scholarly journals The Onset of Systemic Oxidative Stress Associated with the Accumulation of Lipid Peroxidation Product Acrolein in the Skin of Patients with Small-Vessel Vasculitis

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2344
Author(s):  
Vesna Sredoja Tisma ◽  
Stela Bulimbasic ◽  
Danica Galesic Ljubanovic ◽  
Kresimir Galesic ◽  
Jadranka Morovic-Vergles ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Modification ◽  
Protein Adducts ◽  
Small Vessel ◽  
Small Vessel Vasculitis ◽  
Total Serum ◽  
Myeloperoxidase Activity ◽  
Lipid Peroxidation Product ◽  
Systemic Oxidative Stress

Small-vessel vasculitis (SVV) is the inflammation of the vessel wall that can result in hemorrhage and/or ischemia. Among the histological findings in SVV are increased infiltrating neutrophils, which, due to their oxidative burst and myeloperoxidase activity, release excessive reactive oxygen species, triggering a chain reaction of lipid peroxidation and yielding reactive aldehydes such as acrolein. The implication of oxidative stress in the pathogenesis of SVV was studied, focusing on acrolein immunohistochemistry in the affected skin vessels and systemic stress response. Samples from SVV patients and healthy subjects were collected and analyzed for total serum peroxides, total antioxidant capacity, inflammatory and immunological parameters, as well as for the presence of acrolein–protein adducts in the skin tissue specimens. The obtained data showed that systemic redox homeostasis and iron metabolism are altered in SVV patients. Possible biomarkers in the evaluation of oxidative status, disease activity and prevalence were indicated. Furthermore, a strong correlation between the accumulation of acrolein–protein adducts in the skin and the progression of the disease was revealed. Thus, the results of this study demonstrate that SVV is not only associated with systemic oxidative stress but also with tissue-specific oxidative stress that promotes acrolein formation and protein modification correlating with the severity of cutaneous vasculitis.

scholarly journals Oxidative Stress, Lipid Peroxidation, and Loss of Hyaluronic Acid in the Human Vitreous Affected by Synchysis Scintillans

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Loredana Bergandi ◽  
Oleksii A Skorokhod ◽  
Rosalba La Grotta ◽  
Evelin Schwarzer ◽  
Raffaele Nuzzi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Hyaluronic Acid ◽  
Protein Modification ◽  
Vitreous Body ◽  
Thiobarbituric Acid ◽  
No Production ◽  
Lipid Peroxidation Product ◽  
Structural Protein ◽  
Protein Conjugates

The aim of this study was to assess the oxidative stress status in eyes affected by synchysis scintillans and to compare it to vitreoretinal disorders without synchysis scintillans. Human aqueous and vitreous humors were obtained during vitrectomy from thirty-seven otherwise healthy patients that were randomly chosen among patients that had to undergo a 25-gauge pars plana vitrectomy from the central vitreous cavity, for either synchysis scintillans (n = 16) or vitreoretinal disorders without synchysis scintillans (n = 21), such as idiopathic epimacular membrane (n = 12), macular hole (n = 5), or rhegmatogenous retinal detachment (n = 4). The redox parameters thiobarbituric acid reactive substances (TBARS), a measurement of lipid peroxidation, nitrite concentration, an estimate of nitric oxide (NO) production, 4-hydroxynonenal (4-HNE)-protein conjugates, a structural protein modification by lipid peroxidation product 4-HNE, and the antioxidative activities of Cu,Zn-superoxide dismutase (SOD), and catalase were measured in aqueous and vitreous humors and compared between synchysis scintillans affected and not-affected patients. TBARS and nitrite levels of the vitreous humor were significantly higher in patients with synchysis scintillans as compared to patients affected by vitreoretinal disorders without synchysis scintillans. Synchysis scintillans patients had significantly lower activities of SOD and catalase both in aqueous and vitreous humors than patients with vitreoretinal disorders without synchysis. The consequently higher lipoperoxide-dependent 4-HNE production in synchysis scintillans was detectable in aqueous and vitreous humors as a significant increased accumulation of 4-HNE-protein conjugates vs nonsynchysis vitreoretinal disorders. Additionally, hyaluronic acid (HA) was significantly decreased in the vitreous body of synchysis scintillans patients. The data consistently show that synchisis scintillans is accompanied by a redox imbalance with increased oxidative modifications of 4-HNE proteins and loss of HA, both of likely importance for remote damages of the retina. It remains to be proven whether a therapeutic strategy which targets oxidative stress may be effective in the treatment of synchysis patients.

Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Brain Regions ◽  
Protein Adducts ◽  
Antioxidant Systems ◽  
Control Group ◽  
Tbars Level ◽  
Elevated Expression ◽  
Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

scholarly journals Carotid intima-media thickness and oxidative stress markers for assessment of atherosclerosis in children with β thalassemia major

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Geetanjali Jindal ◽  
Prashant Chavan ◽  
Ravinder Kaur ◽  
Shivani Jaswal ◽  
Kamal Kumar Singhal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidized Ldl ◽  
Thalassemia Major ◽  
Lipid Peroxidation Product ◽  
Oxidative Stress Markers ◽  
Lipoprotein A ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Peroxidation Product

<p>The present study evaluates carotid intimamedia thickness (CIMT) in children with β thalassemia major to assess atherosclerosis and its relation to the underlying proposed causative mechanisms <em>via</em> lipid peroxidation product malondialdehyde (MDA), oxidized lowdensity lipoproteins (LDL), total antioxidant level, and lipid profile. A cross sectional study was conducted on 62 children (31 cases and 31 controls). CIMT by high resolution ultrasound and biochemical parameters <em>i.e.</em>, total cholesterol, triglycerides, high-density lipoproteins, LDL, Oxidized LDL, lipoprotein (a), lipid peroxidation product MDA and total antioxidant were measured in enrolled subjects and compared. In our study, CIMT was significantly increased in β thalassemia major patients’ as compared to healthy controls. Mean CIMT in cases was 0.69±0.11 mm and in controls 0.51±0.07 mm. Mean oxidized LDL (EU/mL) in cases 39.3±34.4 (range 14.4 to 160) was significantly raised (P=0.02, t test) as compared to controls 23.9±13.4 (range 12 to 70). In our study we found MDA levels (nmol/mL) to be increased in β thalassemia patients as compared to controls. Mean MDA was 10.0±3.27 (4.41 to 17.48) in cases while in controls was 6.87±4.55 (1.5 to 17.9). Our study results show CIMT as an early marker of atherogenesis in β thalassemia major. Oxidative stress markers are also increased in β thalassemia major patients and lipoprotein (a) shows a positive correlation with CIMT. The present study points towards various atherogenetic mechanisms in β thalassemia major.</p><p> </p><p>本研究评价β重型地中海贫血患儿颈动脉内膜中层厚度（CIMT），以评估动脉粥样硬化，以及与潜在通过血脂过氧化反应产物丙二醛（MDA）、氧化低密度脂蛋白（LDL）、总抗氧化水平和血脂谱所提出致病机制之间的关系。 在62名儿童（31例病例和31例对照）中进行了一项横断面研究。 在入组受试者中通过高分辨率超声和生化指标（即总胆固醇、甘油三酯、高密度脂蛋白、LDL、氧化LDL，脂蛋白（a）、血脂过氧化产物MDA和总抗氧化剂）测量CIMT并进行比较。 在我们的研究中，CIMT在β重型地中海贫血患者中比健康对照组显著增加。 病例组中的平均CIMT为0.69±0.11 mm，对照组0.51±0.07 mm。病例组中平均氧化LDL（EU/mL）为39.3±34.4（从14.4到160的范围）与对照组的23.9±13.4（12至70的范围）相比显著升高（P = 0.02，t检验）。 在我们的研究中，我们发现β地中海贫血患者中的MDA水平（nmol/mL）比对照组更高。 病例组中的平均MDA为10.0±3.27（4.41至17.48），而对照组为6.87±4.55（1.5到17.9）。 我们的研究结果表明，CIMT是β重型地中海贫血动脉粥样硬化的早期标记物。 氧化应激标记物在β重型地中海贫血患者中也有增加，脂蛋白（a）显示出与CIMT呈正相关。 本研究针对β重型地中海贫血中的各种动脉粥样硬化机制。</p>

