Oxidative Stress Evaluation in Patients Treated with Orthodontic Self-ligating Multibracket Appliances: An in Vivo Case-Control Study

Objective: Oxidative stress is a pathologic event induced by a prevalence of oxidant agents on the antioxidant ones, with a consequent alteration of oxide-reducing balance. Introduction: Freeradicals produce damages both in cellular and extra-cellular components; phospholipid membranes, proteins, mitochondrial and nuclear DNA, are the target of the oxidative stress, that can finally cause cellular death due to apoptosis. Materials & Methods: Orthodontic appliances such as brackets, wires, resins and soldering have some components that can be considered as potential allergen, carcinogenic, cytotoxic and gene mutation factors. The primary aim of this research is to evaluate oxidative stress in the saliva of patients treated with multibracket self-ligating vestibular orthodontic appliances; the secondary purpose is to investigate the influence of orthodontic multibracket therapy on oral hygiene and the consequent effect on oxidative stress. Salivary specimens has been collected in a sample of 23 patients were enrolled (12 Female, 11 Male) between 12 and 16 years of age (mean age 14.2). For each patient has been collected a salivary specimen at the following time points; before orthodontic bonding (T1), five weeks (T2) and ten weeks (T3) after orthodontic appliance bonding. Results: Samples has been analysed with a photometer due to SAT Test (Salivary Antioxidant Test). Data obtained show a mean of 2971 mEq/l of anti-oxidant agents before orthodontic treatment, and after five weeks from the bonding the mean was decreased to 2909 mEq/l, instead at ten weeks was increased to 3332 mEq/l. Repeated measures ANOVA did not reveal statistically significant differences between the time points (P = 0.1697). The study did not reveal any correlation between the level of dental hygiene and that of oxidative stress (Pearson Correlation Coefficient R = 0). Conclusion: Orthodontic treatment with multibrackets vestibular metallic appliance seems to be not able to affect oxidative stress during the first ten weeks of therapy.

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Changes in salivary periodontal pathogens after orthodontic treatment: An in vivo prospective study

The Angle Orthodontist ◽

10.2319/070615-450.1 ◽

2015 ◽

Vol 86 (6) ◽

pp. 998-1003 ◽

Cited By ~ 8

Author(s):

Kyungsun Kim ◽

Woo-Sun Jung ◽

Soha Cho ◽

Sug-Joon Ahn

Keyword(s):

Oral Hygiene ◽

Repeated Measures ◽

Orthodontic Treatment ◽

Orthodontic Appliances ◽

Periodontal Pathogens ◽

Time Points ◽

Fixed Orthodontic Appliances ◽

Whole Saliva ◽

Total Bacteria

ABSTRACT Objective: To analyze the initial changes in salivary levels of periodontal pathogens after orthodontic treatment with fixed appliances. Materials and Methods: The subjects consisted of 54 adult patients. The Simplified Oral Hygiene Index, Plaque Index, and Gingival Index were measured as periodontal parameters. Both the plaque and gingival indexes were obtained from the central and lateral incisors and first molars of both arches. Whole saliva and periodontal parameters were obtained at the following four time points: immediately before debonding (T1), 1 week after debonding (T2), 5 weeks after debonding (T3), and 13 weeks after debonding (T4). Repeated measures analysis of variance was used to determine salivary bacterial levels and periodontal parameters among the four time points after quantifying salivary levels of Aggregatibacter actinomycetemcomitans (Aa), Fusobacterium nucleatum (Fn), Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Tannerella forsythia (Tf), and total bacteria using the real-time polymerase chain reaction. Results: All periodontal parameters were significantly decreased immediately after debonding (T2). The salivary levels of total bacteria and Pg were decreased at T3, while Pi and Tf levels were decreased at T4. However, the amount of Aa and Fn remained at similar levels in saliva during the experimental period. Interestingly, Aa and Fn were present in saliva at higher levels than were Pg, Pi, and Tf. Conclusion: The higher salivary levels of Aa and Fn after debonding suggests that the risk of periodontal problems cannot be completely eliminated by the removal of fixed orthodontic appliances during the initial retention period, despite improved oral hygiene.

