scholarly journals The Effect of Selected Dental Materials Used in Conservative Dentistry, Endodontics, Surgery, and Orthodontics as Well as during the Periodontal Treatment on the Redox Balance in the Oral Cavity

2020 ◽  
Vol 21 (24) ◽  
pp. 9684
Author(s):  
Izabela Zieniewska ◽  
Mateusz Maciejczyk ◽  
Anna Zalewska
Keyword(s):  
Oxidative Stress ◽  
Oral Cavity ◽  
Dental Treatment ◽  
Cell Metabolism ◽  
Redox Homeostasis ◽  
Dental Materials ◽  
Redox Balance ◽  
Titanium Implants ◽  
Dental Composite ◽  
Root Canal Filling

Oxidative stress (OS) is a redox homeostasis disorder that results in oxidation of cell components and thus disturbs cell metabolism. OS is induced by numerous internal as well as external factors. According to recent studies, dental treatment may also be one of them. The aim of our work was to assess the effect of dental treatment on the redox balance of the oral cavity. We reviewed literature available in PubMed, Medline, and Scopus databases, including the results from 2010 to 2020. Publications were searched according to the keywords: oxidative stress and dental monomers; oxidative stress and amalgam; oxidative stress and periodontitis, oxidative stress and braces, oxidative stress and titanium; oxidative stress and dental implants, oxidative stress and endodontics treatment, oxidative stress and dental treatment; and oxidative stress and dental composite. It was found that dental treatment with the use of composites, amalgams, glass-ionomers, materials for root canal filling/rinsing, orthodontic braces (made of various metal alloys), titanium implants, or whitening agents can disturb oral redox homeostasis by affecting the antioxidant barrier and increasing oxidative damage to salivary proteins, lipids, and DNA. Abnormal saliva secretion/composition was also observed in dental patients in the course of OS. It is suggested that the addition of antioxidants to dental materials or antioxidant therapy applied during dental treatment could protect the patient against harmful effects of OS in the oral cavity.

scholarly journals Interplay among Oxidative Stress, Methylglyoxal Pathway and S-Glutathionylation

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 19
Author(s):  
Lidia de Bari ◽  
Andrea Scirè ◽  
Cristina Minnelli ◽  
Laura Cianfruglia ◽  
Miklos Peter Kalapos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Function ◽  
Cell Metabolism ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Dependent Manner ◽  
Ros Production ◽  
Glyoxalase Ii ◽  
Cytotoxic Compound ◽  
Oxidative Damages

Reactive oxygen species (ROS) are produced constantly inside the cells as a consequence of nutrient catabolism. The balance between ROS production and elimination allows to maintain cell redox homeostasis and biological functions, avoiding the occurrence of oxidative distress causing irreversible oxidative damages. A fundamental player in this fine balance is reduced glutathione (GSH), required for the scavenging of ROS as well as of the reactive 2-oxoaldehydes methylglyoxal (MGO). MGO is a cytotoxic compound formed constitutively as byproduct of nutrient catabolism, and in particular of glycolysis, detoxified in a GSH-dependent manner by the glyoxalase pathway consisting in glyoxalase I and glyoxalase II reactions. A physiological increase in ROS production (oxidative eustress, OxeS) is promptly signaled by the decrease of cellular GSH/GSSG ratio which can induce the reversible S-glutathionylation of key proteins aimed at restoring the redox balance. An increase in MGO level also occurs under oxidative stress (OxS) conditions probably due to several events among which the decrease in GSH level and/or the bottleneck of glycolysis caused by the reversible S-glutathionylation and inhibition of glyceraldehyde-3-phosphate dehydrogenase. In the present review, it is shown how MGO can play a role as a stress signaling molecule in response to OxeS, contributing to the coordination of cell metabolism with gene expression by the glycation of specific proteins. Moreover, it is highlighted how the products of MGO metabolism, S-D-lactoylglutathione (SLG) and D-lactate, which can be taken up and metabolized by mitochondria, could play important roles in cell response to OxS, contributing to cytosol-mitochondria crosstalk, cytosolic and mitochondrial GSH pools, energy production, and the restoration of the GSH/GSSG ratio. The role for SLG and glyoxalase II in the regulation of protein function through S-glutathionylation under OxS conditions is also discussed. Overall, the data reported here stress the need for further studies aimed at understanding what role the evolutionary-conserved MGO formation and metabolism can play in cell signaling and response to OxS conditions, the aberration of which may importantly contribute to the pathogenesis of diseases associated to elevated OxS.

