Crosstalk between Oxidative Stress and Inflammation in Essential Thrombocythemia (original) (raw)
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Increased oxidative stress in patients with essential thrombocythemia
European review for medical and pharmacological sciences
Essential thrombocythemia (ET) is a clonal disease in which thrombotic and hemorrhagic complications are common. Our aim in this study was to investigate whether oxidative stress in ET patients increased compared to healthy volunteers and to investigate whether there is a relationship between vascular events and oxidative status parameters in ET patients. We determined the serum levels of oxidative status parameters, such as total oxidative status (TOS), total antioxidant status (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) in ET patients. Forty-three ET patients (20 males, 23 females) and 20 healthy volunteers were enrolled. Oxidative status parameters of the patients were compared with those of the controls at time of diagnosis and at 6th-month follow-up. Additionally, oxidative status parameters of patients with ET with a history of vascular event were compared with patients without a vascular event history during diagnosis. Rises in TOS, OSI, and MDA were statist...
Erythrocyte oxidative stress and thrombosis
Expert Reviews in Molecular Medicine
Thrombosis is a common disorder with a relevant burden of morbidity and mortality worldwide, particularly among elderly patients. Growing evidence demonstrated a direct role of oxidative stress in thrombosis, with various cell types contributing to this process. Among them, erythrocytes produce high quantities of intracellular reactive oxygen species (ROS) by NADPH oxidase activation and haemoglobin autoxidation. Concomitantly, extracellular ROS released by other cells in the blood flow can be uptaken and accumulate within erythrocytes. This oxidative milieu can alter erythrocyte membrane structure, leading to an impaired erythrocyte function, and promoting erythrocytes lysis, binding to endothelial cells, activation of platelet and of coagulation factors, phosphatidylserine exposure and release of microvesicles. Moreover, these abnormal erythrocytes are able to adhere to the vessel wall, contributing to thrombin generation within the thrombus. This process results in accelerated ha...
Oxidative Stress and Thrombotic Disorders: Study in Patients with Venous Thromboembolism
https://www.ijhsr.org/IJHSR\_Vol.6\_Issue.1\_Jan2016/29.pdf, 2016
We aimed to investigate biochemical markers and the oxidant/antioxidant balance in patients with venous thromboembolism. This study was conducted as a prospective case-control study. 70 patients with venous thromboembolism enrolled to the study and 80 healthy subjects without risk factors for venous thromboembolism were selected as control group. Venous blood samples were obtained from venous thromboembolism patients during the initial diagnosis and from the control subjects. Biochemical parameters (triglycerides and HDL-cholesterol) and oxidative stress markers (malondialdehyde, carbonyl proteins, superoxide anion expressed as reduced Nitroblue Tetrazolium, nitric oxide expressed as nitrite, reduced glutathione, vitamin C, catalase, superoxide dismutase) were assayed by biochemical methods. Plasma triglyceride was increased and HDL-cholesterol levels were decreased in venous thromboembolism patients compared to control. Malondialdehyde, carbonyl proteins levels and catalase activity were high while nitric oxide and vitamin C were low in venous thromboembolism patients than control. Reduced glutathione concentrations, superoxide anion and superoxide dismutase activity were found not significant respectively. Oxidative stress may be one of the causative factors in venous thromboembolism and probably contributes to additional disorders.
Inflammation, 2014
Instability in circulation, hypoperfusion, hypoxia, and ischemia in pulmonary thromboembolism (PTE) may occur as a result of failure in pulmonary circulation. All these conditions cause inflammation and oxidative stress. We aimed to investigate inflammatory markers, asymmetric dimethylarginine (ADMA) levels, and the oxidant-antioxidant balance in patients with PTE. This study was conducted as a prospective case-control study. Thirty-eight patients with PTE enrolled to the study. Ageand gender-matched 38 healthy subjects without risk factors for pulmonary embolism were selected as control group. Venous blood samples were obtained from the PTE patients during the initial diagnosis and at the first month of treatment and from the control subjects. Interleukine-6 (IL-6), tumor necrosis factor alpha (TNF-α), total antioxidant status (TAS), total oxidant status (TOS), and ADMA levels were measured for all the samples. The results of patients and healthy subjects were compared. The mean age of the control group was 51.81±15.18 years, and the mean age of the patients was 52.90±18.22 years (p=0.770). Deep venous thrombosis was present in 68 % of the patients. While we found significant differences between the patient and control groups in terms of IL-6, TAS, TNF-α, ADMA and oxidative stress index (OSI) values (p=0.001, p=0.011, p=0.038, p=0.028, and p=0.024, respectively), the TOS value was not different between the groups (p=0.080). The ADMA, TNF-α, TAS, TOS, and OSI values of the patients during the initial diagnosis and at the first month of treatment were not different (p>0.05). The results of this study indicate an increased inflammation, endothelial damage, and oxidative stress in PTE. No difference at the first month of therapy suggests ongoing processes. We consider that these markers may be useful in the diagnosis and follow up of PTE.