scholarly journals Oxidative stress in ageing

2017 ◽  
Vol 5 (11) ◽  
pp. 4826 ◽  
Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Free Radical ◽  
Age Groups ◽  
The Body ◽  
Antioxidant Systems ◽  
Lipid Peroxidation Product ◽  
Free Radical Theory ◽  
Radical Theory

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

The effects of oral glutamine on cyclophosphamide-induced nephrotoxicity in rats

2010 ◽  
Vol 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Renal Damage ◽  
Neutrophil Infiltration ◽  
Protein Carbonyl ◽  
Male Rats ◽  
Glutathione Depletion ◽  
Myeloperoxidase Activity ◽  
Protein Carbonyl Content

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.

scholarly journals Association Between Thyroid Hormones, Lipids and Oxidative Stress Markers in Subclinical Hypothyroidism / Povezanost Izme\U Tireoidnih Hormona, Lipida I Markera Oksidativnog Stresa U SubkliniĉKoj Hipotireozi

2015 ◽  
Vol 34 (3) ◽  
pp. 323-331 ◽  
Author(s):  
Maureen Jepkorir Cheserek ◽  
Gui-Rong Wu ◽  
Arsene Ntazinda ◽  
Yong-Hui Shi ◽  
Li-Ye Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thyroid Hormones ◽  
Subclinical Hypothyroidism ◽  
Plasma Lipids ◽  
Plasma Concentrations ◽  
Thyroid Stimulating Hormone ◽  
Overt Hypothyroidism ◽  
Lipid Peroxidation Product ◽  
Free Triiodothyronine

SummaryOxidative stress plays a role in the pathogenesis of many chronic diseases. It is recognized in overt hypothyroidism while its existence in subclinical hypothyroidism (SCH) is not well established. The aim of this study was to determine whether there was increased oxidation of lipids and proteins in SCH, and examine their association with lipids and thyroid hormones.Methods: Male adults (35-59 years) with SCH (n=467) and euthyroid controls (n=190) were studied. Anthropometric measurements, plasma lipids, thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total antioxidant capacity (T-AOC), lipid peroxidation products, malondialdehyde (MDA), advanced oxidation protein products (AOPP) and dityrosine concentrations were measured.Results: Plasma concentrations of MDA were significantly higher (p<0.05) in SCH (8.11±1.39 nmol/mL) compared with euthyroid controls (7.34±1.31 nmol/mL) while AOPP, dityrosine and T-AOC levels were not different. MDA was not associated with TSH (β=-0.019, P=0.759), FT4 (β=-0.062, P=0.323) and FT3 (β=-0.018, P=0.780) in SCH while levels increased with elevated total cholesterol (β=0.229, P=0.001), LDL (β=0.203, P=0.009) and triglycerides (β=0.159, P=0.036) after adjustment for ageand body mass index. T-AOC reduced (β=-0.327, P=0.030) with increased MDA in euthyroid controls and not in SCH (β=-0.068, P=0.349), while levels increased with elevated triglycerides in both groups.Conclusion: Oxidative stress was increased in subclinical hypothyroidism as evidenced by the elevated lipid peroxidation product, malondialdehyde, while protein oxidation was absent. Thus, reduction of oxidative stress may be beneficial in patients with subclinical hypothyroidism

Protein modification by the lipid peroxidation product 4-hydroxynonenal in the spinal cords of amyotrophic lateral sclerosis patients

