marked by the imbalance of LPO-AOS systems disturbance with an accumulation of toxic compounds in tissues which had affected their function. The combined sublethal gamma radiation and immobilization stress disturbed the functional activity of adaptive systems of the body in the early stage of adaptation syndrome. Furthermore, the results show the dominant role of ionizing radiation in it.

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Agarwal, Vyoma. "Correlation of Neurodegenerative Diseases with Oxidative Stress and Nutrition." Chettinad Health City Medical Journal 11, no. 02 (June 30, 2022): 62–68. http://dx.doi.org/10.24321/2278.2044.202217.

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Technology or ease of doing work might be the greatest boon to this era, but it is still a bane for our health and life. Sitting in front of laptops or computers for several hours (sedentary lifestyle), using cell phones, watching television, skipping meals or eating junk/ fast food, lack of physical activities, stress, etc. increase the risk of many lifestyle diseases. All the above-mentioned habits increase the count of free radicals in our body and due to a lack of endogenous and exogenous antioxidants, the body cannot combat oxidative stress. Thus, the chances of occurrence of several chronic diseases like cancer, atherosclerosis, cardiovascular diseases, neurodegenerative diseases, rheumatoid arthritis, chronic inflammations, etc. increase. There are several factors contributing to neurodegeneration of the brain and neurons, in which oxidative stress plays an important role. This review article is the compilation of research done by several other researchers on Neurodegenerative Diseases (NDDs) and is primarily focused on better understanding a few basic questions like the correlation of oxidative stress and nutrition to neurodegeneration, NDDs, their different types, symptoms and causes followed by establishing a relation between oxidative stress and nutrition with the help of several studies carried out by researchers in this context.

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Dowell, Jonathan, Benjamin A. Elser, Rachel E. Schroeder, and Hanna E. Stevens. "Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress." Neuroscience Letters 709 (September 2019): 134368. http://dx.doi.org/10.1016/j.neulet.2019.134368.

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Latorre, Eva, Nyurky Matheus, Elena Layunta, Ana Isabel Alcalde, and José Emilio Mesonero. "IL-10 Counteracts Proinflammatory Mediator Evoked Oxidative Stress in Caco-2 Cells." Mediators of Inflammation 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/982639.

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Oxidative stress is thought to play a key role in the development of intestinal damage in intestinal inflammatory diseases. Several molecules are involved in the intestinal inflammation, either as pro- or anti-inflammatory factors; however, their effects on intestinal oxidative stress seem to be controversial. This work analyzes the contribution of pro- and anti-inflammatory molecules to the balance of oxidative damage in intestinal epithelial cells, as well as their effects on cellular antioxidant enzyme activity. With this purpose, the lipid and protein oxidation, together with the activity of catalase, superoxide dismutase, and glutathione peroxidase, were determined in the Caco-2 cells treated with serotonin, adenosine, melatonin, and TNFα, as proinflammatory factors, and IL-10, as an anti-inflammatory cytokine. The results have shown that all the proinflammatory factors assayed increased oxidative damage. In addition, these factors also inhibited the activity of antioxidant enzymes in the cells, except melatonin. In contrast, IL-10 did not alter these parameters but was able to reduce the prooxidant effects yielded by serotonin, adenosine, melatonin, or TNFα, in part by restoring the antioxidant enzymes activities. In summary, proinflammatory factors may induce oxidative damage in intestinal epithelial cells, whereas IL-10 seems to be able to restore the altered redox equilibrium in Caco-2 cells.

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Vodošek Hojs, Nina, Sebastjan Bevc, Robert Ekart, and Radovan Hojs. "Oxidative Stress Markers in Chronic Kidney Disease with Emphasis on Diabetic Nephropathy." Antioxidants 9, no. 10 (September 27, 2020): 925. http://dx.doi.org/10.3390/antiox9100925.

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Diabetes prevalence is increasing worldwide, especially through the increase of type 2 diabetes. Diabetic nephropathy occurs in up to 40% of diabetic patients and is the leading cause of end-stage renal disease. Various factors affect the development and progression of diabetic nephropathy. Hyperglycaemia increases free radical production, resulting in oxidative stress, which plays an important role in the pathogenesis of diabetic nephropathy. Free radicals have a short half-life and are difficult to measure. In contrast, oxidation products, including lipid peroxidation, protein oxidation, and nucleic acid oxidation, have longer lifetimes and are used to evaluate oxidative stress. In recent years, different oxidative stress biomarkers associated with diabetic nephropathy have been found. This review summarises current evidence of oxidative stress biomarkers in patients with diabetic nephropathy. Although some of them are promising, they cannot replace currently used clinical biomarkers (eGFR, proteinuria) in the development and progression of diabetic nephropathy.

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Hidayati, Alpha Olivia, and Ernawati Hardani. "Analysis Of Risk Factors Oxidative Stress In Obesity Women." Journal of Health 6, no. 1 (January 31, 2019): 51–57. http://dx.doi.org/10.30590/vol6-no1-p51-57.