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DHA reduces oxidative stress following hypoxia-ischemia in newborn piglets: a study of lipid peroxidation products in urine and plasma

Journal of Perinatal Medicine ◽

10.1515/jpm-2016-0334 ◽

2018 ◽

Vol 46 (2) ◽

pp. 209-217 ◽

Cited By ~ 9

Author(s):

Marianne Ullestad Huun ◽

Håvard T. Garberg ◽

Javier Escobar ◽

Consuelo Chafer ◽

Maximo Vento ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Oxygen Species ◽

Major Contributor ◽

Time Points ◽

Newborn Piglets ◽

Hypoxia Group ◽

Hypoxia Ischemia ◽

Anti Oxidant

AbstractBackground:Lipid peroxidation mediated by reactive oxygen species is a major contributor to oxidative stress. Docosahexaenoic acid (DHA) has anti-oxidant and neuroprotective properties. Our objective was to assess how oxidative stress measured by lipid peroxidation was modified by DHA in a newborn piglet model of hypoxia-ischemia (HI).Methods:Fifty-five piglets were randomized to (i) hypoxia, (ii) DHA, (iii) hypothermia, (iv) hypothermia+DHA or (v) sham. All groups but sham were subjected to hypoxia by breathing 8% O2. DHA was administered 210 min after end of hypoxia and the piglets were euthanized 9.5 h after end of hypoxia. Urine and blood were harvested at these two time points and analyzed for F4-neuroprostanes, F2-isoprostanes, neurofuranes and isofuranes using UPLC-MS/MS.Results:F4-neuroprostanes in urine were significantly reduced (P=0.006) in groups receiving DHA. Hypoxia (median, IQR 1652 nM, 610–4557) vs. DHA (440 nM, 367–738, P=0.016) and hypothermia (median, IQR 1338 nM, 744–3085) vs. hypothermia+DHA (356 nM, 264–1180, P=0.006). The isoprostane compound 8-iso-PGF2α was significantly lower (P=0.011) in the DHA group compared to the hypoxia group. No significant differences were found between the groups in blood.Conclusion:DHA significantly reduces oxidative stress by measures of lipid peroxidation following HI in both normothermic and hypothermic piglets.

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Novel QUEST MRI In Vivo Measurement of Noise-induced Oxidative Stress in the Cochlea

Scientific Reports ◽

10.1038/s41598-019-52439-4 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 3

Author(s):

André Kühl ◽

Angela Dixon ◽

Mirabela Hali ◽

Aaron K. Apawu ◽

Antonela Muca ◽

...

Keyword(s):

Oxidative Stress ◽

Hearing Loss ◽

Cell Loss ◽

Hair Cell Loss ◽

Resonance Imaging ◽

In Vivo Measurement ◽

Anti Oxidant ◽

Individual Evaluation ◽

Excised Tissue

Abstract Effective personalized therapeutic treatment for hearing loss is currently not available. Cochlear oxidative stress is commonly identified in the pathogenesis of hearing loss based upon findings from excised tissue, thus suggesting a promising druggable etiology. However, the timing and site(s) to target for anti-oxidant treatment in vivo are not clear. Here, we address this long-standing problem with QUEnch-assiSTed Magnetic Resonance Imaging (QUEST MRI), which non-invasively measures excessive production of free radicals without an exogenous contrast agent. QUEST MRI is hypothesized to be sensitive to noise-evoked cochlear oxidative stress in vivo. Rats exposed to a loud noise event that resulted in hair cell loss and reduced hearing capability had a supra-normal MRI R1 value in their cochleae that could be corrected with anti-oxidants, thus non-invasively indicating cochlear oxidative stress. A gold-standard oxidative damage biomarker [heme oxidase 1 (HO-1)] supported the QUEST MRI result. The results from this study highlight QUEST MRI as a potentially transformative measurement of cochlear oxidative stress in vivo that can be used as a biomarker for improving individual evaluation of anti-oxidant treatment efficacy in currently incurable oxidative stress-based forms of hearing loss.

