UCTD and SLE patients show increased levels of oxidative and DNA damage together with an altered kinetics of DSB repair

Mutagenesis ◽  
2021 ◽  
Author(s):  
Consuelo Micheli ◽  
Alice Parma ◽  
Chiara Tani ◽  
Domenica Di Bello ◽  
Aurora Falaschi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Disease Activity ◽  
Treatment Plan ◽  
Connective Tissue Diseases ◽  
Autoimmune Disorders ◽  
Control Group ◽  
Repair System ◽  
Serological Profile ◽  
Genome Damage

Abstract Immunological tolerance is a critical feature of the immune system; its loss might lead to an abnormal response of lymphocytes causing autoimmune diseases. One of the most important groups belonging to autoimmune disorders is the connective tissue diseases (CTD). CTD are classified among systemic rheumatic diseases and include pathologies such as systemic lupus erythematosus (SLE), and undifferentiated CTD (UCTD). In this study, we evaluated oxidative and genome damage in peripheral blood lymphocytes from patients with SLE and UCTD, further classified on the basis of disease activity and the presence/absence of a serological profile. Oxidative damage was evaluated in cell membrane using the fluorescent fatty acid analogue BODIPY 581/591 C11. The percentage of oxidised lymphocytes in both SLE and UCTD patients was higher than in the control group, and the oxidative stress correlated positively with both disease activity and autoantibody profile. The γH2AX focus assay was used to quantify the presence of spontaneous double strand breaks (DSBs), and to assess the abilities of DSBs repair system after T cells were treated with mitomycin C (MMC). Subjects with these autoimmune disorders showed a higher number of γH2AX foci than healthy controls, but no correlation with diseases activity and presence of serological profile was observed. In addition, patients displayed an altered response to MMC-induced DSBs, which led their peripheral cells to greatly increase apoptosis. Taken together our results confirmed an interplay among oxidative stress, DNA damage and impaired DNA repair, which are directly correlated to the aggressiveness and clinical progression of the diseases. We propose the evaluation of these molecular markers to better characterize SLE and UCTD, aiming to improve the treatment plan and the quality of the patients’ life.

scholarly journals Sulforaphane-Mediated Nrf2 Activation Prevents Radiation-Induced Skin Injury through Inhibiting the Oxidative-Stress-Activated DNA Damage and NLRP3 Inflammasome

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1850
Author(s):  
Jinlong Wei ◽  
Qin Zhao ◽  
Yuyu Zhang ◽  
Weiyan Shi ◽  
Huanhuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Western Blotting ◽  
Nlrp3 Inflammasome ◽  
Fibrous Tissue ◽  
Mouse Skin ◽  
Control Group ◽  
Skin Injury ◽  
Antioxidant Genes ◽  
Radiation Induced

This article mainly observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI). In addition, we will discuss the mechanism of SFN’s protection on RISI. The RISI model was established by the irradiation of the left thigh under intravenous anesthesia. Thirty-two C57/BL6 mice were randomly divided into control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group. At eight weeks after irradiation, the morphological changes of mouse skin tissues were detected by H&E staining. Then, the oxidative stress and inflammatory response indexes in mouse skin tissues, as well as the expression of Nrf2 and its downstream antioxidant genes, were evaluated by ELISA, real-time PCR, and Western blotting. The H&E staining showed the hyperplasia of fibrous tissue in the mouse dermis and hypodermis of the IR group. Western blotting and ELISA results showed that the inflammasome of NLRP3, caspase-1, and IL-1β, as well as oxidative stress damage indicators ROS, 4-HNE, and 3-NT, in the skin tissues of mice in the IR group were significantly higher than those in the control group (p < 0.05). However, the above pathological changes declined sharply after SFN treatment (p < 0.05). In addition, the expressions of Nrf2 and its regulated antioxidant enzymes, including CAT and HO-1, were higher in the skin tissues of SFN and IR/SFN groups, but lower in the control and IR groups (p < 0.05). SFN may be able to suppress the oxidative stress by upregulating the expression and function of Nrf2, and subsequently inhibiting the activation of NLRP3 inflammasome and DNA damage, so as to prevent and alleviate the RISI.