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Obesity is a condition of imbalance in the number of calories entered by the number of calories where the excess is heaped up as body fat. Obesity followed by an increase in fat metabolism will cause Reactive Oxygen Species (ROS) production to increase. This condition causes oxidative stress. Indicators of oxidative stress can be observed from plasma levels of Malondialdehyde (MDA). This study aims to determine the risk factors for oxidative stress in obese women. The results of this study indicate that high fat intake (> 60 g / day) is at risk of increasing MDA-P levels twice. Low fiber consumption (<30 gr / day) gives the risk of an increase in MDA-P levels of 2.09 times. Poor physical activity is a risk factor for MDA-P increase of 1.15 times. High cholesterol (> 200mg / l) and LDL (> 130 mg / l) and low HDL (≤45mg / dl) levels are at risk of increasing MDA-P levels by 1.02 times (cholesterol), 1.13 (LDL) ) and 1.12 (HDL). Based on this study it can be concluded that high fat intake, low fiber intake, low physical activity, high cholesterol and HDL levels and low HDL levels are risk factors for oxidative stress.

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Tomás-Simó, Patricia, Luis D’Marco, María Romero-Parra, Mari Carmen Tormos-Muñoz, Guillermo Sáez, Isidro Torregrosa, Nuria Estañ-Capell, Alfonso Miguel, José Luis Gorriz, and María Jesús Puchades. "Oxidative Stress in Non-Dialysis-Dependent Chronic Kidney Disease Patients." International Journal of Environmental Research and Public Health 18, no. 15 (July 23, 2021): 7806. http://dx.doi.org/10.3390/ijerph18157806.

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Background: Cardiovascular complications are the leading cause of morbidity and mortality at any stage of chronic kidney disease (CKD). Moreover, the high rate of cardiovascular mortality observed in these patients is associated with an accelerated atherosclerosis process that likely starts at the early stages of CKD. Thus, traditional and non-traditional or uremic-related factors represent a link between CKD and cardiovascular risk. Among non-conventional risk factors, particular focus has been placed on anaemia, mineral and bone disorders, inflammation, malnutrition and oxidative stress and, in this regard, connections have been reported between oxidative stress and cardiovascular disease in dialysis patients. Methods: We evaluated the oxidation process in different molecular lines (proteins, lipids and genetic material) in 155 non-dialysis patients at different stages of CKD and 45 healthy controls. To assess oxidative stress status, we analyzed oxidized glutathione (GSSG), reduced glutathione (GSH) and the oxidized/reduced glutathione ratio (GSSG/GSH) and other oxidation indicators, including malondialdehyde (MDA) and 8-oxo-2’-deoxyguanosine (8-oxo-dG). Results: An active grade of oxidative stress was found from the early stages of CKD onwards, which affected all of the molecular lines studied. We observed a heightened oxidative state (indicated by a higher level of oxidized molecules together with decreased levels of antioxidant molecules) as kidney function declined. Furthermore, oxidative stress-related alterations were significantly greater in CKD patients than in the control group. Conclusions: CKD patients exhibit significantly higher oxidative stress than healthy individuals, and these alterations intensify as eGFR declines, showing significant differences between CKD stages. Thus, future research is warranted to provide clearer results in this area.

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Ponugoti, Bhaskar, Guangyu Dong, and Dana T. Graves. "Role of Forkhead Transcription Factors in Diabetes-Induced Oxidative Stress." Experimental Diabetes Research 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/939751.

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Diabetes is a chronic metabolic disorder, characterized by hyperglycemia resulting from insulin deficiency and/or insulin resistance. Recent evidence suggests that high levels of reactive oxygen species (ROS) and subsequent oxidative stress are key contributors in the development of diabetic complications. The FOXO family of forkhead transcription factors including FOXO1, FOXO3, FOXO4, and FOXO6 play important roles in the regulation of many cellular and biological processes and are critical regulators of cellular oxidative stress response pathways. FOXO1 transcription factors can affect a number of different tissues including liver, retina, bone, and cell types ranging from hepatocytes to microvascular endothelial cells and pericytes to osteoblasts. They are induced by oxidative stress and contribute to ROS-induced cell damage and apoptosis. In this paper, we discuss the role of FOXO transcription factors in mediating oxidative stress-induced cellular response.

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Stepanenko, Irina L. "Reactive oxygen species regulate gene networks of stress response." Ecological genetics 2, no. 1 (March 15, 2004): 4–12. http://dx.doi.org/10.17816/ecogen214-12.

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The GeneNet (gnw/genenet/) accumulate information on reactive oxygen species (ROS) signals and reduction/oxidation (redox) regulation of transcription factors. Redox-regulation gene network is the adaptation to oxidative stress and integrative system of local gene networks via key transcription factors. The cross-talk of signals and the interference of gene networks occur in the integrative gene network

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Volkova, M. V., and Y. I. Ragino. "Modern biomarkers of oxidative stress estimated by immuno-enzymal analysis." Ateroscleroz 17, no. 4 (January 13, 2022): 79–92. http://dx.doi.org/10.52727/2078-256x-2021-17-4-79-92.

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The literature review presents the results of studies carried out in the world over the past years, devoted to the study of factors and markers of oxidative stress in the development of therapeutic diseases, especially cardiovascular diseases. The article describes the results of studies using enzyme immunoassay of such biomarkers of oxidative stress as glutathione peroxidase, superoxide dismutase, oxidatively modified low density lipoproteins, carbonylated proteins, as well as the general antioxidant capacity of the blood.

