scholarly journals Activity of ROS-induced processes in the combined preconditioning with amtizol before and after cerebral ischemia in rats

2021 ◽  
Vol 7 (2) ◽  
pp. 49-57
Author(s):  
Olga S. Levchenkova ◽  
Vasiliy E. Novikov ◽  
Viktoriya V. Vorobyova ◽  
Konstantin N. Kulagin
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Rat Brain ◽  
Early Period ◽  
Maximum Level ◽  
Thiobarbituric Acid ◽  
Wistar Rat ◽  
Mitochondrial Fraction ◽  
No Synthase ◽  
The Impact

Introduction: The dose-dependent effect of reactive oxygen species (ROS) in tissues in preconditioning (PreC) and oxidative stress, as well as NO-synthase participation in mitochondrial ROS production determined the study aim – to assess the impact of the neuroprotective method of combined preconditioning (CPreC) on free radical reactions (FRRs) in brain in normoxia and in cerebral ischemia, including in NO-synthase blockade. Materials and methods: The intensity of FRR by iron-induced chemiluminescence (CL), the content of lipid peroxidation products and antioxidant enzyme activity were investigated 1 hr (early period) and 48 hrs (delayed period) after CPreC (amtizol and hypobaric hypoxia) in Wistar rat brain. Some animal groups were operated (common carotid artery bilateral ligation) 1 hr and 48 hrs after CPreC, as well as with preliminary introduction of L-NAME and aminoguanidine. Results and discussion: In normoxia, CPreC led to increase the CL maximum level (Fmax) in the delayed PreC period. The amount of thiobarbituric acid reactive products (TBA-RP), activity of superoxide dismutase (SOD) and catalase in mitochondrial fraction of rat brain did not change in comparison with the intact control in both PreC periods. In cerebral ischemia, oxidative stress was observed. The CPreC use before ischemia caused a decrease in CL parameters and TBA-RP in brain, the maintenance of SOD and high catalase activity. NO-synthase inhibitors partially abolished the antioxidant effect of CPreC in ischemia. Conclusion: CPreC had no influence on FRRs in brain tissue in normoxia, but prevented their excessive activation after ischemia, especially in the delayed period. NO-synthase was involved in the CPreC neuroprotection.

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.

Effect of lipid peroxidation conditions on calcium-dependent activity of phosphodiesterase 3′,5′-cAMP in the rat brain

Biologia ◽  
2006 ◽  
Vol 61 (6) ◽  
Author(s):  
Monika Ďurfinová ◽  
Marta Brechtlová ◽  
Branislav Líška ◽  
Želmíra Barošková
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Rat Brain ◽  
Cell Damage ◽  
Intracellular Camp ◽  
Calcium Dependent ◽  
Cellular Processes ◽  
Phosphodiesterase 3 ◽  
Higher Temperature ◽  
The Impact

Abstract3′,5′-cAMP plays an important role as a second messenger molecule controlling multiple cellular processes in the brain. Its levels are decreased by phosphodiesterases (PDEs), responsible for hydrolysis of intracellular cAMP. A part of the PDE activity is dependent on the effect of calcium, mediated by its binding to calmodulin. During oxidative stress, precisely these changes in calcium concentration are responsible for cell damage. We have examined the effects of oxidative stress conditions on the activity of PDE in rat brain homogenates. We found a different influence of activated lipid peroxidation conditions (Fe2+ with ascorbate and increased temperature) on the calcium-dependent and calcium-independent PDE activity. The inhibition of Ca2+-dependent PDE was observed, while Ca2+-independent PDE was not influenced. We assume that it might be the impact of lipid peroxidation products or any mechanism activated by the higher temperature on the interaction of the Ca2+-dependent isoform of PDE with the complex calcium-calmodulin. Another explanation might be that the formation of the functioning calcium-calmodulin complex is impossible in these conditions.

scholarly journals Effect of Chronic Exposure to Prometryne on Oxidative Stress and Antioxidant Response in Red Swamp Crayfish (Procambarus clarkii)

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Alžběta Stará ◽  
Antonín Kouba ◽  
Josef Velíšek
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Chronic Exposure ◽  
Prolonged Exposure ◽  
Procambarus Clarkii ◽  
Thiobarbituric Acid ◽  
Antioxidant Systems ◽  
Control Group ◽  
Red Swamp Crayfish ◽  
The Impact

