scholarly journals Oxidative Stress and Inflammation in Renal and Cardiovascular Complications of Diabetes

Biology ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 18
Author(s):  
Amelia Charlton ◽  
Jessica Garzarella ◽  
Karin A. M. Jandeleit-Dahm ◽  
Jay C. Jha
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Tissue Injury ◽  
Cardiovascular Complications ◽  
Therapeutic Strategies ◽  
Cellular Damage ◽  
Antioxidant Defenses ◽  
Pathological State ◽  
Oxygen Species ◽  
Emerging Therapies

Oxidative stress and inflammation are considered major drivers in the pathogenesis of diabetic complications, including renal and cardiovascular disease. A symbiotic relationship also appears to exist between oxidative stress and inflammation. Several emerging therapies target these crucial pathways, to alleviate the burden of the aforementioned diseases. Oxidative stress refers to an imbalance between reactive oxygen species (ROS) and antioxidant defenses, a pathological state which not only leads to direct cellular damage but also an inflammatory cascade that further perpetuates tissue injury. Emerging therapeutic strategies tackle these pathways in a variety of ways, from increasing antioxidant defenses (antioxidants and Nrf2 activators) to reducing ROS production (NADPH oxidase inhibitors and XO inhibitors) or inhibiting the associated inflammatory pathways (NLRP3 inflammasome inhibitors, lipoxins, GLP-1 receptor agonists, and AT-1 receptor antagonists). This review summarizes the mechanisms by which oxidative stress and inflammation contribute to and perpetuate diabetes associated renal and cardiovascular disease along with the therapeutic strategies which target these pathways to provide reno and cardiovascular protection in the setting of diabetes.

scholarly journals Reactive oxygen species : A key hallmark of cardiovascullar disease

2019 ◽  
Vol 25 (2) ◽  
Author(s):  
Manorma Singh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Cardiovascular Complications ◽  
The Body ◽  
Oxygen Species

Free radicals and oxidants play a dual role as both toxic and beneficial compounds, since they can be either harmful or helpful to the body. They are produced either from normal cell metabolisms in situ or from external sources (pollution, cigarette smoke, radiation, medication). When an overload of free radicals cannot gradually be destroyed, their accumulation in the body generates a phenomenon called oxidative stress. This process plays a major part in the development of chronic and degenerative illness such as cancer, autoimmune disorders, aging, cataract, rheumatoid arthritis, cardiovascular and neurodegenerative diseases. Cardiovascular diseases (CVDs) have been the prime cause of mortality worldwide for decades. However, the underlying mechanism of their pathogenesis is not fully clear yet. It has been already established that reactive oxygen species (ROS) play a vital role in the progression of CVDs. ROS are chemically unstable reactive free radicals containing oxygen, normally produced by xanthine oxidase, nicotinamide adenine dinucleotide phosphate oxidase, lipoxygenases or mitochondria or due to the uncoupling of nitric oxide synthase in vascular cells. When the equilibrium between production of free radicals and antioxidant capacity of human physiology gets altered due to several pathophysiological conditions, oxidative stress is induced, which in turn leads to tissue injury. The information generated by this review aims to provide updated insights into the understanding of the mechanisms behind cardiovascular complications mediated by ROS.

scholarly journals Age-Related Macular Degeneration: Role of Oxidative Stress and Blood Vessels

2021 ◽  
Vol 22 (3) ◽  
pp. 1296
Author(s):  
Yue Ruan ◽  
Subao Jiang ◽  
Adrian Gericke
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Therapeutic Strategies ◽  
Vision Impairment ◽  
Age Related Macular Degeneration ◽  
Oxygen Species ◽  
Age Related

Age-related macular degeneration (AMD) is a common irreversible ocular disease characterized by vision impairment among older people. Many risk factors are related to AMD and interact with each other in its pathogenesis. Notably, oxidative stress and choroidal vascular dysfunction were suggested to be critically involved in AMD pathogenesis. In this review, we give an overview on the factors contributing to the pathophysiology of this multifactorial disease and discuss the role of reactive oxygen species and vascular function in more detail. Moreover, we give an overview on therapeutic strategies for patients suffering from AMD.