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Zieniewska, Izabela, Mateusz Maciejczyk, and Anna Zalewska. "The Effect of Selected Dental Materials Used in Conservative Dentistry, Endodontics, Surgery, and Orthodontics as Well as during the Periodontal Treatment on the Redox Balance in the Oral Cavity." International Journal of Molecular Sciences 21, no. 24 (December 18, 2020): 9684. http://dx.doi.org/10.3390/ijms21249684.

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Oxidative stress (OS) is a redox homeostasis disorder that results in oxidation of cell components and thus disturbs cell metabolism. OS is induced by numerous internal as well as external factors. According to recent studies, dental treatment may also be one of them. The aim of our work was to assess the effect of dental treatment on the redox balance of the oral cavity. We reviewed literature available in PubMed, Medline, and Scopus databases, including the results from 2010 to 2020. Publications were searched according to the keywords: oxidative stress and dental monomers; oxidative stress and amalgam; oxidative stress and periodontitis, oxidative stress and braces, oxidative stress and titanium; oxidative stress and dental implants, oxidative stress and endodontics treatment, oxidative stress and dental treatment; and oxidative stress and dental composite. It was found that dental treatment with the use of composites, amalgams, glass-ionomers, materials for root canal filling/rinsing, orthodontic braces (made of various metal alloys), titanium implants, or whitening agents can disturb oral redox homeostasis by affecting the antioxidant barrier and increasing oxidative damage to salivary proteins, lipids, and DNA. Abnormal saliva secretion/composition was also observed in dental patients in the course of OS. It is suggested that the addition of antioxidants to dental materials or antioxidant therapy applied during dental treatment could protect the patient against harmful effects of OS in the oral cavity.

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Hughes, Ariel M., H. Tucker Hallmark, Lenka Plačková, Ondrej Novák, and Aaron M. Rashotte. "Clade III cytokinin response factors share common roles in response to oxidative stress responses linked to cytokinin synthesis." Journal of Experimental Botany 72, no. 8 (February 22, 2021): 3294–306. http://dx.doi.org/10.1093/jxb/erab076.

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Abstract Cytokinin response factors (CRFs) are transcription factors that are involved in cytokinin (CK) response, as well as being linked to abiotic stress tolerance. In particular, oxidative stress responses are activated by Clade III CRF members, such as AtCRF6. Here we explored the relationships between Clade III CRFs and oxidative stress. Transcriptomic responses to oxidative stress were determined in two Clade III transcription factors, Arabidopsis AtCRF5 and tomato SlCRF5. AtCRF5 was required for regulated expression of >240 genes that are involved in oxidative stress response. Similarly, SlCRF5 was involved in the regulated expression of nearly 420 oxidative stress response genes. Similarities in gene regulation by these Clade III members in response to oxidative stress were observed between Arabidopsis and tomato, as indicated by Gene Ontology term enrichment. CK levels were also changed in response to oxidative stress in both species. These changes were regulated by Clade III CRFs. Taken together, these findings suggest that Clade III CRFs play a role in oxidative stress response as well as having roles in CK signaling.

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Nopriyati, Rina Novriani, Athuf Thaha, Sarah Diba, Yulia Farida Yahya, and Inda Astri Aryani. "The Role of Oxidative Stress in Atopic Dermatitis." Bioscientia Medicina : Journal of Biomedicine and Translational Research 6, no. 11 (August 12, 2022): 2347–52. http://dx.doi.org/10.37275/bsm.v6i11.603.

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Atopic dermatitis (AD) is a chronic skin inflammation found in children with a varied course caused by external and internal factors. The incidence of AD in industrialized countries is 10-20% in children and 1-3% in adults. The main etiopathogenesis of AD is genetic and skin barrier disorders, immunologic disorders, and environment. Oxidative stress (SO) is the accumulation of reactive oxygen species (ROS) that exceeds the defense capacity of the body's antioxidant system. Uncontrolled ROS production plays a major role in various skin diseases. Oxidative stress can damage the deoxyribonucleic acid (DNA) of keratinocytes through lipid oxidation, as well as disrupt skin barrier function, increase the production of proinflammatory cytokines and worsen AD lesions. The main objectives of this literature review are to determine the role of oxidative stress in AD and antioxidants as adjunctive therapy.

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Klaunig, James E. "Oxidative Stress and Cancer." Current Pharmaceutical Design 24, no. 40 (March 15, 2019): 4771–78. http://dx.doi.org/10.2174/1381612825666190215121712.