Effects of iron-related compounds and bilirubin on redox homeostasis in endometriosis and its malignant transformations

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Hiroshi Shigetomi ◽  
Shogo Imanaka ◽  
Hiroshi Kobayashi
Keyword(s):  
Oxidative Stress ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Heme Iron ◽  
Total Iron ◽  
University Hospital ◽  
Free Iron ◽  
Significant Difference ◽  
Iron Heme ◽  
Related Compounds

Abstract Objectives The balance between oxidative stress and antioxidant defense has been reported to differ between women with endometriosis and patients with its malignant transformation. The aim of this study is to investigate changes in redox balance in endometriosis and endometriosis-related ovarian cancer (EAOC) by simultaneously measuring iron-related compounds and bilirubin. Methods This study included 235 patients with a histopathologically confirmed diagnosis of endometriosis (n=178) and EAOC (n=57). Cyst fluid samples were collected in Nara Medical University hospital from January 2013 to May 2019. The levels of iron-related compounds (total iron, heme iron, free iron, oxyhemoglobin [oxyHb], methemoglobin [metHb], and metHb/oxyHb ratio) and bilirubin were measured. Results Total iron, heme iron, free iron, metHb/oxyHb ratio, and bilirubin were significantly elevated in endometriosis compared to EAOC. In both endometriosis and EAOC, iron-related compounds in the cyst were correlated with each other. There was no statistically significant difference in oxyHb and metHb levels between the two groups, but the metHb/oxyHb ratio was significantly higher in endometriosis than in EAOC. Bilirubin was positively correlated with total iron and free iron in EAOC, but there was no correlation between bilirubin and iron-related compounds in endometriosis. Conclusions Iron-induced oxidative stress in endometriosis may exceed bilirubin-dependent antioxidant capability, while redox homeostasis in EAOC can be maintained by at least bilirubin.

scholarly journals ATM inhibition enhances Auranofin-induced oxidative stress and cell death in lung cell lines

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0244060
Author(s):  
Vanessa Ehrenfeld ◽  
Jan R. Heusel ◽  
Simone Fulda ◽  
Sjoerd J. L. van Wijk
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Ataxia Telangiectasia ◽  
Redox Homeostasis ◽  
Thioredoxin Reductase ◽  
Redox Balance ◽  
Lung Cells ◽  
Chromosomal Breakage ◽  
Atm Kinase ◽  
Cellular Reactive Oxygen Species

Ataxia-Telangiectasia (A-T), a pleiotropic chromosomal breakage syndrome, is caused by the loss of the kinase Ataxia-telangiectasia mutated (ATM). ATM is not only involved in the response to DNA damage, but also in sensing and counteracting oxidative stress. Since a disturbed redox balance has been implicated in the pathophysiology of A-T lung disease, we aimed to further explore the interplay between ATM and oxidative stress in lung cells. Using a kinetic trapping approach, we could demonstrate an interaction between the trapping mutant TRX1-CS and ATM upon oxidative stress. We could further show that combined inhibition of thioredoxin reductase (TrxR) and ATM kinase activity, using Auranofin and KU55933 respectively, induced an increase in cellular reactive oxygen species (ROS) levels and protein oxidation in lung cells. Furthermore, ATM inhibition sensitized lung cells to Auranofin-induced cell death that could be rescued by ROS scavengers. As a consequence, targeted reduction of ATM by TRX1 could serve as a regulator of oxidative ATM activation and contribute to the maintenance of the cellular redox homeostasis. These results highlight the importance of the redox-active function of ATM in preventing ROS accumulation and cell death in lung cells.

scholarly journals Transcriptional regulators of redox balance and other homeostatic processes with the potential to alter neurodegenerative disease trajectory

