scholarly journals Alteration on redox status in saliva of microcephaly children

2021 ◽  
Vol 10 (7) ◽  
pp. e40010716796
Author(s):  
Thayane Miranda Alves ◽  
Cintia Megid Barbieri ◽  
Marco Aurelio Gomes ◽  
Heitor Ceolin Araujo ◽  
Nathália de Oliveira Visquette ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Disorders ◽  
Redox Balance ◽  
Redox Status ◽  
Antioxidant Defenses ◽  
Frap Assay ◽  
Reducing Ability ◽  
Anticonvulsant Medication ◽  
Total Antioxidant ◽  
The Brain

Microcephaly is described as a reduction of the head circumference, due to the premature fusion of the bones of the skull, preventing the brain from growing normally and reaching its maximum development. This condition may result in neurological disorders, phonation and chewing dysfunction, dysphagia and risk of malnutrition. This alteration contributes to oral hygiene impairment, and continuous uses of the antipsychotic and anticonvulsant medication. Thus, the purpose of this study was to evaluate if microcephaly modified redox balance in saliva. Our hypothesis is that in the microcephalic patient's salivary oxidative stress is lower because of the increase in antioxidant defenses. The study included 13 patients with microcephaly (microcephalic group – MC) and 12 patients without neurological disorders (normocephalic group – NC), from zero to ten years old, no edentulous. Saliva was collected using a cotton wool swab, placing it on the child's mouth floor. After centrifugation, supernatants were fractionated and stored at -80 °C for analyses. Lipid oxidative was evaluated by TBARS methods, total antioxidant capacity by the ferric reducing ability (FRAP) assay, uric acid (UA) was quantified by modified Trinder reaction, and superoxide dismutase activity (SOD) by inhibition of the pyrogallol auto-oxidation. Total protein was measured using the method of Lowry.  Compared to NC group, TBARS was significantly lower in MC group, while FRAP, UA and SOD were higher. Our hypothesis was confirmed. MC patients have lower salivary oxidative stress, due to increased oxidant defenses.

scholarly journals Dexamethasone increased the survival rate in Plasmodium berghei-infected mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Danilo Reymão Moreira ◽  
Ana Carolina Musa Gonçalves Uberti ◽  
Antonio Rafael Quadros Gomes ◽  
Michelli Erica Souza Ferreira ◽  
Aline da Silva Barbosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Survival Rate ◽  
Plasmodium Berghei ◽  
Redox Status ◽  
No Synthase ◽  
Ischemia And Reperfusion ◽  
Inos Inhibition ◽  
The Brain ◽  
Plasmodial Infection ◽  
Stimulation Of

AbstractThe present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and subjected to stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice, and the data suggested the participation of oxidative stress in the brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted the survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of brain iNOS by dexamethasone caused a decrease in parasitemia and increased the survival rate of infected animals, suggesting that NO synthesis may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.

Role of Vitamins in Neurodegenerative Diseases: A Review

2021 ◽  
Vol 20 ◽  
Author(s):  
Ravi Ranjan Kumar ◽  
Lovekesh Singh ◽  
Amandeep Thakur ◽  
Shamsher Singh ◽  
Bhupinder Kumar
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Vitamin D ◽  
Vitamin C ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Vitamin D Deficiency ◽  
Neurological Disorders ◽  
The Brain

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity. Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript. Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain.

scholarly journals Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function

2019 ◽  
Vol 57 (3) ◽  
pp. 1317-1331 ◽  
Author(s):  
Gavin Pharaoh ◽  
Daniel Owen ◽  
Alexander Yeganeh ◽  
Pavithra Premkumar ◽  
Julie Farley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Spatial Learning ◽  
Mitochondrial Function ◽  
Coupling Efficiency ◽  
Redox Status ◽  
Cellular Aging ◽  
Age Related ◽  
The Brain ◽  
Circulating Levels

