scholarly journals Crosstalk between Oxidative Stress and Inflammation in Obesity

2020 ◽  
Vol 71 (1) ◽  
pp. 228-232
Author(s):  
Mirela Elena Epingeac ◽  
Mihnea Alexandru Gaman ◽  
Camelia Cristina Diaconu ◽  
Amelia Maria Gaman
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Multifactorial Disease ◽  
Inflammation Markers ◽  
Stress Levels ◽  
Obese Subjects ◽  
The Relationship

Obesity is a multifactorial disease in which oxidative stress and inflammation play important roles. The aim of our study was to evaluate oxidative stress levels and inflammation markers in obese subjects vs. controls and to investigate the relationship between these values. We found increased levels of reactive oxygen species and inflammation markers (fibrinogen, ferritin, CRP, NLR) and decreased levels of antioxidants in obese subjects vs. controls.

The Relationship between Oxidative Stress and Obesity in Prostate Disease

2012 ◽  
Vol 79 (2) ◽  
pp. 156-158 ◽  
Author(s):  
Anna Scavuzzo ◽  
Vincenzo Favilla ◽  
Sebastiano Cimino ◽  
Massimo Madonia ◽  
Giovanni Li Volti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bioactive Substances ◽  
Prostatic Disease ◽  
Prostate Disease ◽  
The Relationship ◽  
And Oxidative Stress

Recent data suggest that chronic increment of reactive oxygen species (ROS) may be involved in the development and progression of chronic prostatic disease, such as BPH and PCa; adipose tissue produces bioactive substances called adipokines, also involved in the production of ROS. Our study aims to evaluate the relationship between obesity and oxidative stress in prostate disease.

Relationship between Ghrelin, reactive Oxygen Species and Oxidative Stress in Hypertensives

2021 ◽  
pp. 130-134
Author(s):  
M.B.S. Sugunakar ◽  
Priscilla Johnson ◽  
Shanthi Silambanan ◽  
Srinivas C.H. ◽  
Lavanya Sekhar
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Healthy Volunteers ◽  
Blood Sample ◽  
Antioxidant Status ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Total Antioxidant ◽  
The Mean ◽  
The Relationship

Globally, hypertension (HTN) is one of the leading cause of premature death as per WHO estimates.1 HTN poses a major public health burden as it is directly responsible for 57% of all stroke deaths and 24% of all coronary heart disease (CHD) deaths in India Oxidative stress refers to a state of elevated levels of reactive oxygen species (ROS) which occurs in several conditions such as hypertension that stimulate either ROS production or a deterioration in antioxidant defenses. Free radical like reactive oxygen species (ROS) were known to be involved in many cellular dysfunctions leading to the development of various lifestyle-related diseasesAlthough few researchers10,11 (Suematsu M 2005, Zwirska-Korczala K 2007) have reported the relationship between oxidative stress and the function of ghrelin, scanty information is available regarding the relationship between ghrelin and antioxidant status in hypertensives. Hence, this study was conducted to explore the association between Ghrelin and antioxidant status in hypertensives. Methodology: Blood Pressure was measured as per the JNC-7 recommendations, using Diamond digital monitor. BP cuff was tied on the right arm, with the subject in sitting position after five minutes of rest and then BP was measured. The AHA classification of hypertension was used to grade hypertension12 Subjects were advised to come for blood sample collection around 7am without having any breakfast the next day. 5ml of blood sample was collected, serum was separated labeled and stored in -200C for analysis. Ghrelin was estimated using sincere biotech ELISA kit E3091Hu HSN-38220090. Total antioxidant activity was measured by ferric reducing antioxidant power (FRAP) ASSAY colorimetric method13 Results: The study subjects were categorized into 3 groups. Group 1 – healthy volunteers; Group 2 – Grade 1 hypertensives (130–139mmHg SBP or 80–89mmHg DBP) and Group 3 – Grade 2 hypertensives (≥140mmHg SBP or ≥90mmHg DBP) The mean Ghrelin levels in Grade1 and Grade 2 hypertensives were lower when compared with healthy volunteers (Table.2, Fig.5) and it was statistically significant (P>0.0001) Similarly, the mean total antioxidant (TAO) levels in Grade 1 and Grade 2 hypertensives were lower when compared with healthy volunteers (Table.1, Fig.4) and it was statistically significant (p=0.000278). Fig.1 shows the correlation between Ghrelin levels and TAO levels. Antioxidant capacity was significantly (p=0.01) higher in the subjects with the higher levels of Ghrelin. Conclusion: It can be concluded that the redox balance changes in the blood of hypertensives. These changes may be compounded by Ghrelin which has an effect on vasodilator action of NO. Our results, therefore, highlight the need for more research to clarify the difference between oxidative stress linked to hypertension and the role of Ghrelin in hypertension. If proven, administration of ghrelin might become a unique new therapy for cardiovascular diseases.