2017 ◽  
Vol 45 (6) ◽  
pp. 1295-1303 ◽  
Author(s):  
Scott W. Burnside ◽  
Giles E. Hardingham
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disease ◽  
Glutamate Uptake ◽  
Redox Homeostasis ◽  
Neuronal Loss ◽  
Redox Balance ◽  
Antioxidant Defences ◽  
Disease Trajectory ◽  
Inflammatory Status ◽  
The Brain

Diverse neurodegenerative diseases share some common aspects to their pathology, with many showing evidence of disruption to the brain's numerous homeostatic processes. As such, imbalanced inflammatory status, glutamate dyshomeostasis, hypometabolism and oxidative stress are implicated in many disorders. That these pathological processes can influence each other both up- and downstream makes for a complicated picture, but means that successfully targeting one area may have an effect on others. This targeting requires an understanding of the mechanisms by which homeostasis is maintained during health, in order to uncover strategies to boost homeostasis in disease. A case in point is redox homeostasis, maintained by antioxidant defences co-ordinately regulated by the transcription factor Nrf2, and capable of preventing not only oxidative stress but also inflammation and neuronal loss in neurodegenerative disease models. The emergence of other master regulators of homeostatic processes in the brain controlling inflammation, mitochondrial biogenesis, glutamate uptake and energy metabolism raises the question as to whether they too can be targeted to alter disease trajectory.

scholarly journals Effect of tirapazamine on selected kidney parameters in rats treated with cisplatin

2019 ◽  
Vol 32 (1) ◽  
pp. 18-22
Author(s):  
Marcin Sysa ◽  
Kamil Pawlowski ◽  
Piotr Slabczynski ◽  
Franciszek Burdan ◽  
Jaroslaw Dudka
Keyword(s):  
Oxidative Stress ◽  
Adverse Effect ◽  
Protein Concentration ◽  
Cell Metabolism ◽  
Redox Balance ◽  
Cytotoxic Agents ◽  
Cytostatic Drugs ◽  
Redox Equilibrium ◽  
Oxidative Stress Parameters ◽  
Stress Parameters

Abstract Hypoxic cancer cells are more aggressive and responsible for more efficient metastasis and recurrence. It seems worth-while, hence, to supplement current cytostatic drugs therapy (i.e. cisplatin) with hypoxia cytotoxic agents (i.e. tirapazamine), the toxicity of which is activated by hypoxia. Cisplatin and tirapazamine can change a redox equilibrium and consequently lead to changes in cell metabolism, fibrosis and apoptosis. The aim of this study was to evaluate the cisplatin/tirapazamine toxicological synergism. In doing so we tested selected kidney oxidative stress parameters, as well as nephrotoxicity markers, in plasma and urine. Once a week for 6 weeks, rats received intraperitoneally two doses of tirapazamine (5 or 10 mg/kg bw), 2 hours before cisplatin (2 mg/kg bw) was applied. Our results show that Tirapazamine (TP) had no significant adverse effect on the redox balance, oxidative stress and kidney function in rats receiving cisplatin (CP). However, TP significantly increased protein concentration in the kidneys of rats. In all tested groups, a significant decrease in NADH concentration in kidneys was recorded, which could indicate disorder in the cell metabolism. TP also was found to have prevented bacterial infection caused by CP. In summary, there was no nephrotoxic synergy of TP with CP at an unacceptable level.

scholarly journals Parkinson Disease-Linked Parkin Mediates Redox Reactions That Lower Oxidative Stress In Mammalian Brain

2020 ◽  
Author(s):  
Daniel N. El Kodsi ◽  
Jacqueline M. Tokarew ◽  
Rajib Sengupta ◽  
Nathalie A. Lengacher ◽  
Andy C. Ng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reductase Activity ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Oxidative Modification ◽  
Reduced Form ◽  
Mammalian Brain ◽  
Anti Oxidant