scholarly journals Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus

2011 ◽  
Vol 34 (3) ◽  
pp. 163 ◽  
Author(s):  
Omur Tabak ◽  
Remise Gelisgen ◽  
Hayriye Erman ◽  
Fusun Erdenen ◽  
Cüneyt Muderrisoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Vascular Complications ◽  
Diabetic Group ◽  
Control Group ◽  
Diabetic Patients ◽  
Serum Samples ◽  
Type 2 Diabetic Patients

Purpose: The purpose of this study was to determine the effects of diabetic complications on oxidation of proteins, lipids, and DNA and to investigate the relationship between oxidative damage markers and clinical parameters. Methods: The study group consisted of 69 type 2 diabetic patients (20 patients without complication, 49 patients with complication) who attended internal medicine outpatient clinics of Istanbul Education and Research Hospital and 19 healthy control subjects. In serum samples of both diabetic patients and healthy subjects, 8-hydroxy-2’deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, Nε-(hexanoyl)lysine (HEL) and 15-F2t-iso-prostaglandin (15-F2t-IsoP). as products of lipooxidative damage, advanced oxidation protein products (AOPP), as markers of protein damage, and paraoxonase1 (PON1) as antioxidant were studied. Results: 15-F2t-IsoP (p < 0.005) and AOPP (p < 0.001) levels were significantly higher in diabetic group than control group while there were no significant differences in levels of 8-OHdG and HEL between the two groups. AOPP (p < 0.001) and 8-OHdG (p < 0.001) were significantly higher in diabetic group with complications compared to diabetic group without complications. Conclusions: Increased formation of free radicals and oxidative stress, under conditions of hyperglycaemia, is one of the probable causes for evolution of complications in diabetes mellitus. Our study supports the hypothesis that oxidant/antioxidant balance is disturbed in diabetic patients.

scholarly journals Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Tarfa Albrahim ◽  
Manal Abdulaziz Binobead
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Leaf Extract ◽  
Liver Toxicity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Glutamyl Transferase ◽  
The Impact

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin-induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P<0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S-transferase (GST) enzyme activities (P<0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

scholarly journals Influence of Insulin Resistance and TNF-αon the Inflammatory Process, Oxidative Stress, and Disease Activity in Patients with Rheumatoid Arthritis

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Neide Tomimura Costa ◽  
Tatiana Mayumi Veiga Iriyoda ◽  
Ana Paula Kallaur ◽  
Francieli Delongui ◽  
Daniela Frizon Alfieri ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Insulin Resistance ◽  
Disease Activity ◽  
Inflammatory Process ◽  
Cross Sectional Study ◽  
Stress Index ◽  
Control Group ◽  
Cross Sectional ◽  
Clinical Trials Registry

The aim of this study was to evaluate the involvement of TNF-αand insulin resistance (IR) in the inflammatory process, oxidative stress, and disease activity in patients with rheumatoid arthritis (RA). This cross-sectional study included 270 subjects (control group,n=97) and RA patients (n=173). RA patients were divided into four groups: the first group without IR and not using antitumor necrosis factor-α(TNF-) (G1, IR− TNF−); the second group without IR and using anti-TNF-α(G2,IR-TNF+); the third group with IR and not using anti-TNF-α(G3, IR+TNF-); and the fourth group with IR and using anti-TNF-α(G4, IR+ TNF+). G3 and G4 had higher (p<0.05) advanced oxidation protein products (AOPPs) and oxidative stress index (OSI) compared to G1. G4 group presented higher (p<0.05) AOPPs and OSI than G2. TRAP was significantly lower in G3 compared to G1. Plasma TNF-αlevels were significantly higher in G4 and G2 compared to G1 (p<0.0001) and G3 (p<0.0001andp<0.01, resp.). The presence of insulin resistance was robustly associated with both oxidative stress and TNF-αlevels. More studies are warranted to verify if IR can be involved in therapeutic failure with TNF-αinhibitors. This trial is registered with Brazilian Clinical Trials Registry Register numberRBR-2jvj92.