The aim of the study was to investigate effects of the triazine herbicide prometryne on red swamp crayfish on the basis of oxidative stress, antioxidant indices in hepatopancreas and muscle, and histopathology of hepatopancreas. Crayfish were exposed to prometryne concentrations of 0.51 μg L−1, 0.144 mg L−1, and 1.144 mg L−1for 11 and 25 days. Indices of oxidative stress (thiobarbituric acid reactive substances (TBARS)), and antioxidant parameters (superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR)) in crayfish muscle and hepatopancreas were measured. Chronic exposure to prometryne did not showed the impact of oxidative damage to cells. Changes activity of the antioxidant enzymes SOD, CAT, and GR were observed in all tested concentrations to prometryne for 11 and 25 days (P<0.01) as compared with the control group. We did not see any differences in histopatological examination to hepatopancreas. Prolonged exposure of prometryne did not result in oxidative damage to cell lipids and proteins, but it led to changes in antioxidant activity in crayfish tissues. Changes in antioxidant systems were also observed in the environmental prometryne concentration of 0.51 μg L−1. The results suggest that antioxidant responses may have potential as biomarkers for monitoring residual triazine herbicides in aquatic environments.

scholarly journals Neither Excessive Nitric Oxide Accumulation nor Acute Hyperglycemia Affects the N-Acetylaspartate Network in Wistar Rat Brain Cells

2020 ◽  
Vol 21 (22) ◽  
pp. 8541
Author(s):  
Marlena Zyśk ◽  
Piotr Pikul ◽  
Robert Kowalski ◽  
Krzysztof Lewandowski ◽  
Monika Sakowicz-Burkiewicz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Wistar Rat ◽  
Diabetic Patients ◽  
Mrna Levels ◽  
Male Adult ◽  
The Impact

The N-acetylaspartate network begins in neurons with N-acetylaspartate production catalyzed by aspartate N-acetyltransferase from acetyl-CoA and aspartate. Clinical studies reported a significant depletion in N-acetylaspartate brain level in type 1 diabetic patients. The main goal of this study was to establish the impact of either hyperglycemia or oxidative stress on the N-acetylaspartate network. For the in vitro part of the study, embryonic rat primary neurons were treated by using a nitric oxide generator for 24 h followed by 6 days of post-treatment culture, while the neural stem cells were cultured in media with 25–75 mM glucose. For the in vivo part, male adult Wistar rats were injected with streptozotocin (65 mg/kg body weight, ip) to induce hyperglycemia (diabetes model) and euthanized 2 or 8 weeks later. Finally, the biochemical profile, NAT8L protein/Nat8l mRNA levels and enzymatic activity were analyzed. Ongoing oxidative stress processes significantly affected energy metabolism and cholinergic neurotransmission. However, the applied factors did not affect the N-acetylaspartate network. This study shows that reduced N-acetylaspartate level in type 1 diabetes is not related to oxidative stress and that does not trigger N-acetylaspartate network fragility. To reveal why N-acetylaspartate is reduced in this pathology, other processes should be considered.

Effect of craniotomy on oxidative stress and its effect on plasma l-carnitine levels

2014 ◽  
Vol 92 (11) ◽  
pp. 913-916 ◽  
Author(s):  
Huan-ting Li ◽  
Zhen-huan Zhao ◽  
Hai-yan Ding ◽  
Le-xin Wang ◽  
Yu Cao
Keyword(s):  
Oxidative Stress ◽  
Plasma Levels ◽  
Plasma Concentrations ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Before And After ◽  
Baseline Values ◽  
The Mean ◽  
Total Antioxidative Capacity ◽  
The Impact

Objective: to investigate the impact of craniotomy on oxidative stress and its effect on levels of plasma l-carnitine (LC). Methods: plasma levels of reactive oxygen species, superoxide dismutase (SOD), glutathion peroxidase (GSH-Px), catalase (CAT), total antioxidative capacity (T-AOC), and thiobarbituric acid reactive substances (TBARS) were measured in 34 patients (26 males and 8 females, mean age 47.7 ± 6.7 years) before and after craniotomy. Plasma levels of LC, acetyl-l-carnitine (ALC), and propionyl-l-carnitine (PLC) were also measured before and after the craniotomy. Results: the plasma concentrations of SOD, GSH-Px, CAT, and T-AOC within the first 4 h after craniotomy were lower than their baseline values (P < 0.05). There were no statistically significant differences in the mean plasma levels of SOD, GSH-Px, CAT, or T-AOC between the baseline and 24 h post-operative values. The level of TBARS at 4 h after the craniotomy was lower than the pre-operative level (P < 0.05), but the 24 h post-operative value was similar to the baseline concentration (P > 0.05). Plasma levels of LC, ALC, and PLC were lower after the craniotomy (P < 0.05), but these levels returned to the baseline levels 24 h after the operation. Conclusions: craniotomy and the associated procedures for surgery/anesthesia temporarily reduce antioxidant activity and plasma levels of l-carnitine.