AbstractAge-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1f/f mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and glucose and insulin tolerance assessed. Mitochondrial function was analyzed in hippocampus, muscle, and visceral fat tissues using high-resolution respirometry O2K as well as redox status and oxidative stress in the cortex. Peripherally, IGF-1 deficiency did not significantly impact muscle mass or mitochondrial function. Aged LID mice were insulin resistant and exhibited ~ 60% less adipose tissue but increased fat mitochondrial respiration (20%). The effects on fat metabolism were attributed to increases in growth hormone. Centrally, IGF-1 deficiency impaired hippocampal-dependent spatial acquisition as well as reversal learning in male mice. Hippocampal mitochondrial OXPHOS coupling efficiency and cortex ATP levels (~ 50%) were decreased and hippocampal oxidative stress (protein carbonylation and F2-isoprostanes) was increased. These data suggest that IGF-1 is critical for regulating mitochondrial function, redox status, and spatial learning in the central nervous system but has limited impact on peripheral (liver and muscle) metabolism with age. Therefore, IGF-1 deficiency with age may increase sensitivity to damage in the brain and propensity for cognitive deficits. Targeting mitochondrial function in the brain may be an avenue for therapy of age-related impairment of cognitive function. Regulation of mitochondrial function and redox status by IGF-1 is essential to maintain brain function and coordinate hippocampal-dependent spatial learning. While a decline in IGF-1 in the periphery may be beneficial to avert cancer progression, diminished central IGF-1 signaling may mediate, in part, age-related cognitive dysfunction and cognitive pathologies potentially by decreasing mitochondrial function.

scholarly journals Reversal of age-associated oxidative stress in mice by PFT, a novel kefir product

2020 ◽  
Vol 34 ◽  
pp. 205873842095014
Author(s):  
Mamdooh Ghoneum ◽  
Shaymaa Abdulmalek ◽  
Deyu Pan
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Redox Homeostasis ◽  
Density Lipoprotein ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Age Related ◽  
Total Antioxidant ◽  
The Brain

Introduction: Oxidative stress is a key contributor to aging and age-related diseases. In the present study, we examine the protective effects of PFT, a novel kefir product, against age-associated oxidative stress using aged (10-month-old) mice. Methods: Mice were treated with PFT orally at a daily dose of 2 mg/kg body weight over 6 weeks, and antioxidant status, protein oxidation, and lipid peroxidation were studied in the brain, liver, and blood. Results: PFT supplementation significantly reduced the oxidative stress biomarkers malondialdehyde (MDA) and nitric oxide; reversed the reductions in glutathione (GSH) levels, total antioxidant capacity (TAC), and anti-hydroxyl radical (AHR) content; enhanced the antioxidant enzyme activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD); inhibited the liver enzyme levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); significantly reduced triglyceride (TG), total cholesterol (TC), and low density lipoprotein (LDL) levels; and significantly elevated high density lipoprotein (HDL) levels. Interestingly, PFT supplementation reversed the oxidative changes associated with aging, thus bringing levels to within the limits of the young control mice in the brain, liver, and blood. We also note that PFT affects the redox homeostasis of young mice and that it is corrected post-treatment with PFT. Conclusion: Our findings show the effectiveness of dietary PFT supplementation in modulating age-associated oxidative stress in mice and motivate further studies of PFT’s effects in reducing age-associated disorders where free radicals and oxidative stress are the major cause.

scholarly journals Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Christonikos Leventelis ◽  
Nikolaos Goutzourelas ◽  
Aikaterini Kortsinidou ◽  
Ypatios Spanidis ◽  
Georgia Toulia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Redox Status ◽  
Protein Carbonyls ◽  
Healthy Individuals ◽  
Thiobarbituric Acid Reactive Substances ◽  
Antioxidant Defence ◽  
Total Antioxidant ◽  
Beneficial Action ◽  
The Impact

Buprenorphine and methadone are two substances widely used in the substitution treatment of patients who are addicted to opioids. Although it is known that they partly act efficiently towards this direction, there is no evidence regarding their effects on the redox status of patients, a mechanism that could potentially improve their action. Therefore, the aim of the present investigation was to examine the impact of buprenorphine and methadone, which are administered as substitutes to heroin-dependent patients on specific redox biomarkers in the blood. From the results obtained, both the buprenorphine (n=21) and the methadone (n=21) groups exhibited oxidative stress and compromised antioxidant defence. This was evident by the decreased glutathione (GSH) concentration and catalase activity in erythrocytes and the increased concentrations of thiobarbituric acid reactive substances (TBARS) and protein carbonyls in the plasma, while there was no significant alteration of plasma total antioxidant capacity (TAC) compared to the healthy individuals (n=29). Furthermore, methadone revealed more severe oxidant action compared to buprenorphine. Based on relevant studies, the tested substitutes mitigate the detrimental effects of heroin on patient redox status; still it appears that they need to be boosted. Therefore, concomitant antioxidant administration could potentially enhance their beneficial action, and most probably, buprenorphine that did not induce oxidative stress in such a severe mode as methadone, on the regulation of blood redox status.

scholarly journals Antioxidant Barrier, Redox Status, and Oxidative Damage to Biomolecules in Patients with Colorectal Cancer. Can Malondialdehyde and Catalase Be Markers of Colorectal Cancer Advancement?