Evaluation of glucose-6-phosphate dehydrogenase serum level in patients with multiple sclerosis and neuromyelitis optica

2020 ◽  
Author(s):  
Niloofar Chitsaz ◽  
Leila Dehghani ◽  
Amir Safi ◽  
Nazgol Esmalian-Afyouni ◽  
Vahid Shaygannejad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Vitamin D ◽  
Serum Level ◽  
Neuromyelitis Optica ◽  
Treatment Plan ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Control Group ◽  
Significant Difference ◽  
Glucose 6 Phosphate Dehydrogenase

Background: Multiple sclerosis (MS) and neuromyelitis optica (NMO) are both demyelinating disorders and oxidative stress is suggested to have a role in their pathogenesis. Glucose-6-phosphate dehydrogenase (G6PD) produces nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. NADPH is not only involved in the synthesis of fatty acids necessary for myelination, but also it is involved in the defense against oxidative stress. Prescribing supplementary vitamin D as a part of the MS treatment plan can increase G6PD gene expression. The aim of this study was to determine the serum level of G6PD in patients with MS and NMO and its relationship with vitamin D, since it is yet to be explored thoroughly. Methods: In this case-control study, subjects were divided into three experimental and control groups. The experimental groups comprised 50 patients with relapsing-remitting MS (RRMS) who had a history of vitamin D consumption, 50 newly-diagnosed MS patients, and 50 patients with NMO. Control group included 65 healthy individuals. Serum level of G6PD was measured and compared among these groups. Results: No significant difference was seen between the G6PD level in patients with MS and NMO, but it should be noted that this level was significantly lower than the healthy group. G6PD serum level was significantly higher in patients with MS who had previously consumed supplementary vitamin D compared to those who had not. Conclusion: G6PD deficiency is observed in patients with MS and NMO. Also, supplementary vitamin D may induce favorable results on the G6PD level.

scholarly journals Fish Oil Supplementation Reduces Markers of Oxidative Stress But Not Muscle Soreness After Eccentric Exercise

2014 ◽  
Vol 24 (2) ◽  
pp. 206-214 ◽  
Author(s):  
Patrick Gray ◽  
Andrew Chappell ◽  
Alison McE Jenkinson ◽  
Frank Thies ◽  
Stuart R. Gray
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Fish Oil ◽  
Eccentric Exercise ◽  
Muscle Soreness ◽  
Protein Carbonyls ◽  
Fish Oils ◽  
Control Group ◽  
Markers Of Oxidative Stress ◽  
Fish Oil Supplementation

Due to the potential anti-inflammatory properties of fish-derived long chain n-3 fatty acids, it has been suggested that athletes should regularly consume fish oils—although evidence in support of this recommendation is not clear. While fish oils can positively modulate immune function, it remains possible that, due to their high number of double bonds, there may be concurrent increases in lipid peroxidation. The current study aims to investigate the effect of fish oil supplementation on exercise-induced markers of oxidative stress and muscle damage. Twenty males underwent a 6-week double-blind randomized placebo-controlled supplementation trial involving two groups (fish oil or placebo). After supplementation, participants undertook 200 repetitions of eccentric knee contractions. Blood samples were taken presupplementation, postsupplementation, immediately, 24, 48, and 72 hr postexercise and muscle soreness/maximal voluntary contraction (MVC) assessed. There were no differences in creatine kinase, protein carbonyls, endogenous DNA damage, muscle soreness or MVC between groups. Plasma thiobarbituric acid reactive substances (TBARS) were lower (p < .05) at 48 and 72 hr post exercise and H2O2 stimulated DNA damage was lower (p < .05) immediately postexercise in the fish oil, compared with the control group. The current study demonstrates that fish oil supplementation reduces selected markers of oxidative stress after a single bout of eccentric exercise.