SUMMARYWe recently hypothesized that parkin plays a role in redox homeostasis and provided evidence that it directly reduces hydrogen peroxide (H2O2) in vitro. Here, we examined this anti-oxidant activity in vivo. Informed by findings in human brain, we demonstrate that elevated oxidative stress promotes parkin insolubility in mice. In normal mouse brain parkin was partially oxidized, e.g., at cysteines 195 and 252, which was augmented by oxidative stress. Although under basal conditions H2O2 levels were unchanged in adult prkn-/- brain, a parkin-dependent reduction of cytosolic H2O2 was observed when mitochondria were impaired, either due to neurotoxicant exposure (MPTP) or Sod2 haploinsufficiency. In accordance, markers of oxidative stress, e.g., protein carbonylation and nitrotyrosination, were elevated in the cytosol but not in mitochondria from prkn-/- mice. Nevertheless, this rise in oxidative stress led to changes in mitochondrial enzyme activities and the metabolism of glutathione in cells and mammalian brain. In parkin’s absence reduced glutathione concentrations were increased including in human cortex. This compensation was not due to new glutathione synthesis but attributed to elevated oxidized glutathione (GSSG)-reductase activity. Moreover, we discovered that parkin also recycled GSSG to its reduced form. With this reaction, parkin became S-glutathionylated, e.g., at cysteines 59 and human-specific 95. This oxidative modification was reversed by glutaredoxin. Our results demonstrate that cytosolic parkin mediates anti-oxidant reactions including H2O2 reduction and glutathione regeneration. These reducing activities lead to a range of oxidative modifications in parkin itself. In parkin-deficient brain oxidative stress rises despite changes to maintain redox balance.

scholarly journals Regulation of redox balance using a biocompatible nanoplatform enhances phototherapy efficacy and suppresses tumor metastasis

2021 ◽  
Vol 12 (1) ◽  
pp. 148-157
Author(s):  
Qunying Jiang ◽  
Min Pan ◽  
Jialing Hu ◽  
Junlin Sun ◽  
Lei Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tumor Metastasis ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Primary Tumors ◽  
Highly Effective

Amplified oxidative stress achieved by modulating redox homeostasis with PDA–MB for highly effective synergistic phototherapy to inhibit primary tumors and metastases.

scholarly journals Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

2020 ◽  
Vol 21 (23) ◽  
pp. 9317
Author(s):  
Javier Checa ◽  
Josep M. Aran
Keyword(s):  
Oxidative Stress ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Structural Cell ◽  
Environmental Threats ◽  
Chronic Lung Diseases ◽  
Cell Components ◽  
Respiratory Pathology

As aerobic organisms, we are continuously and throughout our lifetime subjected to an oxidizing atmosphere and, most often, to environmental threats. The lung is the internal organ most highly exposed to this milieu. Therefore, it has evolved to confront both oxidative stress induced by reactive oxygen species (ROS) and a variety of pollutants, pathogens, and allergens that promote inflammation and can harm the airways to different degrees. Indeed, an excess of ROS, generated intrinsically or from external sources, can imprint direct damage to key structural cell components (nucleic acids, sugars, lipids, and proteins) and indirectly perturb ROS-mediated signaling in lung epithelia, impairing its homeostasis. These early events complemented with efficient recognition of pathogen- or damage-associated recognition patterns by the airway resident cells alert the immune system, which mounts an inflammatory response to remove the hazards, including collateral dead cells and cellular debris, in an attempt to return to homeostatic conditions. Thus, any major or chronic dysregulation of the redox balance, the air–liquid interface, or defects in epithelial proteins impairing mucociliary clearance or other defense systems may lead to airway damage. Here, we review our understanding of the key role of oxidative stress and inflammation in respiratory pathology, and extensively report current and future trends in antioxidant and anti-inflammatory treatments focusing on the following major acute and chronic lung diseases: acute lung injury/respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis.

scholarly journals Increased Systemic Malondialdehyde Levels and Decreased Mo/Co, Mo/Hg2+, Co/Fe2+ Ratios in Patients with Long-Term Dental Titanium Implants and Amalgams

2019 ◽  
Vol 8 (1) ◽  
pp. 86 ◽  
Author(s):  
María Cabaña-Muñoz ◽  
José Parmigiani-Izquierdo ◽  
Fabio Camacho Alonso ◽  
José Merino
Keyword(s):  
Oxidative Stress ◽  
Dental Implants ◽  
Dental Materials ◽  
Dental Amalgam ◽  
Titanium Implants ◽  
Systemic Oxidative Stress ◽  
Hair Samples ◽  
Dental Amalgams ◽  
Titanium Dental Implants

