Reactive Oxygen Species and Their Involvement in Red Blood Cell Damage in Chronic Kidney Disease

Oxidative Medicine and Cellular Longevity, Journal Year: 2021, Volume and Issue: 2021(1)

Published: Jan. 1, 2021

Reactive oxygen species (ROS) released in cells are signaling molecules but can also modify proteins. Red blood perform a major role maintaining the balance of redox blood. The main cytosolic protein RBC is hemoglobin (Hb), which accounts for 95-97%. Most other proteins involved protecting cell from oxidative stress. Hemoglobin factor initiating stress within erythrocyte. RBCs be damaged by exogenous oxidants. Hb autoxidation leads to generation superoxide radical, catalyzed or spontaneous dismutation produces hydrogen peroxide. Both oxidants induce hemichrome formation, heme degradation, and release free iron catalyst radical reactions. To maintain balance, appropriate antioxidants present cytosol, such as dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxiredoxin 2 (PRDX2), well low molecular weight antioxidants: glutathione, ascorbic acid, lipoic α-tocopherol, β-carotene, others. Redox imbalance may associated with overproduction ROS and/or insufficient capacity antioxidant system. Oxidative performs key CKD evidenced high level markers damage proteins, lipids, DNA vivo. In addition ROS, reduced observed, decrease activity SOD, GPx, PRDX2, antioxidants. addition, hemodialysis accompanied low-biocompatibility dialysis membranes activate phagocytic cells, especially neutrophils monocytes, leading respiratory burst. This review shows production under normal conditions its impact on disease progression. red (RBCs) their contribution cardiovascular discussed.

Language: Английский

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Redox changes and cellular senescence in Alzheimer's disease

Redox Biology, Journal Year: 2024, Volume and Issue: 70, P. 103048 - 103048

Published: Jan. 17, 2024

The redox process and cellular senescence are involved in a range of essential physiological functions. However, they also implicated pathological processes underlying age-related neurodegenerative disorders, including Alzheimer's disease (AD). Elevated levels reactive oxygen species (ROS) generated as result abnormal accumulation beta-amyloid peptide (Aβ), tau protein, heme dyshomeostasis is further aggravated by mitochondria dysfunction endoplasmic reticulum (ER) stress. Excessive ROS damages vital components such proteins, DNA lipids. Such damage eventually leads to impaired neuronal function cell death. Heightened oxidative stress can induce via activation the senescence-associated secretory phenotype exacerbate inflammation tissue dysfunction. In this review, we focus on how changes system contribute AD affected perturbations metabolism mitochondrial function. While potential therapeutic strategies targeting have received some attention, more research necessary bring them into clinical application.

Language: Английский

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Reactive Oxygen Species in Venous Thrombosis

International Journal of Molecular Sciences, Journal Year: 2020, Volume and Issue: 21(6), P. 1918 - 1918

Published: March 11, 2020

Reactive oxygen species (ROS) have physiological roles as second messengers, but can also exert detrimental modifications on DNA, proteins and lipids if resulting from enhanced generation or reduced antioxidant defense (oxidative stress). Venous thrombus (DVT) formation resolution are influenced by ROS through modulation of the coagulation, fibrinolysis, proteolysis complement system, well regulation effector cells such platelets, endothelial cells, erythrocytes, neutrophils, mast monocytes fibroblasts. Many conditions that carry an elevated risk venous thrombosis, Antiphospholipid Syndrome, alterations in their redox homeostasis. Dietary pharmacological antioxidants modulate several important processes involved DVT formation, overall effect is unknown there no recommendations regarding use. The development novel treatments aim to abrogate promote its will depend identification targets enable confined site interest order prevent off-target effects mechanisms. Subgroups patients with increased systemic oxidative stress might benefit unspecific treatment, more clinical studies needed bring clarity this issue.

Language: Английский

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Can Meat and Meat-Products Induce Oxidative Stress?

Antioxidants, Journal Year: 2020, Volume and Issue: 9(7), P. 638 - 638

Published: July 20, 2020

High meat and meat-products consumption has been related to degenerative diseases. In addition their saturated fatty acids cholesterol contents, oxidation products generated during production, storage, digestion, metabolization have largely implicated. This review begins by summarizing the concept of main international regulatory agencies while highlighting nutritional importance consumption. The also dials in controversy white/red classification insists need more accurate based on adequate scores. Since one negative arguments that receives comes from association its with increase oxidative stress, compounds (malondialdehyde, thermaloxidized compounds, 4-hydroxy-nonenal, oxysterols, or protein carbonyls) metabolization, are included as a central aspect work. includes future remarks addressed study effects frame diet–gene interactions, stressing knowing genetic variables make individuals susceptible possible stress imbalance antioxidant protection. consumed meat/meat-products personalized nutrition reach plant-food is finally highlighted considering iron plant biophenols microbiota abundance plurality, which turn affect several aspects our physiology metabolism.

