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 effect of acrylamide on sperm oxidative stress, total antioxidant levels, tyrosine phosphorylation, and carboxymethyl-lysine expression: A laboratory study

2021 ◽  
Author(s):  
Mojdeh Hosseinpoor Kashani ◽  
Mina Ramezani ◽  
Zeinab Piravar
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Tyrosine Phosphorylation ◽  
Laboratory Study ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Total Antioxidant ◽  
Carboxymethyl Lysine

Background: Acrylamide (AA) is a reactive molecule produced during food processing at temperatures above 120°C. Objective: To evaluate the impact of different concentrations of AA on human sperm parameters, oxidative stress and total antioxidant capacity (TAC). Materials and Methods: In this laboratory study, semen samples were obtained from healthy donors referred to the Taleghani Hospital, Tehran, Iran between June and July 2019. Samples were divided into four groups (n = 10/each): one control and three treatment groups (0.5, 1, and 2 mM of AA). After 2 hr of exposure to AA, the superoxide dismutase and malondialdehyde levels were measured based on colorimetric methods. The TAC was determined by the ferric-reducing antioxidant power assay. Flow cytometry was performed to measure the intracellular reactive oxygen species generation. Also, immunohistochemistry was done to determine the effect of AA on tyrosine phosphorylation and carboxymethyl-lysine expression. Results: Results of the study demonstrated that the motility and viability of spermatozoa were significantly decreased after AA exposure (p < 0.001). This decrease was also seen in the TAC and superoxide dismutase activity as well as in the phosphotyrosine percentage compared with the control (p < 0.01). However, the carboxymethyllysine and prooxidant activity including reactive oxygen species generation and lipid peroxidation level increased (p < 0.001). Conclusion: Overall, the results confirmed the detrimental effect of AA on human spermatozoa which may be due to oxidative stress and decreased total antioxidant levels. AA may reduce fertility by reducing sperm capacitation and motility. Key words: Acrylamide, Oxidative stress, Antioxidant, Spermatozoa, Infertility.

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.

scholarly journals The reactive oxygen species—total antioxidant capacity score is a new measure of oxidative stress to predict male infertility*

1999 ◽  
Vol 14 (11) ◽  
pp. 2801-2807 ◽  
Author(s):  
Rakesh K. Sharma ◽  
Fabio F. Pasqualotto ◽  
David R. Nelson ◽  
Anthony J. Thomas ◽  
Ashok Agarwal
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Male Infertility ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Total Antioxidant

scholarly journals Assessment of the Antioxidant and Reactive Oxygen Species Scavenging Activity of Methanolic Extract ofCaesalpinia cristaLeaf

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Sourav Mandal ◽  
Bibhabasu Hazra ◽  
Rhitajit Sarkar ◽  
Santanu Biswas ◽  
Nripendranath Mandal
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Antioxidant Activity ◽  
Methanolic Extract ◽  
Reactive Oxygen ◽  
Total Antioxidant Activity ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Total Antioxidant ◽  
Phenolic And Flavonoid

“Oxidative stress” is initiated by reactive oxygen species (ROS), which are responsible for majority of the diseases. However, antioxidants with ROS scavenging ability may have great relevance in the prevention of oxidative stress. The present study was undertaken, using a 70% methanolic extract ofCaesalpinia cristaleaves, to examine differentin vitrotests in diversified fields including total antioxidant activity, scavenging activities for various ROS, iron chelating activity and phenolic and flavonoid contents. Total antioxidant activity was evaluated as trolox equivalent antioxidant capacity value of 0.546 ± 0.014. The extract was investigated for different ROS scavenging activities and IC50values were found to be 0.44 ± 0.1 mg/ml, 24.9 ± 0.98 μg/ml, 33.72 ± 0.85 μg/ml, 61.13 ± 3.24 μg/mL and 170.51 ± 4.68 μg/mL for hydroxyl, superoxide, nitric oxide, singlet oxygen and hypochlorous acid, respectively; however, no significant results were obtained in scavenging of hydrogen peroxide and peroxynitrite anion. The extract was found to be a potent iron chelator with IC50= 279.85 ± 4.72 μg/mL. The plant extract (100 mg) yielded 50.23 ± 0.003 mg/mL gallic acid equivalent phenolic content and 106.83 ± 0.0003 mg/mL quercetin equivalent flavonoid content. In thein vivoexperiments, the extract treatment showed significant increase in the level of superoxide dismutase, catalase, glutathione-S-transferase and reduced glutathione. In a word, it may be concluded that 70% methanol extract ofC. cristaleaves acts as an antioxidant and ROS scavenger; which may be due to the presence of phenolic and flavonoid compounds.

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.

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.

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.

Sign in / Sign up

Export Citation Format

Share Document