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Background: Cancer is considered a major cause of death worldwide. The etiology of cancer is linked to environmental and genetic inheritance causes. Approximately 90 percent of all human cancers have an environmental cause (non-genetic inheritance) predominantly through lifestyle choices (smoking, diet, UV radiation) while the remaining due to infections and chemical exposure. Cancer is a multistage process that involves mutational changes and uncontrolled cell proliferation. Research has firmly established a causal and contributory role of oxidative stress and oxidative damage in cancer initiation and progression. Methods: The purpose of this article is to review the role that oxidative stress and reactive oxygen species play in the development of cancer. Both endogenous and exogenous sources of reactive oxygen species result in increased oxidative stress in the cell. Excess reactive oxygen fumed can result in damage to and modification of cellular macromolecules most importantly genomic DNA that can produce mutations. In addition, oxidative stress modulates gene expression of downstream targets involved in DNA repair, cell proliferation and antioxidants. The modulation of gene expression by oxidative stress occurs in part through activation or inhibition of transcription factors and second messengers. The role of single nuclear polymorphism for oxidative DNA repair and enzymatic antioxidants is important in determining the potential human cancer risk. Conclusion: oxidative stress and the resulting oxidative damage are important contributors to the formation and progression of cancer.

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Żelaźniewicz, Agnieszka, Judyta Nowak, Agata Groyecka, Piotr Sorokowski, Małgorzata Dobrowolska, and Bogusław Pawłowski. "Empathy and Oxidative Stress in Healthy Adults." Sustainability 12, no. 12 (June 18, 2020): 4959. http://dx.doi.org/10.3390/su12124959.

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Empathy is crucial for normal and effective social functioning, enabling comprehension and prediction of actions in social environments. Despite its importance for maintaining social relationships in human groups, the physiological correlates of empathy are not fully known. The aim of this study was to test whether empathy is related to oxidative stress level, that may result both from internal disturbances and influence of external adverse factors. Seventy-four healthy women (Mage = 26.23, SDage = 2.88) and one hundred and one men (Mage = 28.09, SDage = 3.03) took part in the study. Participants’ empathy was evaluated with self-assessment questionnaire—Empathy Quotient (EQ). Oxidative stress level was measured with serum 8-OH-dG, a product of oxidative DNA damage. The results showed that empathy is negatively related to oxidative stress level in men but not in women, when controlled for testosterone level. Revealed sex differences may be explained by men’s greater vulnerability to various adverse conditions and harmful factors. Men, compared to women, seem to be more susceptible to behavioral changes, induced by increased oxidative stress level. The study adds to growing evidence showing that many physiological mechanisms, other than hormonal factors, that may be also related with environmental harmful factors, are related to behavioral, affective and cognitive phenomena.

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Yermukhambetova, R. Zh, A. Zh Dogabayev, A. A. Bari, and Zh K. Masalimov. "Oxidative stress response in plants to combined abiotic and biotic stress factors." BULLETIN of the L.N. Gumilyov Eurasian National University. BIOSCIENCE Series 122, no. 1 (2018): 48–53. http://dx.doi.org/10.32523/2616-7034-2018-122-1-48-53.

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SHIMOSAWA, Tatsuo. "Mechanical Stress and Humoral Factors Linked to the Induction of Oxidative Stress." Hypertension Research 29, no. 9 (2006): 643–44. http://dx.doi.org/10.1291/hypres.29.643.

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Motataianu, Anca, Georgiana Serban, Laura Barcutean, and Rodica Balasa. "Oxidative Stress in Amyotrophic Lateral Sclerosis: Synergy of Genetic and Environmental Factors." International Journal of Molecular Sciences 23, no. 16 (August 19, 2022): 9339. http://dx.doi.org/10.3390/ijms23169339.

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Amyotrophic lateral sclerosis (ALS) is a grievous neurodegenerative disease whose survival is limited to only a few years. In spite of intensive research to discover the underlying mechanisms, the results are fairly inconclusive. Multiple hypotheses have been regarded, including genetic, molecular, and cellular processes. Notably, oxidative stress has been demonstrated to play a crucial role in ALS pathogenesis. In addition to already recognized and exhaustively studied genetic mutations involved in oxidative stress production, exposure to various environmental factors (e.g., electromagnetic fields, solvents, pesticides, heavy metals) has been suggested to enhance oxidative damage. This review aims to describe the main processes influenced by the most frequent genetic mutations and environmental factors concurring in oxidative stress occurrence in ALS and the potential therapeutic molecules capable of diminishing the ALS related pro-oxidative status.

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Bayarsaikhan, Govigerel, Delger Bayarsaikhan, Jaewon Lee, and Bonghee Lee. "Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress." Antioxidants 11, no. 5 (May 9, 2022): 936. http://dx.doi.org/10.3390/antiox11050936.

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Oxidative stress and inflammation cannot be considered as diseases themselves; however, they are major risk factors for the development and progression of the pathogenesis underlying many illnesses, such as cancer, neurological disorders (including Alzheimer’s disease and Parkinson’s disease), autoimmune and metabolic disorders, etc. According to the results obtained from extensive studies, oxidative stress–induced biomolecules, such as advanced oxidation protein products, advanced glycation end products, and advanced lipoxidation end products, are critical for an accelerated level of inflammation and oxidative stress–induced cellular damage, as reflected in their strong affinity to a wide range of scavenger receptors. Based on the limitations of antioxidative and anti-inflammatory molecules in practical applications, targeting such interactions between harmful molecules and their cellular receptors/signaling with advances in gene engineering technology, such as CRISPR or TALEN, may prove to be a safe and effective alternative. In this review, we summarize the findings of recent studies focused on the deletion of scavenger receptors under oxidative stress as a development in the therapeutic approaches against the diseases linked to inflammation and the contribution of advanced glycation end products (AGEs), advanced lipid peroxidation products (ALEs), and advanced oxidation protein products (AOPPs).