Language: Английский

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Abnormal Iron and Lipid Metabolism Mediated Ferroptosis in Kidney Diseases and Its Therapeutic Potential

Metabolites, Journal Year: 2022, Volume and Issue: 12(1), P. 58 - 58

Published: Jan. 10, 2022

Ferroptosis is a newly identified form of regulated cell death driven by iron-dependent phospholipid peroxidation and oxidative stress. has distinct biological morphology characteristics, such as shrunken mitochondria when compared to other known deaths. The regulation ferroptosis includes different molecular mechanisms multiple cellular metabolic pathways, including glutathione/glutathione peroxidase 4(GPX4) signaling which are involved in the amino acid metabolism activation GPX4; iron import/export storage/release intracellular through iron-regulatory proteins (IRPs), lipid unsaturated fatty acids membranes. plays an essential role pathology various kidneys diseases, acute kidney injury (AKI), chronic disease (CKD), autosomal dominant polycystic (ADPKD), renal carcinoma (RCC). Targeting with its inducers/initiators inhibitors can modulate progression diseases animal models. In this review, we discuss characteristics ferroptosis-based mechanisms, highlighting potential main ferroptosis-associated pathways treatment prevention diseases.

Language: Английский

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Ferroptosis and metabolic syndrome and complications: association, mechanism, and translational applications

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 14

Published: Jan. 8, 2024

Metabolic syndrome is a medical condition characterized by several metabolic disorders in the body. Long-term raise risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Therefore, it essential to actively explore aetiology (MetS) its comorbidities provide effective treatment options. Ferroptosis new form cell death that iron overload, lipid peroxide accumulation, decreased glutathione peroxidase 4(GPX4) activity, involves pathological processes variety diseases. Lipid deposition caused diseases overload significant syndrome, providing theoretical conditions for developing ferroptosis. Recent studies have found major molecules ferroptosis are linked common consequences, such as T2DM atherosclerosis. In this review, we first discussed mechanics ferroptosis, regulatory function inducers inhibitors significance loading MetS. Next, summarized role pathogenesis MetS, obesity, diabetes, Finally, relevant ferroptosis-targeted therapies raised some crucial issues concern directions future Mets-related treatments research.

Language: Английский

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Heme oxygenase-nitric oxide crosstalk-mediated iron homeostasis in plants under oxidative stress

Free Radical Biology and Medicine, Journal Year: 2022, Volume and Issue: 182, P. 192 - 205

Published: March 1, 2022

Language: Английский

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System biology-based investigation of Silymarin to trace hepatoprotective effect

Computers in Biology and Medicine, Journal Year: 2022, Volume and Issue: 142, P. 105223 - 105223

Published: Jan. 6, 2022

Language: Английский

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Stem cell-derived vessels-on-chip for cardiovascular disease modeling

Cell Reports, Journal Year: 2024, Volume and Issue: 43(4), P. 114008 - 114008

Published: March 26, 2024

The metabolic syndrome is accompanied by vascular complications. Human in vitro disease models are hence required to better understand dysfunctions and guide clinical therapies. Here, we engineered an open microfluidic vessel-on-chip platform that integrates human pluripotent stem cell-derived endothelial cells (SC-ECs). design enables seamless integration with state-of-the-art analytical technologies, including single-cell RNA sequencing, proteomics mass spectrometry, high-resolution imaging. Beyond previous systems, report SC-EC maturation means of barrier formation, arterial toning, high nitric oxide synthesis levels under gravity-driven flow. Functionally, corroborate the hallmarks early-onset atherosclerosis low sample volumes cell numbers flow conditions determining proteome secretome changes SC-ECs stimulated oxidized low-density lipoprotein free fatty acids. More broadly, our organ-on-chip modeling patient-specific tissue has potential become a general tool for animal-free research.

Language: Английский

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Carbon monoxide–induced metabolic switch in adipocytes improves insulin resistance in obese mice

JCI Insight, Journal Year: 2018, Volume and Issue: 3(22)

Published: Nov. 14, 2018

Obesity is characterized by accumulation of adipose tissue and one the most important risk factors in development insulin resistance. Carbon monoxide–releasing (CO-releasing) molecules (CO-RMs) have been reported to improve metabolic profile obese mice, but underlying mechanism remains poorly defined. Here, we show that oral administration CORM-401 mice fed a high-fat diet (HFD) resulted significant reduction body weight gain, accompanied marked improvement glucose homeostasis. We further unmasked an action believe be novel, which CO accumulates visceral uncouples mitochondrial respiration adipocytes, ultimately leading concomitant switch toward glycolysis. This was enhanced systemic sensitivity, as indicated lower blood increased Akt phosphorylation. Our findings indicate transient uncoupling activity elicited repetitive associated with gain sensitivity during HFD. Thus, prototypic compounds release could investigated for developing promising insulin-sensitizing agents.

Language: Английский

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