scholarly journals Postponed effect of neostigmine on oxidative homeostasis

2014 ◽  
Vol 7 (3) ◽  
pp. 134-138
Author(s):  
Miroslav Pohanka
Keyword(s):  
Oxidative Stress ◽  
Molecular Weight ◽  
Thiobarbituric Acid ◽  
Low Molecular Weight ◽  
Glutathione S Transferase ◽  
Antioxidant Power ◽  
Ache Inhibitors ◽  
Ferric Reducing Antioxidant Power ◽  
The Impact

ABSTRACT Cholinesterases are enzymes able to hydrolyze the neurotransmitter acetylcholine and thus to terminate transmission. Once the enzymes are inhibited, excitotoxicity can appear in the adjacent cells. It is well known that oxidative stress is involved in the toxicity of cholinesterase inhibitors. Commonly, stress follows inhibition of cholinesterases and disappears shortly afterwards. In the present experiment, it was decided to test the impact of an inhibitor, neostigmine, on oxidative stress in BALB/c mice after a longer interval. The animals were sacrificed three days after onset of the experiment and spleens and livers were collected. Reduced glutathione (GSH), glutathione reductase (GR), glutathione S-transferase (GST), thiobarbituric acid reactive substances (TBARS), ferric reducing antioxidant power (FRAP), caspase-3 and activity of acetylcholinesterase (AChE) were assayed. The tested markers were not altered with exceptions of FRAP. The FRAP values indicate accumulation of low molecular weight antioxidants in the examined organs. The role of low molecular weight antioxidants in the toxicity of AChE inhibitors is discussed.

P0851THE DIFFERENTIAL IMPACT OF INTRAVENOUS IRON IN A MODEL OF EXPERIMENTAL URAEMIA ON TISSUE MARKERS OF OXIDATIVE STRESS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sunil Bhandari ◽  
Faisal Nuhu ◽  
Anne Marie Seymour
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Cardiac Tissue ◽  
Intravenous Iron ◽  
Thiobarbituric Acid ◽  
Iron Therapy ◽  
Sprague Dawley ◽  
Post Surgery ◽  
Parenteral Iron ◽  
The Impact

Abstract Background and Aims Uraemia leads to changes in cardiac structure, metabolic remodelling and anaemia, key factors in the development of heart failure in patients with chronic kidney disease (CKD). Previous studies have identified abnormalities in mitochondrial function in experimental uraemia, potentially impairing energy provision and enhancing oxidative stress. The aim of this study was to characterise oxidant status and changes in mitochondrial function in uraemia and the impact of iron therapy. Method Experimental uraemia was induced in male Sprague-Dawley rats via a subtotal nephrectomy and parenteral iron administration at 6 weeks post-surgery (10mg/Kg body weight). Pro-oxidant activities and antioxidant capacities (oxidised glutathione (GSSG) relative to reduced (GSH)) in both sham and uraemic animals and lipid peroxidation (thiobarbituric acid-reactive substances (TBARS) was measured. Mitochondrial function was assessed using the SEAHORSE analyser. Results Oxidative stress was increased in cardiac tissue (69% increase in GSSG/GSH ratio, 38% rise in TBARS and significantly (79%) upregulated NADPH oxidase activity. Glutathione peroxidase (GPx) and glutathione reductase (GR) activities were significantly increased by 30%. Iron reduced GSSG/GSH ratio and TBARS by 62% and 51% respectively. Iron therapy was also associated with significantly increased aconitase activity. Parenteral iron improved respiratory reserve in cardiac mitochondria and skeletal mitochondria suggests IV iron restores mitochondrial function. Conclusion Uraemia leads or oxidative stress and mitochondrial dysfunction in cardiac tissue. Iron therapy reduces oxidative stress and improves cardiac mitochondrial function. This might lead to reduced adverse cardiovascular outcomes in CKD.

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