scholarly journals Role of Klotho as a Modulator of Oxidative Stress Associated with Ovarian Tissue Cryopreservation

2021 ◽  
Vol 22 (24) ◽  
pp. 13547
Author(s):  
Boram Kim ◽  
Hyunho Yoon ◽  
Tak Kim ◽  
Sanghoon Lee
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Tissue Damage ◽  
Ovarian Tissue ◽  
Reactive Oxygen ◽  
Ovarian Tissue Cryopreservation ◽  
Oxygen Species ◽  
Klotho Protein ◽  
Induced Apoptosis ◽  
Tissue Cryopreservation

Ovarian tissue cryopreservation is the only option for preserving fertility in adult and prepubertal cancer patients who require immediate chemotherapy or do not want ovarian stimulation. However, whether ovarian tissue cryopreservation can ameliorate follicular damage and inhibit the production of reactive oxygen species in cryopreserved ovarian tissue remains unclear. Oxidative stress is caused by several factors, such as UV exposure, obesity, age, oxygen, and cryopreservation, which affect many of the physiological processes involved in reproduction, from maturation to fertilization, embryonic development, and pregnancy. Here, freezing and thawing solutions were pre-treated with N-acetylcysteine (NAC) and klotho protein upon the freezing of ovarian tissue. While both NAC and klotho protein suppressed DNA fragmentation by scavenging reactive oxygen species, NAC induced apoptosis and tissue damage in mouse ovarian tissue. Klotho protein inhibited NAC-induced apoptosis and restored cellular tissue damage, suggesting that klotho protein may be an effective antioxidant for the cryopreservation of ovarian tissue.

scholarly journals Sildenafil Reduces Expression and Release of IL-6 and IL-8 Induced by Reactive Oxygen Species in Systemic Sclerosis Fibroblasts

2020 ◽  
Vol 21 (9) ◽  
pp. 3161 ◽  
Author(s):  
Luigi Di Luigi ◽  
Paolo Sgrò ◽  
Guglielmo Duranti ◽  
Stefania Sabatini ◽  
Daniela Caporossi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Systemic Sclerosis ◽  
Tissue Damage ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Dermal Fibroblasts ◽  
Vascular Damage ◽  
Oxygen Species ◽  
Phosphodiesterase Type 5 Inhibitor

Oxidative stress linked to vascular damage plays an important role in the pathogenesis of systemic sclerosis (SSc). Indeed, vascular damage at nailfold capillaroscopy in patients with Raynaud’s Phenomenon (RP) is a major risk factor for the development of SSc together with the presence of specific autoantiobodies. Here, we investigated the effects of the phosphodiesterase type 5 inhibitor (PDE5i) sildenafil, currently used in the management of RP, in modulating the proinflammatory response of dermal fibroblasts to oxidative stress in vitro. Human fibroblasts isolated from SSc patients and healthy controls were exposed to exogenous reactive oxygen species (ROS) (100 µM H2O2), in the presence or absence of sildenafil (1 µM). Treatment with sildenafil significantly reduced dermal fibroblast gene expression and cellular release of IL-6, known to play a central role in the pathogenesis of tissue damage in SSc and IL-8, directly induced by ROS. This reduction was associated with suppression of STAT3-, ERK-, NF-κB-, and PKB/AKT-dependent pathways. Our findings support the notion that the employment of PDE5i in the management of RP may be explored for its efficacy in modulating the oxidative stress-induced proinflammatory activation of dermal fibroblasts in vivo and may ultimately aid in the prevention of tissue damage caused by SSc.

scholarly journals In vitro Studies on Calcium Oxalate Induced Apoptosis Attenuated by Didymocarpus pedicellata

2021 ◽  
Vol 12 (6) ◽  
pp. 7342-7355
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Calcium Oxalate ◽  
Reactive Oxygen ◽  
Ethanolic Extract ◽  
Sem Analysis ◽  
Oxygen Species ◽  
Induced Apoptosis

The present study focuses on exploring the antilithiatic potential of Didymocarpus pedicellata, which is valuable in managing renal disorders. Urolithiasis is an idiopathic disorder with a high recurrence and an incidence rate and is of major concern worldwide due to partial and unsatisfactory relief. Calcium oxalate crystals in contact with renal epithelial cells (HK2), causing reactive oxygen species overproduction, oxidative stress, apoptosis resulting in crystal adhesion and internalization. Crystals were modulated by cotreatment with ethanolic extract of D. pedicellata. Cell toxicity assay was assessed using flow cytometry. Cell-crystal interaction, adhesion, and internalization were visualized through Scanning electron microscopy (SEM) analysis and hematoxylin-eosin staining. The lithogenic induction caused impairment of renal function due to oxidative stress, measured by ROS levels. Cell death assays were detected by dual staining methods. Fluorimeter evaluation pointed to active caspase 3 mediated cell death (apoptotic) in oxalate injured cells was attenuated by Didymocarpus pedicellata extract. Alterations in cell adhesion were observed by immunocytochemistry. The current study revealed that the Didymocarpus pedicellata was endowed with antiurolithiatic activity as it displayed increased viability, reduced oxidative stress due to lowered production of intracellular reactive oxygen species (ROS), and decreased apoptosis when oxalate injured HK2 cells were cotreated with the extract.

scholarly journals Obesity, bariatric surgery and oxidative stress

2017 ◽  
Vol 63 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Roberta Cattaneo Horn ◽  
Gabriela Tassotti Gelatti ◽  
Natacha Cossettin Mori ◽  
Ana Caroline Tissiani ◽  
Mariana Spanamberg Mayer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Bariatric Surgery ◽  
Ascorbic Acid ◽  
Body Weight ◽  
Tissue Damage ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Obese Women