The Thrombotic Events in Polycythemia Vera Patients May Be Related to Increased Oxidative Stress
Medical Principles and Practice, 2014
oxidative status parameters of patients with PV and a history of a vascular event were compared with those of patients with no history of a vascular event. Results: The TOS, OSI and MDA values were significantly higher in the patients than in the control group at the time of diagnosis. At 6 months after phlebotomy and 100 mg/day acetyl salicylic acid therapy, the TOS, OSI and MDA values were significantly lower in the patients when compared to the pretreatment values. The TOS and OSI levels were notably higher in the patients with a vascular-event history than in those without this history. Conclusion: Oxidative stress parameters were increased in PV patients.
Evaluation of oxidative stress balance in acute deep vein thrombosis
Turkish Journal of Biochemistry, 2015
Objective: The purpose of this study was to show the association between oxidative stress and deep venous thrombosis (DVT) by determining total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI) values in patients with DVT and to take precautionary measures to balance oxidative status. Methods: TOS, TAS and OSI levels in serum from 52 individuals with DVT and 45 without DVT were compared. Results: TOS and OSI levels were significantly higher in patients with DVT compared with the control group (p<0.0001), but no difference was observed in TAS levels (p=0.118). The patient group was divided into two subgroups, idiopathic and secondary DVT. TOS and OSI levels were significantly higher patients with both idiopathic DVT and secondary DVT compared to the control group (p<0.0001). TAS levels were significantly higher in patients with idiopathic DVT than in the control group, but no difference was observed in the patients with secondary DVT. Conclusion: Specificity and sensitivity values obtained from the receiver operating characteristic (ROC) curve show that TOS and OSI are both markers that can be used in the diagnosis of DVT. Also, determination of oxidative stress markers may guide clinicians to take necessary precautions to balance oxidative stress in the patients.
Angioplasty, Various Techniques and Challenges in Treatment of Congenital and Acquired Vascular Stenoses, 2012
Angioplasty, Various Techniques and Challenges in Treatment of Congenital and Acquired Vascular Stenoses 64 generation to H 2 O 2 , which transformed further by catalase, glutathion plus glutathion peroxydase. Under hypoxic condition several sources of free radicals activated, e.g. the NADPH oxydase, xanthin oxidase, and others. ROS generated by hypoxia disrupts respiratory chain, causing a vicious cycle, manifested in modification in permeability transmission, loss of membrane potential, altering the function of mitochondrial complex I, III, and generating ubisemiquinon radical, which donates its electron to oxygen resulting in superoxyde anion. In reduced oxygen tension complex II switches its activity from succinate dehydrogenase to fumarate reductase (Henrich M et al, 2004.), Kolamunne RT et al 2011). Chronic sever hypoxia induces ATP depletion, and cell death. In the course of hypoxia, ATP generation decrees, exhausting the ATP sources, which responsible for the overflow of hypoxanthine, an ATP metabolite. Hypoxanthine in normoxyc condition metabolized further by xanthine dehydrogenase to xanthine (by means of nicotinamide adenine dinucleotide (NAD) as cofactor), but during hypoxia xanthin dehydrogenase converted to xanthin oxidase, which is unable to catalyse this conversion, but in the presence of high oxygen level in reoxygenation phase it continuously generates toxic ROS, because it uses oxygen as cofactor. ROS are effective oxidizing and reducing agents that directly damage cellular membranes, leading to impairment of membrane ion channels, disturbing cellular ionic balance resulting in cell swelling. ROS can activate leucocytes as well, and induce chemotaxis, cytokine release, leukocyte infiltration into the injured tissues, and due to endothelium dysfunction, a systemic reperfusion inflammatory response occurs. The most serious consequences of IR are the development of remote organ injuries in non-ischemic organs and can induce systemic inflammatory response injury (SIRS) or multiorgan failure syndrome (MOFS) which are responsible for of 20-40% of death in intensive care units (Levy JH, and Tanaka KA 2003). Tough reconstruction of the flow in the occluded vessels is not without risk, because of the generated volume, pressure and metabolic load, accompanied by further tissue damages resulting in the so-called reperfusion injury. The main components of the molecular pathophysiological cascades are the activated circulating cells, first of all the white blood cells (WBC), mainly the neutrophils, due to their intensive free radical production, but, thrombocytes (PLT), red blood cells (RBC), and the cells of the vessel wall (endothelial cells and smooth muscle cells) also participate in the free radical production and the tissue damage (Roth and Hejjel 2003). In the early reperfusion the release of inflammatory cytokines, such as tumor necrosis factor alpha (TNF) increase too. These events together with the elevated Ca 2+ levels inside the attached cells threat the integrity of the whole