Introduction: the biological safety of dental biomaterials has been questioned in human studies. Material and Methods: Several heavy metals/oligoelements were compared by Inductive Coupled Mass Spectrometry (ICP-MS) in hair samples from 130 patients (n = 54 patients with long-term titanium dental implants and amalgams (A + I group), 51 patients with long-term dental amalgam alone (A group), as well as controls (n = 25: without dental materials) of similar age. All patients (except controls) had had titanium dental implants and/or dental amalgams for at least 10 years (average: 17). We evaluated whether A + I patients could present higher systemic malondialdehyde levels (MDA) as compared to the A group. Results: The A + I group have lower molybdenum levels (A + I) and reduced Mo/Co and Mo/Fe2+ ratios, which could predispose them to oxidative stress by raising MDA levels as compared to the A group alone; our findings suggest that higher Co levels could enhance oxidative stress in the A + I group. However, there were no differences on metals from titanium alloy (Ti-6Al), Cr from crowns or Hg2+, Sn, Zn2+, Cu2+ levels between the A + I and A groups. Conclusion: patients with long-term dental titanium and amalgams have systemic oxidative stress due to rising MDA levels and lower Mo/Co and Mo/Fe2+ ratios than those with amalgams alone.

scholarly journals A Systematic Review of Exposure to Bisphenol A from Dental Treatment

2019 ◽  
Vol 4 (2) ◽  
pp. 106-115 ◽  
Author(s):  
T. Marzouk ◽  
S. Sathyanarayana ◽  
A.S. Kim ◽  
A.L. Seminario ◽  
C.M. McKinney
Keyword(s):  
Systematic Review ◽  
Bisphenol A ◽  
Dental Treatment ◽  
Dental Materials ◽  
Library Science ◽  
Dental Composite ◽  
Endocrine Disrupting Chemical ◽  
Endocrine Disrupting ◽  
Before And After ◽  
Open Question

Introduction: Dental composite restorations and dental sealants containing bisphenol A glycidyl methacrylate (BisGMA) are commonly used materials in dentistry. Bisphenol A (BPA) is used to manufacture BisGMA and can be a by-product in BisGMA-based dental materials. BPA is an endocrine-disrupting chemical that may affect reproductive, psychological, cognitive, and endocrine-related health. We conducted a systematic review of clinical studies that measured urinary BPA (uBPA) concentrations before and after dental treatment to evaluate the extent to which individuals are exposed to BPA from dental treatment. Methods: Eligibility included studies that measured uBPA concentrations before and after dental treatment with any type of resin-based dental material. We searched PubMed, Cochrane, Web of Science, Virtual Health Library, Science Direct, ProQuest, and Clinical Trials with no date or language restrictions to identify published studies. We summarized eligible studies across participant characteristics, amount of treatment, and time of follow-up measures. Because methods of measuring uBPA varied, our primary outcome was the direction and percentage change between baseline and 24 h posttreatment and at later time points as available. Results: We identified 1,190 abstracts and 7 eligible studies: 4 in children and 3 in adults. In all studies, BPA concentrations increased 24 h after treatment. The 2 studies with the largest sample sizes found statistically significant increases >40% in uBPA concentrations at 24 h posttreatment (both P values <0.01). The 1 study to examine uBPA concentrations beyond 1 mo posttreatment found that concentrations returned to baseline by 14 d after treatment and remained at baseline 6 mo after treatment. Conclusions: Our findings suggest that uBPA concentrations increase 24 h after dental treatment. One study showed that uBPA concentrations return to baseline by 14 d. Additional research is needed to determine the magnitude of change from pre– to post–dental treatment and the trajectory of uBPA concentrations posttreatment. Knowledge Transfer Statement: BPA is an endocrine-disrupting chemical that may have negative human health effects. Our findings suggest that urinary BPA concentrations increase in the short term after dental treatment. The extent to which such an increase may affect the health of patients remains an open question, particularly since there are no established thresholds for safety or harm related to BPA exposure.

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