scholarly journals The Evaluation of Oxidative Stress Levels in Obesity

2019 ◽  
Vol 70 (6) ◽  
pp. 2241-2244 ◽  
Author(s):  
Mirela Elena Epingeac ◽  
Mihnea Alexandru Gaman ◽  
Camelia Cristina Diaconu ◽  
Mohamed Gad ◽  
Amelia Maria Gaman
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Antioxidant Capacity ◽  
Total Cholesterol ◽  
Reactive Oxygen ◽  
Oxygen Radical ◽  
Oxygen Species ◽  
Free Oxygen Radical ◽  
Free Oxygen ◽  
Obese Subjects

The association between elevated values of reactive oxygen species and a decreased antioxidant capacity defines oxidative stress. Oxidative stress involvement is blamed in many diseases, including obesity. We evaluated oxidative stress levels by FORT (Free Oxygen Radical Testing � reactive oxygen species levels) and FORD (Free Oxygen Radical Defence � antioxidant capacity value) assays in obese subjects vs. controls. FORT values were high and FORD values were low in obese patients vs. controls, notably in obese subjects with comorbidities (diabetes, hypertension, dyslipidaemia, coronary heart disease, anaemia, hepatic steatosis). We found positive correlations between FORT values and total cholesterol, uric acid, triglycerides, LDL, body mass index, HDL/total cholesterol ratio, and negative correlations between FORT and age, HDL. FORD levels correlated oppositely to FORT. Our results suggest that obesity and oxidative stress are linked.

How does endothelin induce vascular oxidative stress in mineralocorticoid hypertension?

2006 ◽  
Vol 110 (2) ◽  
pp. 205-206 ◽  
Author(s):  
David M. Pollock
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Vascular Wall ◽  
Organ Damage ◽  
Oxygen Species ◽  
New Evidence ◽  
Vascular Oxidative Stress ◽  
The Relationship ◽  
And Oxidative Stress

Endothelin and reactive oxygen species have been identified as important mediators in the pathogenesis of hypertension and associated end-organ damage. In the present issue of Clinical Science, Callera and co-workers have provided new evidence that endothelin stimulates mitochondria to generate reactive oxygen species in the vascular wall during mineralocorticoid-induced hypertension in the rat. These studies open a new line of investigation that could be important for the development of therapeutic strategies; however, there still remains a great deal of uncertainty about the mechanisms that define the relationship between endothelin and oxidative stress in hypertension.

Crosstalk between Oxidative Stress, Chronic Inflammation and Disease Progression in Essential Thrombocythemia

2019 ◽  
Vol 70 (10) ◽  
pp. 3486-3489
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Disease Progression ◽  
Chronic Inflammation ◽  
Essential Thrombocythemia ◽  
Reactive Oxygen ◽  
Low Grade ◽  
Oxygen Species ◽  
Inflammation Markers ◽  
Leukemic Transformation

