Antioxidant and prooxidant systems in patients with ischemic insult

2021 ◽  
Vol 19 (3) ◽  
pp. 281-290
Author(s):  
Svetlana G. Belokoskova ◽  
Sergey G. Tsikunov
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ischemic Stroke ◽  
Affective Disorders ◽  
Ischemia Reperfusion ◽  
Antioxidant Systems ◽  
Antioxidant Protection ◽  
Residual Symptoms ◽  
Brain Functions

The literature review presents current information on the role of oxidative stress in the pathogenesis of cerebral ischemia / reperfusion. In patients with ischemic stroke, activation of enzymatic and non-enzymatic links of antioxidant defense in the form of an increase in the blood and cerebrospinal fluid of the activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, the content of glutathione reflects the presence of compensatory reserves, is a favorable factor for the restoration of brain functions. An increase in the content of markers of lipid peroxidation in various biological environments in patients with strokes, mainly malondialdehyde, even in combination with an increase in the content of markers of antioxidant protection, indicates its insufficiency and an unfavorable prognosis of the disease. An increase in the content of markers of lipid peroxidation, mainly malondialdehyde, in patients with strokes in various biological environments, even in combination with an increase content in markers of antioxidant protection, indicates its insufficiency, an unfavorable prognosis of the disease. The presence of affective disorders and the persistence of residual manifestations of ischemic stroke may be due to permanent oxidative stress. When choosing a therapy aimed at increasing the activity of antioxidant protection and reducing the toxic effect of prooxidants, one should take into account the severity and dynamics of metabolic disorders. In the presence of data reflecting insufficient activity of antioxidant systems in combination with increased activity of prooxidant systems, the appointment of drugs that reduce the severity of oxidative stress in the early stages of stroke is indicated. Therapy including antioxidant drugs is also indicated in patients with post-stroke affective disorders and with residual symptoms of stroke.

scholarly journals Nitric Oxide Donors as Neuroprotective Agents after an Ischemic Stroke-Related Inflammatory Reaction

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Marisol Godínez-Rubí ◽  
Argelia E. Rojas-Mayorquín ◽  
Daniel Ortuño-Sahagún
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Inflammatory Response ◽  
Ischemia Reperfusion ◽  
Therapeutic Window ◽  
Nitric Oxide Donors ◽  
Neuroprotective Agents

Cerebral ischemia initiates a cascade of detrimental events including glutamate-associated excitotoxicity, intracellular calcium accumulation, formation of Reactive oxygen species (ROS), membrane lipid degradation, and DNA damage, which lead to the disruption of cellular homeostasis and structural damage of ischemic brain tissue. Cerebral ischemia also triggers acute inflammation, which exacerbates primary brain damage. Therefore, reducing oxidative stress (OS) and downregulating the inflammatory response are options that merit consideration as potential therapeutic targets for ischemic stroke. Consequently, agents capable of modulating both elements will constitute promising therapeutic solutions because clinically effective neuroprotectants have not yet been discovered and no specific therapy for stroke is available to date. Because of their ability to modulate both oxidative stress and the inflammatory response, much attention has been focused on the role of nitric oxide donors (NOD) as neuroprotective agents in the pathophysiology of cerebral ischemia-reperfusion injury. Given their short therapeutic window, NOD appears to be appropriate for use during neurosurgical procedures involving transient arterial occlusions, or in very early treatment of acute ischemic stroke, and also possibly as complementary treatment for neurodegenerative diseases such as Parkinson or Alzheimer, where oxidative stress is an important promoter of damage. In the present paper, we focus on the role of NOD as possible neuroprotective therapeutic agents for ischemia/reperfusion treatment.

Pathophysiology of Ischemic Stroke: Role of Oxidative Stress

2020 ◽  
Vol 26 (34) ◽  
pp. 4246-4260 ◽  
Author(s):  
Sofía Orellana-Urzúa ◽  
Ignacio Rojas ◽  
Lucas Líbano ◽  
Ramón Rodrigo
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Physical Disability ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Therapeutic Interventions ◽  
Oxygen Species ◽  
Tissue Plasminogen ◽  
Brain Tissue Damage

Stroke is the second leading cause of mortality and the major cause of adult physical disability worldwide. The currently available treatment to recanalize the blood flow in acute ischemic stroke is intravenous administration of tissue plasminogen activator (t-PA) and endovascular treatment. Nevertheless, those treatments have the disadvantage that reperfusion leads to a highly harmful reactive oxygen species (ROS) production, generating oxidative stress (OS), which is responsible for most of the ischemia-reperfusion injury and thus causing brain tissue damage. In addition, OS can lead brain cells to apoptosis, autophagy and necrosis. The aims of this review are to provide an updated overview of the role of OS in brain IRI, providing some bases for therapeutic interventions based on counteracting the OS-related mechanism of injury and thus suggesting novel possible strategies in the prevention of IRI after stroke.

scholarly journals The role of oxidative stress and antioxidant defence system in periodontitis

2020 ◽  
Vol 54 (2) ◽  
pp. 75-82
Author(s):  
Vesna Obradović
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Periodontal Disease ◽  
Inflammatory Process ◽  
Molecular Mechanisms ◽  
Signal Pathways ◽  
Antioxidant Protection ◽  
Oxidation Stress ◽  
Antioxidant Defence System