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Staphylococcus aureus Infection Induced Oxidative Imbalance in Neutrophils: Possible Protective Role of Nanoconjugated Vancomycin

ISRN Pharmacology ◽

10.5402/2012/435214 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 4

Author(s):

Subhankari Prasad Chakraborty ◽

Panchanan Pramanik ◽

Somenath Roy

Keyword(s):

Oxidative Stress ◽

Staphylococcus Aureus ◽

Cell Damage ◽

Treated Group ◽

Protective Role ◽

Control Group ◽

Similar Dose ◽

Cellular Components

Staphylococcus aureus infection causes oxidative stress in neutrophils. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The present study was aimed to test the protective role of nanoconjugated vancomycin against vancomycin-sensitive Staphylococcus aureus (VSSA) and vancomycin-resistant Staphylococcus aureus (VRSA) infection induced oxidative stress in neutrophils. VSSA- and VRSA-infection were developed in Swiss mice by intraperitoneal injection of 5×106 CFU/mL bacterial solutions. Nanoconjugated vancomycin was treated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, and nitrite generation and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative imbalance in neutrophils.

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Electron Microscopy in Rat Brain Slices Reveals Rapid Accumulation of Cisplatin on Ribosomes and Other Cellular Components Only in Glia

Chemotherapy Research and Practice ◽

10.1155/2014/174039 ◽

2014 ◽

Vol 2014 ◽

pp. 1-5 ◽

Cited By ~ 3

Author(s):

Lidia Zueva ◽

Yomarie Rivera ◽

Lilia Kucheryavykh ◽

Serguei N. Skatchkov ◽

Misty J. Eaton ◽

...

Keyword(s):

Electron Microscopy ◽

Organic Cation ◽

Nuclear Dna ◽

Staining Method ◽

Brain Slices ◽

High Electron ◽

Rapid Accumulation ◽

Cellular Components ◽

Direct Attack

Cisplatin is a widely used, effective anticancer drug. Its use, however, is associated with several side effects including nephrotoxicity and neurotoxicity. It is known that cisplatin is accumulated in cells by the organic cation transport system and reacts with nucleotides, damaging them, but the precise target of cisplatin-induced neurotoxicity remains obscure. Here we report direct visualization of cisplatin inside brain cells using in vivo “cisplatin staining,” a technique that takes advantage of the high electron density of cisplatin, which contains platinum (atomic mass=195). After applying 0.1% cisplatin to living brain slices for 30 min, we fixed the tissue and observed the accumulated cisplatin using electron microscopy. We found that cisplatin was localized mainly to ribosomes associated with endoplasmic reticulum (EPR) in glial cells and to the myelin sheath formed by oligodendrocytes around neuronal axons. Staining of nuclear DNA was moderate. Our in vivo “cisplatin staining” method validated that the main target of cisplatin is a direct attack on myelin and the RNA contained in ribosomes.

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The essential iron-sulfur protein Rli1 is an important target accounting for inhibition of cell growth by reactive oxygen species

Molecular Biology of the Cell ◽

10.1091/mbc.e12-05-0413 ◽

2012 ◽

Vol 23 (18) ◽

pp. 3582-3590 ◽

Cited By ~ 49

Author(s):

Alawiah Alhebshi ◽

Theodora C. Sideri ◽

Sara L. Holland ◽

Simon V. Avery

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Ribosomal Subunit ◽

Reactive Oxygen ◽

Oxygen Species ◽

Sulfur Protein ◽

Iron Sulfur Protein ◽

Cellular Components

Oxidative stress mediated by reactive oxygen species (ROS) is linked to degenerative conditions in humans and damage to an array of cellular components. However, it is unclear which molecular target(s) may be the primary “Achilles’ heel” of organisms, accounting for the inhibitory action of ROS. Rli1p (ABCE1) is an essential and highly conserved protein of eukaryotes and archaea that requires notoriously ROS-labile cofactors (Fe-S clusters) for its functions in protein synthesis. In this study, we tested the hypothesis that ROS toxicity is caused by Rli1p dysfunction. In addition to being essential, Rli1p activity (in nuclear ribosomal-subunit export) was shown to be impaired by mild oxidative stress in yeast. Furthermore, prooxidant resistance was decreased by RLI1 repression and increased by RLI1 overexpression. This Rlip1 dependency was abolished during anaerobicity and accentuated in cells expressing a FeS cluster–defective Rli1p construct. The protein's FeS clusters appeared ROS labile during in vitro incubations, but less so in vivo. Instead, it was primarily55FeS-cluster supply to Rli1p that was defective in prooxidant-exposed cells. The data indicate that, owing to its essential nature but dependency on ROS-labile FeS clusters, Rli1p function is a primary target of ROS action. Such insight could help inform new approaches for combating oxidative stress–related disease.