Investigating the Effect of Fresh Frozen Plasma and Albumin on DNA Damage and Oxidative Stress Biomarkers in Poisoning Cases by Organophosphates

Drug Research ◽  
2020 ◽  
Vol 71 (01) ◽  
pp. 10-16
Author(s):  
Saeed Afzali ◽  
Manoochehr Karami ◽  
Nejat Kheyripour ◽  
Akram Ranjbar
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Fresh Frozen Plasma ◽  
Adjunctive Treatment ◽  
Control Group ◽  
Oxidative Stress Biomarkers ◽  
Significant Difference ◽  
Antioxidant Parameters ◽  
Fresh Frozen ◽  
Frozen Plasma

AbstractThe efficacy of albumin and fresh frozen plasma (FFP) and their effects on biomarkers of oxidative stress has been evaluated. In a randomized clinical control trial, 33 poisoned patients by Organophosphate (OP) were enrolled in the research and divided into three groups. The first group underwent conventional treatments by atropine and pralidoxime (control group); the second and third groups, in addition to traditional treatments, received albumin and FFP. Cholinesterase (ChE) enzyme activity, total antioxidant capacity (TAC), serum thiol groups (TTG), malonyl aldehyde (MDA) and DNA damage were measured in all treatment and control groups. Patients were matched in terms of demographic characteristics at the beginning of the study. ChE activity was increased in all three groups during treatment, which was more noticeable in the FFP group and was statistically significant in both albumin and FFP group compared to the control group (p<0.05). TAC increased, and TTG decreased in FFP and albumin groups compared to the control group; no significant difference was observed. MDA decreased in albumin and FFP and was significantly different in the FFP group compared to the control group (p<0.05). The amount of DNA damage in FFP and albumin groups decreased, and there was a significant difference compared to the control group (p<0.05). According to the results of this study, due to the decrease of oxidative damage parameters and the increase of antioxidant parameters in albumin and specially FFP groups, FFP may be considered as an adjunctive treatment for OP poisoning.

Baicalein (5,6,7-trihydroxyflavone) reduces oxidative stress-induced DNA damage by upregulating the DNA repair system

2012 ◽  
Vol 28 (6) ◽  
pp. 421-433 ◽  
Author(s):  
Ki Cheon Kim ◽  
In Kyung Lee ◽  
Kyoung Ah Kang ◽  
Hye Sun Kim ◽  
Sam Sik Kang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Repair System

scholarly journals The maternal effect in infantile autism: elevated DNA damage degree in patients and their mothers

2016 ◽  
Vol 62 (4) ◽  
pp. 466-470 ◽  
Author(s):  
L.N. Porokhovnik ◽  
S.V. Kostyuk ◽  
E.S. Ershova ◽  
S.M. Stukalov ◽  
N.N. Veiko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Maternal Effect ◽  
Infantile Autism ◽  
Reproductive Age ◽  
Control Group ◽  
Healthy Children ◽  
Tail Moment ◽  
Autistic Children ◽  
Comet Tail

Infantile autism is a common disorder of mental development, which is characterized by impairments in the communicative, cognitive and speech spheres and obsessional stereotyped behaviour. Although in most cases, pathogenic factors remain unclear, infantile autism has a significant hereditary component, however, its etiology is also under the influence of environmental factors, including the condition of the mother's body during pregnancy (“maternal effect”). Oxidative stress is assumed to play a key role in the pathogenesis of infantile autism. It is known that oxidative stress has a prominent genotoxic effect, which is realized through inducing single and double strand breaks of the nuclear DNA. We evaluated the degree of DNA damage in patients with infantile autism and their mothers using DNA comet assay. The comet tail moment and DNA per cent ratio in the tail were assessed for each individual. The two parameters appeared to be strongly correlated (r=0.90). Mean and median values of both parameters were considerably higher in the sample of autistic children, than in age-matching healthy controls. Interestingly, these parameters were also elevated in healthy mothers of autistic children, with no difference from the values in the group of autistic children. The control group of healthy women of reproductive age, who had no children with autism, differed by the DNA comet tail moment from the group of mothers of autistic children, but did not differ significantly from the control group of healthy children. The results suggest that there are genotoxic factors in mentally healthy mothers of autistic children, which can determine the pathological process in the foeti via environmental “maternal effect” during gestation.

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