Cerium oxide nanozyme attenuates periodontal bone destruction by inhibiting ROS-NFκB pathway

Nanoscale ◽  
2022 ◽  
Author(s):  
Yijun Yu ◽  
Sheng Zhao ◽  
Deao Gu ◽  
Bijun Zhu ◽  
Hanxiao Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Bone Resorption ◽  
Inflammatory Disease ◽  
Tissue Damage ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Oxygen Species ◽  
Nfκb Pathway ◽  
Excess Reactive Oxygen Species

Periodontitis, an inflammatory disease of oxidative stress, occurs due to the excess reactive oxygen species (ROS) contributing to cell and tissue damage that in turn leads to alveolar bone resorption...

Oxidative stress and its implications in chronic kidney disease

2015 ◽  
Author(s):  
Nosratola D. Vaziri
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Tissue Damage ◽  
Oxygen Radicals ◽  
Inflammatory Cells ◽  
Control Mechanisms ◽  
Oxygen Species ◽  
Low Levels

Reactive oxygen species (ROS) are produced at low levels physiologically and their production conveys signals and has specific functions. Control mechanisms ensure that this does not cause damage. ROS are highly reactive and cytotoxic and are also deliberately produced by inflammatory cells (granulocytes, macrophages) to kill pathogens. If these chemicals are released inappropriately or excessively, or if control mechanisms are under-functioning, bystander or unintended tissue damage may be caused. The concept of oxidative stress is based on the idea that in certain states, commonly inflammatory states, release of oxygen radicals may be excessive, or control mechanisms weakened, so that tissue damage occurs. In CKD, both overproduction and diminished control may apply. No effective therapies acting via these pathways have been established so far though there remain some candidates.

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.

The Redox Potential of a Heme Cofactor in Nitrosomonas europaea Cytochrome c Peroxidase: A Polarizable QM/MM Study

2021 ◽  
Author(s):  
Elizabeth Anotonovna Karnaukh ◽  
Ksenia B Bravaya
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cytochrome C ◽  
Redox Potential ◽  
Redox Reactions ◽  
Cytochrome C Peroxidase ◽  
Biological Processes ◽  
Oxygen Species ◽  
Heme Cofactor ◽  
Excess Reactive Oxygen Species

Redox reactions are crucial to biological processes that protect organisms against oxidative stress. Metalloenzymes, such as peroxidases which reduce excess reactive oxygen species into water, play a key role in...

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 Depletion of Neutrophils Protects Against L-Arginine-Induced Acute Pancreatitis in Mice

2015 ◽  
Vol 35 (6) ◽  
pp. 2111-2120 ◽  
Author(s):  
Guolin Chen ◽  
Feng Xu ◽  
Jing Li ◽  
Shiqi Lu
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Pancreatitis ◽  
Inflammatory Disease ◽  
Tissue Damage ◽  
Cell Damage ◽  
Ros Generation ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Plasma Cytokines ◽  
Neutrophil Depletion

Background/Aims: Acute pancreatitis (AP) is an inflammatory disease characterized by acinar cell damage and inflammation of the pancreas with infiltration of leukocytes, predominantly neutrophils. We investigated whether neutrophil depletion protects against experimental AP induced by L-arginine. Methods: AP was induced in C57BL/6 mice via two intraperitoneal L-arginine (4 g/kg) injections. Mice were pretreated with 250 and 100 µg anti-Gr-1 antibody via intraperitoneal injection at 24 and 4 h, respectively, before L-arginine challenge for neutrophil depletion. At 48 and 72 h after injection, the severity of AP was determined with the aid of biochemical and histological analyses. Amylase and MPO activity was detected using specific assay kits. The plasma cytokines levels were detected using ELISA. Results: Neutrophil depletion resulted in significantly reduced plasma amylase levels in pancreas, myeloperoxidase (MPO) activity in pancreas and lung, reactive oxygen species (ROS) generation and cell apoptosis, and decreased circulating neutrophil, tissue damage as well as expression levels of nuclear factor NF-κB. Conclusion: Neutrophil depletion is capable of reducing tissue damage of pancreas and lung in mice with acute pancreatitis.