Biomolecules ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 637 ◽  
Author(s):  
Zińczuk ◽  
Maciejczyk ◽  
Zaręba ◽  
Romaniuk ◽  
Markowski ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Oxidative Damage ◽  
Redox Status ◽  
Control Group ◽  
Tumour Invasion ◽  
Reducing Ability ◽  
Glycation End Products ◽  
Total Antioxidant ◽  
Oxidative Damage To Proteins ◽  
Oxidant Status

This study is the first to assess the diagnostic utility of redox biomarkers in patients with colorectal cancer (CRC). Antioxidant barrier (Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), uric acid (UA), reduced glutathione (GSH)), redox status (total antioxidant (TAC)/oxidant status (TOS), ferric reducing ability (FRAP)), and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), malondialdehyde (MDA)) were measured in serum/plasma samples of 50 CRC patients. The activity of SOD was significantly higher whereas the activity of CAT, GPx and GR was considerably lower in CRC patients compared to the control group (p < 0.0001). Levels of UA, TOS, and OSI and concentrations of AGE, AOPP, and MDA were significantly higher, and the levels of GSH, TAC, and FRAP were considerably lower in CRC patients compared to the healthy controls (p < 0.0001). AUC for CAT with respect to presence of lymph node metastasis was 0.7450 (p = 0.0036), whereas AUC for MDA according to the depth of tumour invasion was 0.7457 (p = 0.0118). CRC is associated with enzymatic/non-enzymatic redox imbalance as well as increased oxidative damage to proteins and lipids. Redox biomarkers can be potential diagnostic indicators of CRC advancement.

scholarly journals Lack of Association between Nuclear Factor Erythroid-Derived 2-Like 2 Promoter Gene Polymorphisms and Oxidative Stress Biomarkers in Amyotrophic Lateral Sclerosis Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Annalisa LoGerfo ◽  
Lucia Chico ◽  
Loredana Borgia ◽  
Lucia Petrozzi ◽  
Anna Rocchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amyotrophic Lateral Sclerosis ◽  
Gene Promoter ◽  
Redox Balance ◽  
Nuclear Factor ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Reducing Ability ◽  
Als Patients ◽  
Lateral Sclerosis

Oxidative stress involvement has been strongly hypothesized among the possible pathogenic mechanisms of motor neuron degeneration in amyotrophic lateral sclerosis (ALS). The intracellular redox balance is finely modulated by numerous complex mechanisms critical for cellular functions, among which the nuclear factor erythroid-derived 2-like 2 (NFE2L2/Nrf2) pathways. We genotyped, in a cohort of ALS patients(n=145)and healthy controls(n=168), three SNPs inNrf2gene promoter: −653 A/G, −651 G/A, and −617 C/A and evaluated, in a subset(n=73)of patients, advanced oxidation protein products (AOPP), iron-reducing ability of plasma (FRAP), and plasma thiols (-SH) as oxidative damage peripheral biomarkers.Nrf2polymorphisms were not different among patients and controls. Increased levels of AOPP(P<0.05)and decreased levels of FRAP(P<0.001)have been observed in ALS patients compared with controls, but no difference in -SH values was found. Furthermore, no association was found between biochemical markers of redox balance andNrf2polymorphisms. These data confirm an altered redox balance in ALS and indicate that, while being abnormally modified compared to controls, the oxidative stress biomarkers assessed in this study are independent from the −653 A/G, −651 G/A, and −617 C/ANrf2SNPs in ALS patients.

scholarly journals Elevated DNA Damage, Oxidative Stress, and Impaired Response Defense System Inflicted in Patients With Myocardial Infarction

2017 ◽  
Vol 24 (5) ◽  
pp. 780-789 ◽  
Author(s):  
Sumayya Shahzad ◽  
Asif Hasan ◽  
Abul Faiz Faizy ◽  
Somaiya Mateen ◽  
Naureen Fatima ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Myocardial Infarction ◽  
Membrane Damage ◽  
Redox Status ◽  
Antioxidant Potential ◽  
Total Antioxidant ◽  
Coronary Events ◽  
Grace Score ◽  
Score Risk