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Isomeric O-methyl cannabidiolquinones with dual BACH1/NRF2 activity

10.1101/2020.06.16.153981 ◽

2020 ◽

Author(s):

Laura Casares ◽

Juan Diego Unciti ◽

Maria Eugenia Prados ◽

Diego Caprioglio ◽

Maureen Higgins ◽

...

Keyword(s):

Oxidative Stress ◽

Multiple Sclerosis ◽

Neurodegenerative Diseases ◽

Cell Models ◽

Therapeutic Approaches ◽

Neuroprotective Effects ◽

Anti Oxidant ◽

Anti Inflammatory ◽

The Brain

ABSTRACTOxidative stress and inflammation in the brain are two key hallmarks of neurodegenerative diseases (NDs) such as Alzheimer’s, Parkinson’s, Huntington’s and multiple sclerosis. The axis NRF2-BACH1 has anti-inflammatory and anti-oxidant properties that could be exploited pharmacologically to obtain neuroprotective effects. Activation of NRF2 or inhibition of BACH1 are, individually, promising therapeutic approaches for NDs. Compounds with dual activity as NRF2 activators and BACH1 inhibitors, could therefore potentially provide a more robust antioxidant and anti-inflammatory effects, with an overall better neuroprotective outcome. The phytocannabinoid cannabidiol (CBD) inhibits BACH1 but lacks significant NRF2 activating properties. Based on this scaffold, we have developed a novel CBD derivative that is highly effective at both inhibiting BACH1 and activating NRF2. This new CBD derivative provides neuroprotection in cell models of relevance to Huntington’s disease, setting the basis for further developments in vivo.

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Evaluation of anti-oxidant status in-vitro and in-vivo in hydro-alcoholic extract of Eugenia caryophyllus

International Journal of Pharmacology and Toxicology ◽

10.14419/ijpt.v4i1.5880 ◽

2016 ◽

Vol 4 (1) ◽

pp. 19

Author(s):

Roma Ghai ◽

Kandasamy Nagarajan ◽

Jitendra Singh ◽

Shiwam Swarup ◽

Minu Keshari

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Antioxidant Property ◽

Total Phenolic ◽

Alcoholic Extract ◽

Flavonoid Content ◽

Anti Oxidant ◽

Oxidant Status

Free radicals mediated oxidative stress is the major risk factor for many chronic diseases like atherosclerosis, diabetes mellitus, arthritis, cancer, ageing and neurodegenerative diseases. Therapy with anti-oxidants is gradually gaining lot of importance for treatment of such diseases. Hydro-alcoholic extract of Eugenia caryophyllus was studied for its in-vivo antioxidant activity using two different animal models viz. Triton induced hyperlipidemia and High fat diet induced hyperlipidemia. Total phenolic content and total flavonoid content, DPPH assay was also carried out for in vitro anti-oxidant efficacy. Total protein, lipid peroxidation (MDA), reduced glutathione, superoxide dismutase and catalase were evaluated in the liver tissue in Triton induced hyperlipidemia and diet induced hyperlipidemia models. The study findings indicated significant in-vivo and in-vitro antioxidant property that may be related to the amount of polyphenols and flavonoids present in the extract. These results clearly indicate that Eugenia caryophyllus is effective against free radical mediated oxidative stress.