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Hopps, Eugenia, and Gregorio Caimi. "Protein Oxidation in Metabolic Syndrome." Clinical & Investigative Medicine 36, no. 1 (February 1, 2013): 1. http://dx.doi.org/10.25011/cim.v36i1.19399.

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Purpose: Oxidative stress plays a pivotal role in the pathogenesis of the metabolic syndrome and in the progression of its complications. Carbonylated proteins are a stable marker of severe oxidative stress because damage to the protein structure is irreversible and may cause an inhibition of their enzymatic activity or an increased susceptibility to proteolysis. There are few data regarding protein oxidation in metabolic syndrome, although elevated levels of carbonyl groups are often detected in subjects with obesity, diabetes mellitus, hypertension or dyslipidemia, well-known components of the metaboic syndrome. In particular, obesity, insulin resistance and diabetes mellitus are frequently associated with increased protein carbonylation. A relationship between insulin resistance, protein oxidative stress and inflammation has also been suggested as well as protein oxidation products are correlated with overexpression of resistin, TNF-α and IL-6. Conclusion: Therapeutic interventions based on lifestyle modifications and pharmacological agents in order to correct all the main risk factors influence oxidative stress and protein carbonylation.

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Man, Andy W. C., Huige Li, and Ning Xia. "Impact of Lifestyles (Diet and Exercise) on Vascular Health: Oxidative Stress and Endothelial Function." Oxidative Medicine and Cellular Longevity 2020 (September 26, 2020): 1–22. http://dx.doi.org/10.1155/2020/1496462.

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Healthy lifestyle and diet are associated with significant reduction in risk of obesity, type 2 diabetes, and cardiovascular diseases. Oxidative stress and the imbalance between prooxidants and antioxidants are linked to cardiovascular and metabolic diseases. Changes in antioxidant capacity of the body may lead to oxidative stress and vascular dysfunction. Diet is an important source of antioxidants, while exercise offers many health benefits as well. Recent findings have evidenced that diet and physical factors are correlated to oxidative stress. Diet and physical factors have debatable roles in modulating oxidative stress and effects on the endothelium. Since endothelium and oxidative stress play critical roles in cardiovascular and metabolic diseases, dietary and physical factors could have significant implications on prevention of the diseases. This review is aimed at summarizing the current knowledge on the impact of diet manipulation and physical factors on endothelium and oxidative stress, focusing on cardiovascular and metabolic diseases. We discuss the friend-and-foe role of dietary modification (including different diet styles, calorie restriction, and nutrient supplementation) on endothelium and oxidative stress, as well as the potential benefits and concerns of physical activity and exercise on endothelium and oxidative stress. A fine balance between oxidative stress and antioxidants is important for normal functions in the cells and interfering with this balance may lead to unfavorable effects. Further studies are needed to identify the best diet composition and exercise intensity.

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Francisco, Bosch-Morell, Mérida Salvador, and Navea Amparo. "Oxidative Stress in Myopia." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/750637.

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Myopia affected approximately 1.6 billion people worldwide in 2000, and it is expected to increase to 2.5 billion by 2020. Although optical problems can be corrected by optics or surgical procedures, normal myopia and high myopia are still an unsolved medical problem. They frequently predispose people who have them to suffer from other eye pathologies: retinal detachment, glaucoma, macular hemorrhage, cataracts, and so on being one of the main causes of visual deterioration and blindness. Genetic and environmental factors have been associated with myopia. Nevertheless, lack of knowledge in the underlying physiopathological molecular mechanisms has not permitted an adequate diagnosis, prevention, or treatment to be found. Nowadays several pieces of evidence indicate that oxidative stress may help explain the altered regulatory pathways in myopia and the appearance of associated eye diseases. On the one hand, oxidative damage associated with hypoxia myopic can alter the neuromodulation that nitric oxide and dopamine have in eye growth. On the other hand, radical superoxide or peroxynitrite production damage retina, vitreous, lens, and so on contributing to the appearance of retinopathies, retinal detachment, cataracts and so on. The objective of this review is to suggest that oxidative stress is one of the key pieces that can help solve this complex eye problem.

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Mansego, Maria L., Josep Redon, Sergio Martinez-Hervas, Jose T. Real, Fernando Martinez, Sebastian Blesa, Veronica Gonzalez-Albert, Guillermo T. Saez, Rafael Carmena, and Felipe J. Chaves. "Different Impacts of Cardiovascular Risk Factors on Oxidative Stress." International Journal of Molecular Sciences 12, no. 9 (September 20, 2011): 6146–63. http://dx.doi.org/10.3390/ijms12096146.

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Heales, S. J. R. "Oxidative stress and neuronal mitochondrial function. Factors dictating susceptibility." Journal of Neurochemistry 85 (May 8, 2003): 3. http://dx.doi.org/10.1046/j.1471-4159.85.s2.3_2.x.