Hyperglycemia Induces Generation of Reactive Oxygen Species and Accelerates Apoptotic Cell Death in Salivary Gland Cells

Pathobiology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Naoyuki Matsumoto ◽  
Daisuke Omagari ◽  
Ryoko Ushikoshi-Nakayama ◽  
Tomoe Yamazaki ◽  
Hiroko Inoue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salivary Gland ◽  
Tissue Injury ◽  
Ros Production ◽  
Oxygen Species ◽  
Saliva Secretion ◽  
Salivary Gland Tissue ◽  
Gland Tissue

<b><i>Introduction:</i></b> Type-2 diabetes mellitus (T2DM) is associated with several systemic vascular symptoms and xerostomia. It is considered that hyperglycemia-induced polyuria and dehydration cause decreased body-water volume, leading to decreased saliva secretion and, ultimately, xerostomia. In T2DM, increased production of reactive oxygen species (ROS) causes tissue damage to vascular endothelial cells as well as epithelial tissue, including pancreas and cornea. Hence, a similar phenomenon may occur in other tissues and glands in a hyperglycemic environment. <b><i>Methods:</i></b> Salivary gland tissue injury was examined, using T2DM model mouse (db/db). Transferase‐mediated dUTP nick‐end labeling (TUNEL) was conducted to evaluate tissue injury. The levels of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine, Bax/Bcl-2 ratio were measured as indicator of oxidative stress. Moreover, in vitro ROS production and cell injury was evaluated by mouse salivary gland-derived normal cells under high-glucose condition culture. <b><i>Results:</i></b> In vivo and in vitro analysis showed a higher percentage of TUNEL-positive cells and higher levels of MDA and 8-hydroxy-2′-deoxyguanosine in salivary gland tissue of db/db mice. This suggests damage of saliva secretion-associated lipids and DNA by hyperglycemic-induced oxidative stress. To analyze the mechanism by which hyperglycemia promotes ROS production, mouse salivary gland-derived cells were isolated. The cell culture with high-glucose medium enhanced ROS production and promotes apoptotic and necrotic cell death. <b><i>Conclusion:</i></b> These findings suggest a novel mechanism whereby hyperglycemic-induced ROS production promotes salivary gland injury, resulting in hyposalivation.

scholarly journals NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Renal Tissue ◽  
Oxygen Species ◽  
Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

Thioredoxins in cardiovascular disease

2015 ◽  
Vol 93 (11) ◽  
pp. 903-911 ◽  
Author(s):  
Thomas F. Whayne ◽  
Narasimham Parinandi ◽  
Nilanjana Maulik
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Hormone Replacement ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Causative Factor ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Vascular Endothelial Dysfunction ◽  
Familial Combined Hyperlipidemia ◽  
Disulfide Reduction

Key thioredoxin (Trx) system components are nicotinamide adenine dinucleotide phosphate (NADPH), Trx reductase (TrxR), and Trx. TrxR catalyzes disulfide reduction in Trx with NADPH as cofactor. Because Trx is an antioxidant, oxidative stress results in an increase in Trx, which has a reduced disulfide component. If Trx is suppressed, oxidative stress in higher. In contrast a decrease in oxidative stress is associated with low Trx levels. Trx is involved in inflammation, apoptosis, embryogenesis, and cardiovascular disease (CVD). This review focuses on the Trx system in CVD. Abnormal Trx binding occurs in mouse familial combined hyperlipidemia; however, this has not been confirmed in humans. Congestive heart failure is a manifestation of many CVDs, which may be improved by attenuating oxidative stress through the suppression of Trx and decreased reactive oxygen species. Angiotensin II is associated with hypertension and other CVDs, and its receptor blockade results in decreased oxidative stress with reduced Trx levels. Inflammation is a major causative factor of CVDs, and myocarditis as an example, is associated with increased Trx levels. Vascular endothelial dysfunction has an association with CVD. This dysfunction is alleviated by hormone replacement therapy, which involves decreased oxidative stress and Trx levels. Diabetes mellitus has a major association with CVDs; increase in Trx levels may reflect insulin resistance. Identification of Trx system abnormalities may lead to innovative approaches to treat multiple CVDs and other pathologies.

scholarly journals Roles of Superoxide dismutase(SOD) , Malondialdehyde (MDA), 8-iso-prostaglandinF2α ( 8-iso-PGF2α)as oxidative stress in development and progression of Brest cancer in Iraqi females patients