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In vitrofolate supplementation alleviates oxidative stress, mitochondria-associated death signalling and apoptosis induced by 7-ketocholesterol

British Journal Of Nutrition ◽

10.1079/bjn20041259 ◽

2004 ◽

Vol 92 (6) ◽

pp. 887-894 ◽

Cited By ~ 32

Author(s):

R.-F. S. Huang ◽

H.-C. Yaong ◽

S.-C. Chen ◽

Y.-F. Lu

Keyword(s):

Oxidative Stress ◽

Nuclear Dna ◽

High Dose ◽

Protective Effects ◽

Folate Supplementation ◽

Mitochondria Membrane Potential ◽

Induced Apoptosis ◽

Apoptotic Damage

Folate has recently been proposed as a new antioxidant. Folate supplementation may have a protective effect in counteracting oxidant-induced apoptotic damage. The present studies were undertaken to examine whether there is a direct link between folate levels, antioxidant capability and reduced apoptotic damage. Using anin vitrocellular model of 7-ketocholesterol (KC)-induced apoptosis, U937 cells were pre-cultured with a folate-deficient medium supplemented with various levels of folate (2–1500μmol/l) before treatment with 7-KC. Apoptotic markers, mitochondria-associated death signals and levels of reactive oxygen species were assayed. After treatment with 7-KC for 30h, low and high levels of folate supplementation significantly (P<0.05) reduced nuclear DNA loss. Only high levels of folate supplementation (>1000μmol/l) were effective in counteracting 7-KC-promoted apoptotic membrane phosphatidylserine exposure and DNA laddering. The attenuation of 7-KC-induced apoptotic damage by high-dose folate supplementation coincided with a partial normalization of mitochondria membrane potential dissipation, a suppression of cytochromecrelease and an inhibition of procaspase 3 activation. The prevention of mitochondrial dysfunctions and apoptotic processes was associated with antioxidant actions of high-dose folate by a marked scavenging of intracellular superoxide. Collectively, our present results demonstrate thatin vitrofolate supplementation exerts differentially protective effects against 7-KC-induced damage. High-dose supplementation alleviates oxidative stress, mitochondria-associated death signalling and apoptosis induced by 7-KC. However, thein vivorelevance is not clear and requires further study.

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Endometriosis Susceptibility to Dapsone-Hydroxylamine-Induced Alterations Can Be Prevented by Licorice Intake: In Vivo and In Vitro Study

International Journal of Molecular Sciences ◽

10.3390/ijms22168476 ◽

2021 ◽

Vol 22 (16) ◽

pp. 8476

Author(s):

Chiara Sabbadin ◽

Alessandra Andrisani ◽

Gabriella Donà ◽

Elena Tibaldi ◽

Anna Maria Brunati ◽

...

Keyword(s):

Oxidative Stress ◽

In Vitro Study ◽

Carbonic Anhydrase Activity ◽

Control Group ◽

Beneficial Effects ◽

Licorice Extract ◽

Anti Oxidant ◽

Gynecological Disease

Endometriosis, an estrogen-dependent chronic gynecological disease, is characterized by a systemic inflammation that affects circulating red blood cells (RBC), by reducing anti-oxidant defenses. The aim of this study was to investigate the potential beneficial effects of licorice intake to protect RBCs from dapsone hydroxylamine (DDS-NHOH), a harmful metabolite of dapsone, commonly used in the treatment of many diseases. A control group (CG, n = 12) and a patient group (PG, n = 18) were treated with licorice extract (25 mg/day), for a week. Blood samples before (T0) and after (T1) treatment were analyzed for: i) band 3 tyrosine phosphorylation and high molecular weight aggregates; and ii) glutathionylation and carbonic anhydrase activity, in the presence or absence of adjunctive oxidative stress induced by DDS-NHOH. Results were correlated with plasma glycyrrhetinic acid (GA) concentrations, measured by HPLC–MS. Results showed that licorice intake decreased the level of DDS-NHOH-related oxidative alterations in RBCs, and the reduction was directly correlated with plasma GA concentration. In conclusion, in PG, the inability to counteract oxidative stress is a serious concern in the evaluation of therapeutic approaches. GA, by protecting RBC from oxidative assault, as in dapsone therapy, might be considered as a new potential tool for preventing further switching into severe endometriosis.

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