Essential thrombocythemia (ET) is a Philadelphia-negative chronic myeloproliferative neoplasm characterized by acquired somatic mutations: JAK2, CALR or MPL. It is associated with low-grade chronic inflammation, oxidative stress, overproduction of reactive oxygen species (ROS) and antioxidant deficiency. In ET, chronic inflammation and oxidative stress contribute to the genomic instability, the clonal evolution to myelofibrosis and the leukemic transformation. We evaluated ROS levels and the total antioxidant capacity (TAC) in 62 ET patients and investigated the relationship between ROS, TAC, chronic inflammation, leukocytosis, JAK2V617F mutation, and disease progression to myelofibrosis or leukemic transformation. We observed increased levels of ROS and inflammation markers and a decreased TAC in ET patients vs. controls. The acute myeloid leukaemia transformation associated increased levels of oxidative stress and inflammation markers and increased leukocyte counts, while myelofibrosis progression associated an increase in ROS and serum ferritin. Keywords: essential thrombocythemia, reactive oxygen species, inflammation, JAK2V617F

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Oxidative Stress Levels, JAK2V617F Mutational Status and Thrombotic Complications in Patients with Essential Thrombocythemia

2019 ◽  
Vol 70 (8) ◽  
pp. 2822-2825 ◽  
Author(s):  
Cornel Moisa ◽  
Mihnea Alexandru Gaman ◽  
Camelia Cristina Diaconu ◽  
Amelia Maria Gaman
Keyword(s):  
Oxidative Stress ◽  
Essential Thrombocythemia ◽  
Myeloproliferative Neoplasm ◽  
Oxygen Species ◽  
Mutational Status ◽  
Increased Risk ◽  
Stress Levels ◽  
Total Antioxidant ◽  
Thrombotic Complications ◽  
The Relationship

Essential thrombocythemia (ET) is a BCR-ABL1-negative myeloproliferative neoplasm associated with thrombotic and haemorrhagic complications. Reactive oxygen species (ROS) overexpression induces a growth advantage to JAK2V617F-positive clones and, in association with a higher number of immature platelets, leukocytosis, and additional cardiovascular risk factors, leads to an increased risk for thrombotic events. We evaluated oxidative stress by measuring ROS levels and the total antioxidant capacity (TAC) in 62 ET patients and investigated the relationship between oxidative stress, JAK2V617F mutational status and the development of thrombotic events. We found higher oxidative stress levels in JAK2V617F-positive vs. JAK2V617F-negative ET cases with no significant differences between homozygous and heterozygous genotypes. Increased ROS levels and thrombotic events were more frequent in ET patients with old age at diagnosis, higher haematocrit levels or leukocytosis.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

scholarly journals Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4138
Author(s):  
Yeon-Jin Cho ◽  
Sun-Hye Choi ◽  
Ra-Mi Lee ◽  
Han-Sung Cho ◽  
Hyewhon Rhim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Akt Signaling ◽  
Atp Depletion ◽  
Oxygen Species ◽  
Akt Signaling Pathway ◽  
Neuroprotective Effects ◽  
Lpa1 Receptor

Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

scholarly journals How to express the antioxidant properties of substances properly?

2021 ◽  
Author(s):  
Małgorzata Olszowy-Tomczyk
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Literature Review ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
The Body ◽  
Universal Method ◽  
Oxygen Species ◽  
Good Tool

AbstractOxidative stress, associated with an imbalance between the oxidants (reactive oxygen species) and the antioxidants in the body, contributes to the development of many diseases. The body’s fight against reactive oxygen species is supported by antioxidants. Nowadays, there are too many analytical methods, but there is no one universal technique for assessing antioxidant properties. Moreover, the applied different ways of expressing the results lead to their incompatibility and unreasonable interpretation. The paper is a literature review concerning the most frequent ways of antioxidant activities expression and for an easy and universal method of the obtained results discussion. This paper is an attempt to point out their disadvantages and advantages. The manuscript can support the searching interpretation of the obtained results which will be a good tool for the development of a number of fields, especially medicine what can help in the future detection and treatment of many serious diseases. Graphic abstract

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