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Kim, Juewon, Si Y. Cho, Donghyun Cho, Su H. Kim, Dae B. Seo, and Song S. Shin. "Oxidative Stress & FoxO Transcription Factors in Cardiovascular Aging." Current Medicinal Chemistry 24, no. 9 (May 3, 2017): 943–49. http://dx.doi.org/10.2174/0929867323666161213100140.

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Nabhan, Ashraf Fawzy, Lerine B. El-Din, Amal Hamed Rabie, and Gehan M. Fahmy. "Impact of intrapartum factors on oxidative stress in newborns." Journal of Maternal-Fetal & Neonatal Medicine 22, no. 10 (January 2009): 867–72. http://dx.doi.org/10.1080/14767050902994614.

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Wood, Lisa G., Dominic A. Fitzgerald, Peter G. Gibson, David M. Cooper, Clare E. Collins, and Manohar L. Garg. "Oxidative Stress in Cystic Fibrosis: Dietary and Metabolic Factors." Journal of the American College of Nutrition 20, no. 2 (April 2001): 157–65. http://dx.doi.org/10.1080/07315724.2001.10719028.

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McMahon, Michael, Yiguo Zhang, and John Hayes. "Oxidative stress and the Nrf1 and Nrf2 transcription factors." Toxicology Letters 172 (October 2007): S10. http://dx.doi.org/10.1016/j.toxlet.2007.05.047.

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Waeber, Bernard, and François Feihl. "Oxidative stress: A pivotal link among cardiovascular risk factors?" Current Hypertension Reports 7, no. 4 (August 2005): 229–30. http://dx.doi.org/10.1007/s11906-005-0015-2.

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Rodrigues-Díez, Raquel, and Mercedes Salaices. "Cardiovascular risk factors and oxidative stress in young people." Clínica e Investigación en Arteriosclerosis (English Edition) 29, no. 5 (September 2017): 216–17. http://dx.doi.org/10.1016/j.artere.2017.09.002.

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Santos, Leonardo, Carlos Escande, and Ana Denicola. "Potential Modulation of Sirtuins by Oxidative Stress." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9831825.

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Sirtuins are a conserved family of NAD-dependent protein deacylases. Initially proposed as histone deacetylases, it is now known that they act on a variety of proteins including transcription factors and metabolic enzymes, having a key role in the regulation of cellular homeostasis. Seven isoforms are identified in mammals (SIRT1–7), all of them sharing a conserved catalytic core and showing differential subcellular localization and activities. Oxidative stress can affect the activity of sirtuins at different levels: expression, posttranslational modifications, protein-protein interactions, and NAD levels. Mild oxidative stress induces the expression of sirtuins as a compensatory mechanism, while harsh or prolonged oxidant conditions result in dysfunctional modified sirtuins more prone to degradation by the proteasome. Oxidative posttranslational modifications have been identifiedin vitroandin vivo, in particular cysteine oxidation and tyrosine nitration. In addition, oxidative stress can alter the interaction with other proteins, like SIRT1 with its protein inhibitor DBC1 resulting in a net increase of deacetylase activity. In the same way, manipulation of cellular NAD levels by pharmacological inhibition of other NAD-consuming enzymes results in activation of SIRT1 and protection against obesity-related pathologies. Nevertheless, further research is needed to establish the molecular mechanisms of redox regulation of sirtuins to further design adequate pharmacological interventions.

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Numakawa, Tadahiro, Tomoya Matsumoto, Yumiko Numakawa, Misty Richards, Shigeto Yamawaki, and Hiroshi Kunugi. "Protective Action of Neurotrophic Factors and Estrogen against Oxidative Stress-Mediated Neurodegeneration." Journal of Toxicology 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/405194.

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Oxidative stress is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Low levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are important for maintenance of neuronal function, though elevated levels lead to neuronal cell death. A complex series of events including excitotoxicity, Ca2+overload, and mitochondrial dysfunction contributes to oxidative stress-mediated neurodegeneration. As expected, many antioxidants like phytochemicals and vitamins are known to reduce oxidative toxicity. Additionally, growing evidence indicates that neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and estrogens significantly prevent neuronal damage caused by oxidative stress. Here, we review and discuss recent studies addressing the protective mechanisms of neurotrophic factors and estrogen within this system.

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Chang, Tuanjie, and Lingyun Wu. "Methylglyoxal, oxidative stress, and hypertension." Canadian Journal of Physiology and Pharmacology 84, no. 12 (December 2006): 1229–38. http://dx.doi.org/10.1139/y06-077.

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Pathogenic mechanisms for essential hypertension are unclear despite striking efforts from numerous research teams over several decades. Increased production of reactive oxygen species (ROS) has been associated with the development of hypertension and the role of ROS in hypertension has been well documented in recent years. In this context, it is important to better understand pathways and triggering factors for increased ROS production in hypertension. This review draws a causative linkage between elevated methylglyoxal level, methylglyoxal-induced production of ROS, and advanced glycation end products in the development of hypertension. It is proposed that elevated methylglyoxal level and resulting protein glycation and ROS production may be the upstream links in the chain reaction leading to the development of hypertension.

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Santos, Fátima Milhano, Joana Mesquita, João Paulo Castro-de-Sousa, Sergio Ciordia, Alberto Paradela, and Cândida Teixeira Tomaz. "Vitreous Humor Proteome: Targeting Oxidative Stress, Inflammation, and Neurodegeneration in Vitreoretinal Diseases." Antioxidants 11, no. 3 (March 6, 2022): 505. http://dx.doi.org/10.3390/antiox11030505.