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 Oxidative stress in pregnancy and reproduction

2016 ◽  
Vol 9 (3) ◽  
pp. 113-116 ◽  
Author(s):  
Kate Duhig ◽  
Lucy C Chappell ◽  
Andrew H Shennan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Preterm Labour ◽  
Membrane Integrity ◽  
Cellular Membrane ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Overwhelming Evidence ◽  
Excess Reactive Oxygen Species ◽  
In Pregnancy

Oxidative stress is implicated in the pathophysiology of many reproductive complications including infertility, miscarriage, pre-eclampsia, fetal growth restriction and preterm labour. The presence of excess reactive oxygen species can lead to cellular damage of deoxyribonucleic acids, lipids and proteins. Antioxidants protect cells from peroxidation reactions, limiting cellular damage and helping to maintain cellular membrane integrity. There is overwhelming evidence for oxidative stress causing harm in reproduction. However, there is sparse evidence that supplementation with commonly used antioxidants (mostly vitamins C and E) makes any difference in overcoming oxidative stress or reversing disease processes. There may be potential for antioxidant therapy to ameliorate or prevent disease, but this requires a thorough understanding of the mechanism of action and specificity of currently used antioxidants.

scholarly journals The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yunyan Zhang ◽  
Yuzhi Yang ◽  
Mingxue Xu ◽  
Jingwen Zheng ◽  
Yuchan Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Bone Formation ◽  
Alveolar Bone ◽  
Bone Development ◽  
Reactive Oxygen ◽  
Enzyme Linked Immunosorbent Assay ◽  
Oxygen Species ◽  
Periodontal Tissues ◽  
Ros Accumulation

The status of reactive oxygen species (ROS) correlates closely with the normal development of the oral and maxillofacial tissues. Oxidative stress caused by ROS accumulation not only affects the development of enamel and dentin but also causes pathological changes in periodontal tissues (periodontal ligament and alveolar bone) that surround the root of the tooth. Although previous studies have shown that ROS accumulation plays a pathologic role in some oral and maxillofacial tissues, the effects of ROS on alveolar bone development remain unclear. In this study, we focused on mandibular alveolar bone development of mice deficient in superoxide dismutase1 (SOD1). Analyses were performed using microcomputerized tomography (micro-CT), TRAP staining, immunohistochemical (IHC) staining, and enzyme-linked immunosorbent assay (ELISA). We found for the first time that slightly higher ROS in mandibular alveolar bone of SOD1(-/-) mice at early ages (2-4 months) caused a distinct enlargement in bone size and increased bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and expression of alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2), and osteopontin (OPN). With ROS accumulation to oxidative stress level, increased trabecular bone separation (Tb.Sp) and decreased expression of ALP, Runx2, and OPN were found in SOD1(-/-) mice at 6 months. Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN. These results indicate that redox imbalance caused by SOD1 deficiency has dual effects (promotion or inhibition) on mandibular alveolar bone development, which is closely related to the concentration of ROS and the stage of growth. We present a valuable model here for investigating the effects of ROS on mandibular alveolar bone formation and highlight important roles of ROS in regulating tissue development and pathological states, illustrating the complexity of the redox signal.

Novel antioxidative nanotherapeutics in a rat periodontitis model: Reactive oxygen species scavenging by redox injectable gel suppresses alveolar bone resorption

Biomaterials ◽  
2016 ◽  
Vol 76 ◽  
pp. 292-301 ◽  
Author(s):  
Makiko Saita ◽  
Junya Kaneko ◽  
Takenori Sato ◽  
Shun-suke Takahashi ◽  
Satoko Wada-Takahashi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Reactive Oxygen ◽  
Oxygen Species

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.

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