2020 ◽  
Vol 25 (1) ◽  
pp. 1-4
Author(s):  
Ferdous Abbas Jabir ◽  
Ahmed Sabah Shaker
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Patients ◽  
Antioxidant Defenses ◽  
Blood Levels ◽  
P Value ◽  
Oxygen Species ◽  
Breast Cancer Patients ◽  
Markers Of Oxidative Stress ◽  
The Mean

               Oxidative stress occurs as a result of disturbance in the balance between the production of reactive oxygen species (free radicals) and antioxidant defenses. Markers of oxidative stress were measured the markers of oxidative stress in breast cancer patients after diagnosis of breast cancer and compared these plasma blood levels controls This study was conducted to three markers of oxidative stress ;these are (SOD) enzyme ,malondialdehyde (MDA)and8-iso-prostaglandinF2α plasma of patients with breast cancer and compare with controls .In this study ;  the mean MDA (ng/ml) levels for the breast cancer patients and the controls were55.91±3.31 and40.61±3.76  respectively, while the SOD (pg/ml) levels were1530.37±80.4 and1851.4 9±93.65  respectively and the 8-iso-PGF2α (ng/ml ) levels were 40.16±3.31 and 30.16±2.34  difference of the mean were statistically significant (p value <0.05).                                                                                                                       

Abstract 132: A Novel Hydrogen Sulfide (H 2 S) Prodrug, SG1002, Protects Against Myocardial Oxidative Damage and Hypertrophic Signaling via Induction of Cystathionine Β-Synthase (CBS) and Antioxidant Proteins

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Kazi N Islam ◽  
Erminia Donnarumma ◽  
Erinn Donnelly ◽  
David J Lefer
Keyword(s):  
Oxidative Stress ◽  
Clinical Utility ◽  
Culture Media ◽  
Therapeutic Strategies ◽  
Oxidation Products ◽  
Cellular Damage ◽  
Serum Starvation ◽  
Antioxidant Proteins ◽  
Hypertrophic Signaling ◽  
Cells Cultured

Background: Endogenously produced H 2 S is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H 2 S levels have proven cardioprotective in models of acute myocardial infarction and heart failure (HF). The present study was under taken to investigate the effects of a novel H 2 S prodrug, SG1002, on stress induced hypertrophic signaling in murine HL1 cardiomyocytes. Methods: HL1 cells were maintained either in serum starvation (1%) or serum containing (10%) media followed by treatment either with SG1002 or H 2 O 2 , or endothelin-1 (ET-1)/phenylephrine (Phe) or in combination. Treated cells were analyzed for specific experimental needs. Results: SG1002 significantly increased cellular levels of the H 2 S producing enzyme, CBS, as well as production of H 2 S and nitrosothiol in HL1 cells cultured both in serum starvation or serum containing media. SG1002 significantly inhibited H 2 O 2 and ET-1/Phe induced oxidative stress in both culture media as measured by advanced protein oxidation products and MDA levels. Expression of ANP and BNP were markedly attenuated by SG1002 treatment. Cells cultured in media supplemented with serum containing H 2 O 2 /(ET-1 or Phe) or in 1% serum exhibited decreased levels of CBS, SOD1, and catalase. When the HL1 cells were coincubated with SG1002 cellular damage from oxidative stress was significantly attenuated accompanied by an increase in CBS expression. Conclusion: Our data clearly demonstrate that SG1002 attenuates myocardial cellular damage via increasing antioxidant proteins. SG1002 directly increases H 2 S levels and upregulates CBS. Studies are currently underway to evaluate the clinical utility of SG1002 in HF.

Exploring the Potentials of Antioxidants in Retarding Ageing

2017 ◽  
pp. 166-195 ◽  
Author(s):  
Minu Kesheri ◽  
Swarna Kanchan ◽  
Rajeshwar P. Sinha
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Growth And Development ◽  
Aging Process ◽  
Reactive Oxygen ◽  
Normal Growth ◽  
Antioxidant Defenses ◽  
Oxygen Species ◽  
Biotic Stresses ◽  
Living Organisms