organism, destroying the crucial macromolecules, proteins, lipids and nucleic acids (Arato et al. 2005) , (Blaisdell FW 1989). Reactive oxygen species are Janus-faced agents. They have important role in eliminating pathogen microorganisms from the body, and can regulate cell growth and differentiation. ROS can act as important signalling molecules, in the circulation and participate in the maintenance of intra-and extracellular milieu. They can induce redox sensitive transcription factors, regulate redox sensitive signalization cascades and can act as secondary messengers (Kathy K et al 2000) , (Dröge W, 2002). Oxygen free radicals can act as second messengers and they are able to influence the function of enzymes, and transcription factors, leading to the induction of genes are sensitive to them (Li W et al 2008). Their intra-and extracellular levels are regulated by SOD and catalase (the enzymes are present in almost all living organisms are exposed to oxygen) and other antioxidant, respectively. On the other hand they can cause endothelial dysfunction due to eliminating vital nitrogenous monoxides
Oxidative stress's impact on red blood cells Unveiling implications for health and disease
Medicine, 2024
Oxidative stress, a condition characterized by an imbalance between reactive oxygen species (ROS) production and the body's ability to detoxify them, has emerged as a pivotal factor in the pathophysiology of various diseases. Red blood cells (RBCs), essential components of the circulatory system, are particularly susceptible to oxidative damage due to their high oxygencarrying capacity and the abundance of vulnerable biomolecules. This review comprehensively explores the intricate mechanisms underlying oxidative stress-induced damage to red blood cells and the subsequent implications for overall health and disease. We delve into the sources of ROS generation within RBCs, including metabolic processes and external factors, shedding light on the delicate redox balance that governs cellular homeostasis. The impact of oxidative stress on red blood cells extends beyond the confines of their primary physiological role, as these cells actively participate in immune responses, inflammation modulation, and nitric oxide metabolism. Consequently, understanding the implications of oxidative stress on RBCs provides valuable insights into the broader landscape of health and disease. In conclusion, this review underscores the critical role of oxidative stress in influencing red blood cell physiology and its far-reaching implications for human health. Elucidating the molecular intricacies of this relationship not only enhances our understanding of fundamental biological processes but also paves the way for the development of targeted therapeutic interventions to mitigate the adverse effects of oxidative stress on red blood cells and, by extension, on overall health. Abbreviations: RBCs = red blood cells, RNS = reactive nitrogen species, ROS = reactive oxygen species.
Inflammation, oxidative stress, and atherosclerosis
2004
Background: Accelerated atherosclerosis is the major cause of mortality in patients on chronic hemodialysis (HD). Inflammation, increased oxidative stress and endothelial activation or dysfunction might be the major factors leading to high cardiovascular mortality rate in HD patients. Also, C667T mutation of methylenetetrahydrofolate reductase (MTHFR) might be associated with accelerated atherosclerosis. Aim: The present study was designed to clarify the role of inflammation, oxidative stress parameters, endothelial activation or dysfunction and genotyping of MTHFR enzyme which affect the level of homocysteine and their relation to carotid artery intima-media thickness (CIMT) as indicators of atherosclerosis. Subjects & Methods: 44 chronic hemodialysis (HD) patients and 40 healthy subjects were included in the study. Serum highly sensitive C reactive protein (hs-CRP) and IL-6 were measured as inflammatory markers, soluble vascular cell adhesion molecule-1 (sVCAM-1) was measured as a marker of endothelial activation and dysfunction. Serum thiobarbituric acid reactive substances (TBARS), total nitric oxide (NO), total peroxides (TP), total antioxidant capacity (TAC) and oxidative stress index (OSI) levels were determined as oxidative stress markers. Common carotid intima media thickness (CC-IMT) was assessed by carotid artery ultrasonography, genotyping of MTHFR enzyme which affect the level of homocysteine was analyzed by PCR-RFLIP technique. Results: Chronic HD patients had elevated levels of inflammatory markers (hs-CRP and IL-6), enhanced endothelial activation or dysfunction demonstrated by elevated VCAM-1 as compared by healthy controls. Also, they had enhanced oxidative stress indicated by the higher levels of NO, TBARS, TP, OSI and lower levels of TAC as compared to controls. Hemodialysis patients had significantly higher CC-IMT levels. There is a significant positive correlation between inflammatory cytokines (hs-CRP and IL-6), and each of TBARS, total NO, TP and OSI with CC-IMT Also, the previous parameters negatively correlated with TAC. There is no significant difference in the genotype of C667T MTHFR between patients and controls, but that mutation especially the TT genotype is associated with development of atherosclerosis as indicated by the increase of CC-IMT.