Background: Ischemic tissue damage in myocardial infarction (MI) is allied with the exaggerated production of reactive oxygen species (ROS) beyond the countering capability of chain-breaking radical scavengers, fallouts in the form of oxidatively burdened myocardial tissue. Methods: One hundred and twenty five patients with MI were included in the study to evaluate the dynamics of redox status of patients by monitoring the antioxidant potential, biomarkers of oxidative stress, lipid indices, RBC membrane damage when compared to healthy individuals in patients with MI congregated on the basis of Global Registry of Acute Coronary Events (GRACE) score, risk factors, and age. Results: Higher levels of malondialdehyde, 8-hydroxy-2-deoxyguanosine, lipid indices, ROS content, and membrane deterioration in erythrocytes were seen in patients with MI. Furthermore, reduced activities of erythrocyte antioxidant enzymes and lower concentrations of antioxidant molecules, plus reduced total antioxidant capacity, were observed in plasma of all patients with MI with respect to control. However, elevation in oxidative stress was found to be significantly marked in patients having GRACE score >100, risk factors, and MI >45 years when compared to patients with GRACE score ≤100, without risk factors, and MI ≤45 years, respectively. Conclusion: These findings indicate the existence of increased oxidative damage and reduced antioxidant potential in patients with MI have a potent relationship with their GRACE risk score, risk factors, and age.

scholarly journals A 11C-Labeled 1,4-Dihydroquinoline Derivative as a Potential PET Tracer for Imaging of Redox Status in Mouse Brain

2015 ◽  
Vol 35 (12) ◽  
pp. 1930-1936 ◽  
Author(s):  
Toshimitsu Okamura ◽  
Maki Okada ◽  
Tatsuya Kikuchi ◽  
Hidekatsu Wakizaka ◽  
Ming-Rong Zhang
Keyword(s):  
Mouse Brain ◽  
Initial Velocity ◽  
Brain Homogenate ◽  
Redox Balance ◽  
Redox Status ◽  
Cationic Form ◽  
Pet Tracer ◽  
Positron Emission ◽  
The Brain

A disturbance in redox balance has been implicated in the pathogenesis of a number of diseases. This study sought to examine the feasibility of imaging brain redox status using a 11C-labeled dihydroquinoline derivative ([11C]DHQ1) for positron emission tomography (PET). The lipophilic PET tracer [11C]DHQ1 was rapidly oxidized to its hydrophilic form in mouse brain homogenate. The redox modulators diphenyleneiodonium and apocynin significantly reduced the initial velocity of [11C]DHQ1 oxidation, and apocynin also caused concentration-dependent inhibition of the initial velocity. Moreover, [11C]DHQ1 readily entered the brain by diffusion after administration and underwent oxidation into the hydrophilic cationic form, which then slowly decreased. By contrast, apocynin treatment inhibited the in vivo oxidation of [11C]DHQ1 to the hydrophilic cationic form, leading to a rapid decrease of radioactivity in the brain. Thus, the difference in the [11C]DHQ1 kinetics reflects the alteration in redox status caused by apocynin. In conclusion, [11C]DHQ1 is a potential PET tracer for imaging of redox status in the living brain.

scholarly journals Assessment of total (anti)oxidant status in goat kids

2021 ◽  
Vol 64 (1) ◽  
pp. 139-146
Author(s):  
Stefano Cecchini ◽  
Francesco Fazio
Keyword(s):  
Radical Scavenging Activity ◽  
Analytical Data ◽  
Radical Scavenging ◽  
Redox Balance ◽  
Reactive Oxygen Metabolites ◽  
Strongly Correlated ◽  
Antioxidant Assays ◽  
Reducing Ability ◽  
Total Antioxidant ◽  
Oxidant Status

Abstract. The redox potential of goat serum was assessed by different spectrophotometric assays. Among them, three methods are commonly applied for the evaluation of the oxidative (reactive oxygen metabolites, ROMs, and total oxidant status, TOS) and nitrosative (NO⚫ metabolites, NOx) stress, and four methods for the evaluation of the antioxidant status: the total antioxidant capacity (TAC) based on the ferric reducing ability of plasma (FRAP), the total antioxidant activity (TAA) based on the reduction of the coloured ABTS⚫+ radical cation, the free radical scavenging activity (FRSA) based on the reduction of the purple DPPH⚫, and the total thiol levels (TTLs) based on their interaction with DTNB to form a highly coloured anion. Besides, myeloperoxidase (MPO) and ceruloplasmin oxidase (CP) activities were also assessed. Except for TAA, analytical data showed a great inter-individual variation for both oxidant and antioxidant assays. ROMs were strongly correlated with CP, while TOS with MPO and TAC. Furthermore, a tendency between TOS and FRSA was shown. NOx was correlated with TAC and TAA, and a tendency with TOS was shown. No correlations appeared among the antioxidant assays, even if a tendency between TAC and TAA was evidenced, but TAC was correlated with MPO activity. The observed correlation between ROMs and CP is discussed as a possible analytical interference. The absence of correlation among the antioxidant biomarkers suggests the simultaneous use of a panel of tests to verify any changes in the redox balance, mainly in livestock in which reference values for each biomarker are lacking.

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