In retrospect to the rise in the occurrence of ageing related disorders and the everlasting desire to overcome ageing, exploring the causes, mechanisms and therapies to curb ageing becomes relevant. Reactive Oxygen Species (ROS) are commonly generated during normal growth and development. However abiotic and biotic stresses enhance the level of ROS which in turn pose the threat of oxidative stress. Ability to perceive ROS and to speedily commence antioxidant defenses is crucial for the survival as well as longevity of living cells. Therefore living organisms are bestowed with antioxidants to combat the damages caused by oxidative stress. This chapter aims to elucidate an overview of the process of ageing, generation and enhancement of reactive oxygen species, damages incurred by oxidative stress, its amelioration strategies, therapeutic and biotechnological potentials of antioxidants and various sources of bioactive compounds significant in retardation of aging process.

scholarly journals Endoplasmic Reticulum Stress: A Critical Molecular Driver of Endothelial Dysfunction and Cardiovascular Disturbances Associated with Diabetes

2019 ◽  
Vol 20 (7) ◽  
pp. 1658 ◽  
Author(s):  
Hatem Maamoun ◽  
Shahenda Abdelsalam ◽  
Asad Zeidan ◽  
Hesham Korashy ◽  
Abdelali Agouni
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Endoplasmic Reticulum ◽  
Endothelial Cell ◽  
Er Stress ◽  
Cardiovascular Complications ◽  
Endothelial Cell Dysfunction ◽  
Cell Dysfunction ◽  
Obesity And Diabetes

Physical inactivity and sedentary lifestyle contribute to the widespread epidemic of obesity among both adults and children leading to rising cases of diabetes. Cardiovascular disease complications associated with obesity and diabetes are closely linked to insulin resistance and its complex implications on vascular cells particularly endothelial cells. Endoplasmic reticulum (ER) stress is activated following disruption in post-translational protein folding and maturation within the ER in metabolic conditions characterized by heavy demand on protein synthesis, such as obesity and diabetes. ER stress has gained much interest as a key bridging and converging molecular link between insulin resistance, oxidative stress, and endothelial cell dysfunction and, hence, represents an interesting drug target for diabetes and its cardiovascular complications. We reviewed here the role of ER stress in endothelial cell dysfunction, the primary step in the onset of atherosclerosis and cardiovascular disease. We specifically focused on the contribution of oxidative stress, insulin resistance, endothelial cell death, and cellular inflammation caused by ER stress in endothelial cell dysfunction and the process of atherogenesis.

scholarly journals Curcumin Ameliorates Lead-Induced Hepatotoxicity by Suppressing Oxidative Stress and Inflammation, and Modulating Akt/GSK-3β Signaling Pathway

Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 703 ◽  
Author(s):  
Ahlam Alhusaini ◽  
Laila Fadda ◽  
Iman H. Hasan ◽  
Enas Zakaria ◽  
Abeer M. Alenazi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Tissue Injury ◽  
Elevated Serum ◽  
Antioxidant Defenses ◽  
Exact Role ◽  
Toxic Heavy Metal ◽  
Tnf Α ◽  
Gsk 3Β

Lead (Pb) is a toxic heavy metal pollutant with adverse effects on the liver and other body organs. Curcumin (CUR) is the principal curcuminoid of turmeric and possesses strong antioxidant and anti-inflammatory activities. This study explored the protective effect of CUR on Pb hepatotoxicity with an emphasis on oxidative stress, inflammation and Akt/GSK-3β signaling. Rats received lead acetate and CUR and/or ascorbic acid (AA) for seven days and samples were collected for analyses. Pb(II) induced liver injury manifested by elevated serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), as well as histopathological alterations, including massive hepatocyte degeneration and increased collagen deposition. Lipid peroxidation, nitric oxide, TNF-α and DNA fragmentation were increased, whereas antioxidant defenses were diminished in the liver of Pb(II)-intoxicated rats. Pb(II) increased hepatic NF-κB and JNK phosphorylation and caspase-3 cleavage, whereas Akt and GSK-3β phosphorylation was decreased. CUR and/or AA ameliorated liver function, prevented tissue injury, and suppressed oxidative stress, DNA damage, NF-κB, JNK and caspase-3. In addition, CUR and/or AA activated Akt and inhibited GSK-3β in Pb(II)-induced rats. In conclusion, CUR prevents Pb(II) hepatotoxicity via attenuation of oxidative injury and inflammation, activation of Akt and inhibition of GSK-3β. However, further studies scrutinizing the exact role of Akt/GSK-3β signaling are recommended.

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