Summary Introduction: Obesity refers to the accumulation of fatty tissues and it favors the occurrence of oxidative stress. Alternatives that can contribute to body weight reduction have been investigated in order to reduce the production of reactive oxygen species responsible for tissue damage. The aim of the current study was to assess whether the oxidant and antioxidant markers of obese women before and after bariatric surgery were able to reduce oxidative damage. Method: We have assessed 16 morbidly obese women five days before and 180 days after the surgery. The control group comprised 16 non-obese women. Levels of thiobarbituric acid-reactive substances, carbonylated proteins, reduced glutathione and ascorbic acid were assessed in the patients' plasma. Results: Levels of lipid peroxidation and protein carbonylation in the pre-surgical obese women were higher than those of the controls and post-surgical obese women. Levels of reduced glutathione in the pre-surgical obese women were high compared to the controls, and declined after surgery. Levels of ascorbic acid fell in the pre--surgical obese women compared to the control and post-surgical obese women. Conclusion: Body weight influences the production of reactive oxygen species. Bariatric surgery, combined with weight loss and vitamin supplementation, reduces cellular oxidation, thus reducing tissue damage.

scholarly journals Peranan Stres Oksidatif pada Proses Penyembuhan Luka

2018 ◽  
Vol 5 (2) ◽  
pp. 22
Author(s):  
Handy Arief ◽  
M Aris Widodo
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Free Radical ◽  
Tissue Damage ◽  
Healing Process ◽  
Reactive Oxygen ◽  
Wound Healing Process ◽  
Oxygen Species

Wound healing is a complex dynamic process characterized by a series of events that occur in almost all type of tissue damage. In the early phase of the inflammatory response, neutrophils and macrophages enters into the injured tissue and the cells produce reactive oxygen species that can give a beneficial or detrimental effects. Oxidative stress is a condition occurs that shows imbalance between prooxidant or free radical and antioxidant that have a function to maintain the condition of the tissue damage that occurs. So Oxidative stress occurs when the production of Reactive Oxygen Species occurring is higher than the antioxidants existing as an intrinsic defense. Reactive Oxygen Species and Reactive Nitrogen Species are important components in the healing process of wounds and is necessary to be in the state of homeostasis to prevent oksidatif stress. The major components of ROS are superoxide (O2•), hydroxyl radical (OH•) and hydrogen peroxide (H2O2), which includes RNS are nitric oxide (NO•), nitrous oxide (NO2•), nitroxyl anion (HNO) and peroxynitrite (ONOO-) which could be form by the reaction between superoxide and nitric oxide. The existence of excessive O2 amount in the wound and the presence of excess NO can increase the incidence of oxidative stress that interfere with wound healing process. Oxidative stress plays a role in the inflammatory phase, proliferation and remodeling phase by increasing angiogenesis and affect other cells including endothelial cells in secreting NO. So the strategy in controlling oxidative stress is by increasing antioxidant level which is a scavenger to free radical excessive superoxide formation so preventing interference with the wound healing process. 

scholarly journals Regulation of reactive oxygen species by p53: implications for nitric oxide-mediated apoptosis

2010 ◽  
Vol 298 (6) ◽  
pp. H2192-H2200 ◽  
Author(s):  
Daniel A. Popowich ◽  
Ashley K. Vavra ◽  
Christopher P. Walsh ◽  
Hussein A. Bhikhapurwala ◽  
Nicholas B. Rossi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Oxygen Species ◽  
Antioxidant Protein ◽  
Intracellular Ros ◽  
Stressed Cells ◽  
Induced Apoptosis

Nitric oxide (NO) induces vascular smooth muscle cell (VSMC) apoptosis in part through activation of p53. Traditionally, p53 has been thought of as the gatekeeper, determining if a cell should undergo arrest and repair or apoptosis following exposure to DNA-damaging agents, depending on the severity of the damage. However, our laboratory previously demonstrated that NO induces apoptosis to a much greater extent in p53−/− compared with p53+/+ VSMC. Increased reactive oxygen species (ROS) within VSMC has been shown to induce VSMC apoptosis, and recently it was found that the absence of, or lack of, functional p53 leads to increased ROS and oxidative stress within different cell types. This study investigated the differences in intracellular ROS levels between p53−/− and p53+/+ VSMC and examined if these differences were responsible for the increased susceptibility to NO-induced apoptosis observed in p53−/− VSMC. We found that p53 actually protects VSMC from NO-induced apoptosis by increasing antioxidant protein expression [i.e., peroxiredoxin-3 (PRx-3)], thereby reducing ROS levels and cellular oxidative stress. We also observed that the NO-induced apoptosis in p53−/− VSMC was largely abrogated by pretreatment with catalase. Furthermore, when the antioxidant protein PRx-3 and its specific electron acceptor thioredoxin-2 were silenced within p53+/+ VSMC with small-interfering RNA, not only did these cells exhibit greater ROS production, but they also exhibited increased NO-induced apoptosis similar to that observed in p53−/− VSMC. These findings suggest that ROS mediate NO-induced VSMC apoptosis and that p53 protects VSMC from NO-induced apoptosis by decreasing intracellular ROS. This research demonstrates that p53 has antioxidant functions in stressed cells and also suggests that p53 has antiapoptotic properties.

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.

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.

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