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Oxidative stress is defined as an unbalance between pro-oxidants and antioxidants, as evidenced by an increase in reactive oxygen and reactive nitrogen species production over time. It is important in the pathophysiology of retinal disorders such as diabetic retinopathy, age-related macular degeneration, retinal detachment, and proliferative vitreoretinopathy, which are the focus of this article. Although the human organism’s defense mechanisms correct autoxidation caused by endogenous or exogenous factors, this may be insufficient, causing an imbalance in favor of excessive ROS production or a weakening of the endogenous antioxidant system, resulting in molecular and cellular damage. Furthermore, modern lifestyles and environmental factors contribute to increased chemical exposure and stress induction, resulting in oxidative stress. In this review, we discuss the current information about oxidative stress and the vitreous proteome with a special focus on vitreoretinal diseases. Additionally, we explore therapies using antioxidants in an attempt to rescue the body from oxidation, restore balance, and maximize healthy body function, as well as new investigational therapies that have shown significant therapeutic potential in preclinical studies and clinical trial outcomes, along with their goals and strategic approaches to combat oxidative stress.

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Hussain, Tarique, Bie Tan, Yulong Yin, Francois Blachier, Myrlene C. B. Tossou, and Najma Rahu. "Oxidative Stress and Inflammation: What Polyphenols Can Do for Us?" Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/7432797.

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Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. Oxidative stress can activate a variety of transcription factors, which lead to the differential expression of some genes involved in inflammatory pathways. The inflammation triggered by oxidative stress is the cause of many chronic diseases. Polyphenols have been proposed to be useful as adjuvant therapy for their potential anti-inflammatory effect, associated with antioxidant activity, and inhibition of enzymes involved in the production of eicosanoids. This review aims at exploring the properties of polyphenols in anti-inflammation and oxidation and the mechanisms of polyphenols inhibiting molecular signaling pathways which are activated by oxidative stress, as well as the possible roles of polyphenols in inflammation-mediated chronic disorders. Such data can be helpful for the development of future antioxidant therapeutics and new anti-inflammatory drugs.

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Haque, Md Mamunul, Dhiraj P. Murale, Yun Kyung Kim, and Jun-Seok Lee. "Crosstalk between Oxidative Stress and Tauopathy." International Journal of Molecular Sciences 20, no. 8 (April 22, 2019): 1959. http://dx.doi.org/10.3390/ijms20081959.

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Tauopathy is a collective term for neurodegenerative diseases associated with pathological modifications of tau protein. Tau modifications are mediated by many factors. Recently, reactive oxygen species (ROS) have attracted attention due to their upstream and downstream effects on tauopathy. In physiological conditions, healthy cells generate a moderate level of ROS for self-defense against foreign invaders. Imbalances between ROS and the anti-oxidation pathway cause an accumulation of excessive ROS. There is clear evidence that ROS directly promotes tau modifications in tauopathy. ROS is also highly upregulated in the patients’ brain of tauopathies, and anti-oxidants are currently prescribed as potential therapeutic agents for tauopathy. Thus, there is a clear connection between oxidative stress (OS) and tauopathies that needs to be studied in more detail. In this review, we will describe the chemical nature of ROS and their roles in tauopathy.

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Mulford, K. E., and J. S. Fassler. "Association of the Skn7 and Yap1 Transcription Factors in the Saccharomyces cerevisiae Oxidative Stress Response." Eukaryotic Cell 10, no. 6 (April 8, 2011): 761–69. http://dx.doi.org/10.1128/ec.00328-10.

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ABSTRACT Saccharomyces cerevisiae Skn7p is a stress response transcription factor that undergoes aspartyl phosphorylation by the Sln1p histidine kinase. Aspartyl phosphorylation of Skn7p is required for activation of genes required in response to wall stress, but Skn7p also activates oxidative stress response genes in an aspartyl phosphorylation-independent manner. The presence of binding sites for the Yap1p and Skn7p transcription factors in oxidative stress response promoters and the oxidative stress-sensitive phenotypes of SKN7 and YAP1 mutants suggest that these two factors work together. We present here evidence for a DNA-independent interaction between the Skn7 and Yap1 proteins that involves the receiver domain of Skn7p and the cysteine-rich domains of Yap1p. The interaction with Yap1p may help partition the Skn7 protein to oxidative stress response promoters when the Yap1 protein accumulates in the nucleus.

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Kacarevic, Dragana, Natasa Bogavac-Stanojevic, Vesna Spasojevic-Kalimanovska, Dragana Bojanin, Tatjana Milenkovic, Aleksandra Stefanovic, Marija Mihajlovic, et al. "Factors associated with oxidative stress status in pediatric patients with type 1 diabetes mellitus." Journal of Pediatric Endocrinology and Metabolism 33, no. 5 (May 26, 2020): 591–98. http://dx.doi.org/10.1515/jpem-2019-0555.