1998 ◽  
Vol 44 (5) ◽  
pp. 819-824 ◽  
Author(s):  
Ward A. Pedersen ◽  
Weiming Fu ◽  
Jeffrey N. Keller ◽  
William R. Markesbery ◽  
Stanley Appel ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Amyotrophic Lateral Sclerosis ◽  
Protein Modification ◽  
Lipid Peroxidation Product ◽  
Peroxidation Product ◽  
Lateral Sclerosis

scholarly journals Model of specific diagnostics of ovarian cancer stages

2012 ◽  
Vol 93 (5) ◽  
pp. 739-743
Author(s):  
I I Antoneeva ◽  
T V Abakumova ◽  
T P Gening ◽  
S O Gening ◽  
S S Pirmamedova
Keyword(s):  
Ovarian Cancer ◽  
Lipid Peroxidation ◽  
Tumor Tissue ◽  
Reductase Activity ◽  
Clinical Stage ◽  
Phagocytic Index ◽  
Diagnostic Tools ◽  
Myeloperoxidase Activity ◽  
Lipid Peroxidation Product ◽  
Gynecology And Obstetrics

Aim. To develop the model of specific diagnostics of III-IV stages of ovarian cancer. Methods. 404 patients with I-IV stages of primary ovarian cancer according to International Federation of Gynecology and Obstetrics classification were examined. Ultrasonography of genitalia and internal organs, chest X-ray in order to detect possible remote metastases, cytological, histological and immunohistological examination of tumor mass, as well as «lipid peroxidation - antioxidants» system condition of tumor tissue and patients’ serum were examined. Results. Elevated level of a lipid peroxidation product, malondialdehyde, was found in tumor tissue of patients with ovarian cancer, with levels of malondialdehyde growing from clinical stage I to clinical stage III of the disease. Leukocyte counts of peripheral blood statistically significantly decreased at stages I-III and elevated at stage IV. However, aerobic and anaerobic cytotoxicity of neutrophils decreases. An algorithm of supplementary diagnostic tools use to define the stage of ovarian cancer was developed, as well as differentiation coefficient calculation formula. Conclusion. Defining the serum levels of malondialdehyde, catalase and glutathione reductase activity allows to calculate the coefficient for differentiation between stages III and IV of ovarian cancer, and detection of cation proteins level, myeloperoxidase activity and phagocytic index allows to calculate the coefficient for differentiation between stages II and III of ovarian cancer.

scholarly journals Formation of DNA etheno adducts in rodents and humans and their role in carcinogenesis.

1998 ◽  
Vol 45 (1) ◽  
pp. 145-161 ◽  
Author(s):  
A Barbin
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vinyl Chloride ◽  
Dietary Factors ◽  
Lipid Peroxidation Product ◽  
Environmental Carcinogens ◽  
Increased Risk ◽  
Substitution Mutations ◽  
New Biomarkers

Ethenobases are exocyclic adducts formed with DNA by some environmental carcinogens such as vinyl chloride or urethane. In the last few years, they have received a renewed interest due to the development of sensitive techniques of analysis that made it possible to measure their formation in vivo. This minireview summarizes the information gained recently from the work of several laboratories, including ours. Increased levels of DNA etheno adducts have been measured in target tissues from rodents exposed to vinyl chloride or urethane. Hepatic tumours caused by exposure to vinyl chloride in humans and in rats and lung tumours induced by urethane in mice exhibit base pair substitution mutations in the ras and p53 genes which seem to be exposure-specific and consistent with the promutagenic properties of ethenobases. Background levels of etheno adducts have been detected in DNA from non-exposed humans or animals, pointing to an alternative, endogenous pathway of formation. This background may be affected by dietary factors. It could arise from the reaction of trans-4-hydroxy-2-nonenal (or its epoxide 2,3-epoxy-4-hydroxynonanal), a lipid peroxidation product, with nucleic acid bases. Elevated levels of etheno adducts are found in hepatic DNA from humans and rodents with genetic predisposition to oxidative stress and lipid peroxidation in the liver, and with an associated increased risk of liver cancer. These data suggest that DNA ethenobases could serve as new biomarkers of oxidative stress/lipid peroxidation.

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