The prevalence of periodontal disease is very high in the adult population. According to research results, as much as 46% of the total population was affected by periodontal disease in the period from 2010 to 2012, which would mean that 64.7 million people had periodontitis, of which 8% had a severe form of this disease. Having in mind the clinical and socioeconomic significance of periodontitis, this review aims to present in a comprehensive way the pathogenetic aspects of periodontitis with a special emphasis on oxidative stress and antioxidant protection mechanisms as possible molecular mechanisms for the development of periodontitis in adults. Oxidation stress is involved in the progression of periodontitis as a chronic inflammatory disease of periodontium, which occurs as a result of imbalance between host response and bacterial infection. At the same time there is a decreased antioxidant activity and salivary gland capacity, which contributes to the further development of this disease. MDA is the most common lipid peroxidation derivative that occurs in periodontitis. All of the mentioned literature data suggest that the elevated MDA values may be due to both local and systemic oxidative stress as a response to inflammatory periodontal disease alone or in combination with other systemic disorders and smoking. The harmful effects of ROS during oxidative stress occur through lipid peroxidation processes and irreversible protein modification to cell apoptosis and programmed cell death. In addition to the two most important signal pathways, caspase pathway and NADPH oxidase-4 pathway, several other signaling pathways mediate in oxidative cell damage: PERK/NRF2 signal path, JNK / mitogen-activating pathway (MAP). When a clinically visible inflammatory process occurs in periodontium, this usually presents a condition that is more or less irreversible. In parodontology, therefore, the idea of introducing biochemical analyzes to diagnose the inflammatory process in parodontium is still open before it can be seen at the clinical level. For this reason, the significance of the role of oxidative stress, the antioxidant protection of the organism and the molecular mechanisms by which damage occurs is an indisputable importance. Assessment and measurement of biomarkers of oxidative stress and antioxidant enzymes can play a central role in monitoring biochemical indicators of parodontium state and even assist with various methods of treatment of periodontal disease.

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

scholarly journals Protective Role of Glutathione in the Hippocampus after Brain Ischemia

2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Excitatory Amino Acid ◽  
Ischemia Reperfusion ◽  
Thiol Group ◽  
Protective Role ◽  
Key Factor ◽  
Rate Limiting ◽  
Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

scholarly journals Comparison of coenzyme Q10 or fish oil for prevention of intermittent hypoxia-induced oxidative injury in neonatal rat lungs

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Christina D’Agrosa ◽  
Charles L. Cai ◽  
Faisal Siddiqui ◽  
Karen Deslouches ◽  
Stephen Wadowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lung Injury ◽  
Fish Oil ◽  
Coenzyme Q10 ◽  
Intermittent Hypoxia ◽  
Oxidative Injury ◽  
Adverse Outcomes ◽  
Neonatal Rat ◽  
Antioxidant Systems

Abstract Background Neonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats. Methods Newborn rats were exposed to two clinically relevant IH paradigms at birth (P0): (1) 50% O2 with brief hypoxia (12% O2); or (2) room air (RA) with brief hypoxia (12% O2), until P14 during which they were supplemented with daily oral CoQ10, fish oil, or olive oil from P0 to P14. Pups were studied at P14 or placed in RA until P21 with no further treatment. Lungs were assessed for histopathology and morphometry; biomarkers of oxidative stress and lipid peroxidation; and antioxidants. Results Of the two neonatal IH paradigms 21%/12% O2 IH resulted in the most severe outcomes, evidenced by histopathology and morphometry. CoQ10 was effective for preserving lung architecture and reduction of IH-induced oxidative stress biomarkers. In contrast, fish oil resulted in significant adverse outcomes including oversimplified alveoli, hemorrhage, reduced secondary crest formation and thickened septae. This was associated with elevated oxidants and antioxidants activities. Conclusions Data suggest that higher FiO2 may be needed between IH episodes to curtail the damaging effects of IH, and to provide the lungs with necessary respite. The negative outcomes with fish oil supplementation suggest oxidative stress-induced lipid peroxidation.

scholarly journals Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 45
Author(s):  
Helena Beatriz Ferreira ◽  
Tânia Melo ◽  
Artur Paiva ◽  
Maria do Rosário Domingues
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Profile ◽  
Inflammatory Responses ◽  
Molecular Level ◽  
Lipid Hydroperoxides ◽  
Lipid Species ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine.

The role of lipid peroxidation in pathogenesis of ischemic damage and the antioxidant protection of the heart

1982 ◽  
Vol 77 (5) ◽  
pp. 465-485 ◽  
Author(s):  
F. Z. Meerson ◽  
V. E. Kagan ◽  
Yu. P. Kozlov ◽  
L. M. Belkina ◽  
Yu. V. Arkhipenko
Keyword(s):  
Lipid Peroxidation ◽  
Ischemic Damage ◽  
Antioxidant Protection

Role of Free Radicals and Lipid Peroxidation in Gastric Mucosal Injury Induced by Ischemia-Reperfusion in Rats

1989 ◽  
Vol 24 (sup162) ◽  
pp. 55-58 ◽  
Author(s):  
S. Ueda ◽  
T. Yoshikawa ◽  
S. Takahashi ◽  
H. Ichikawa ◽  
M. Yasuda ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury

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.

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