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AbstractBackgroundOxidative stress is implicated in both, the onset and the progression of type 1 diabetes mellitus (T1DM). There is accumulated evidence of increased biomarkers of oxidative stress in newly diagnosed, T1DM patients without complications, and in those with advanced disease. In this cross-sectional study, we investigated factors affecting oxidative stress status in pediatric patients with T1DM.MethodsAdvanced oxidation protein products (AOPP), prooxidant-antioxidant balance (PAB), total sulfhydryl (SH) groups, and superoxide dismutase (SOD) activity were determined in 170 children and adolescents with T1DM. Principal component analysis was used to investigate clustering of clinical and laboratory variables associated with elevated oxidative stress and reduced antioxidative defense biomarkers.ResultsFactor analysis extracted five factors, interpreted as (1) “weight status factor” including age, BMI, waist and hip circumferences; (2) “proatherogenic factor” that included LDL-cholesterol, non-HDL-cholesterol, and triglycerides; (3) “metabolic control factor” including glucose and HbA1c; (4) “renal marker factor” with positive loading of urinary albumin excretion rate and negative loading of GFR; and (5) “antiatherogenic factor” that included HDL-cholesterol. High AOPP levels were independently predicted by “proatherogenic” (OR: 2.32; 95% CI: 1.44–3.71; p < 0.001), “metabolic control” (OR: 2.24; 95% CI: 1.35–3.73; p < 0.01), and “renal marker” (OR: 1.65; 95% CI: 1.03–2.65; p < 0.05) factors. “Renal marker factor” was a significant predictor of PAB (OR: 0.52; 95% CI: 0.34–0.81; p < 0.01). Regarding antioxidative defense markers, reduced SH groups were predicted by “proatherogenic factor” (OR: 0.56; 95% CI: 0.34–0.94; p < 0.05), while “weight status factor” predicted lower SOD activity (OR: 1.66; 95% CI: 1.03–2.67; p < 0.05).ConclusionsCardiometabolic risk factors and renal function are associated with oxidative stress in pediatric T1DM patients.

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MOREL, Yannick, and Robert BAROUKI. "Repression of gene expression by oxidative stress." Biochemical Journal 342, no. 3 (September 5, 1999): 481–96. http://dx.doi.org/10.1042/bj3420481.

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Gene expression is modulated by both physiological signals (hormones, cytokines, etc.) and environmental stimuli (physical parameters, xenobiotics, etc.). Oxidative stress appears to be a key pleiotropic modulator which may be involved in either pathway. Indeed, reactive oxygen species (ROS) have been described as second messengers for several growth factors and cytokines, but have also been shown to rise following cellular insults such as xenobiotic metabolism or enzymic deficiency. Extensive studies on the induction of stress-response genes by oxidative stress have been reported. In contrast, owing to the historical focus on gene induction, less attention has been paid to gene repression by ROS. However, a growing number of studies have shown that moderate (i.e. non-cytotoxic) oxidative stress specifically down-regulates the expression of various genes. In this review, we describe the alteration of several physiological functions resulting from oxidative-stress-mediated inhibition of gene transcription. We will then focus on the repressive oxidative modulation of various transcription factors elicited by ROS.

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Maria, Vadala, Palmieri Beniamino, Malagoli Andrea, and Laurino Carmen. "Oxidative stress, plasma/salivary antioxidant status detection and health risk factors." Asian Journal of Medical Sciences 8, no. 1 (January 3, 2017): 32–41. http://dx.doi.org/10.3126/ajms.v8i1.15134.

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Background: Oxidative stress is involved in the pathophysiology of several diseases such as cardiovascular disorders, cancer, neurodegeneration.Aims and Objectives: Our study evaluated the oxidant/antioxidant status on a cohort of healthy patients matched with some independent variables as a basic individual redox balance monitor on a disease-prevention perspective.Materials and Methods: The anecdotic, retrospective and observational study included 200 apparently healthy volunteers after formal informed consent release whose personal history and physical examination had been recorded specifically on the following items: age, previous diseases, sport activities, smoking habit, balanced/unbalanced nutrition, current absence/presence of inflammatory processes, oral health hygiene, administration of oral contraceptives or hormone replacement therapy in postmenopausal women. No drug treatment was admitted in the recruited patients, up to 6 months before the evaluation. The laboratory instruments used were Point of care FRAS 4 Evolvo (H&D, Parma, Italy) measuring the oxidative stress in plasma samples and antioxidant capacity in plasma and saliva samples.Results: Two-hundred patients were recruited. Statistically relevant differences were observed in oxidative stress-related variables, namely a significant relationship between plasma oxidative stress level and female gender (p<0.01), between saliva antioxidant level and age (p=0.01), between plasma antioxidant level and unbalanced diet (p<0.01), between plasma oxidative stress level and inflammation in the oral cavity (p=0.04), and between saliva antioxidant level and inflammation in the oral cavity (p<0.01).Conclusions: A relationship between oxidative/antioxidant status and health risk factors has been outlined in our study; the achieved data are quite helpful, in the clinical practice, providing additional information on individual general health conditions, putatively related to prevention diagnosis, prognosis, and treatment effectiveness in some specific diseases.Asian Journal of Medical Sciences Vol.8(1) 2017 32-41

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Journal articles on the topic 'Oxidative stress factors'

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