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1.
Oxid Med Cell Longev ; 2022: 1058813, 2022.
Article in English | MEDLINE | ID: covidwho-1962449

ABSTRACT

Background: Activation of the immune system response is associated with the generation of oxidative stress (OS). Several alterations are involved in OS, such as excessive production of reactive oxygen species (ROS) and decreased antioxidant activity, which together lead to an imbalance in redox status. The role of OS during SARS-CoV-2 infection is not fully understood. The aim of this study was to determine OS biomarkers and assess their usefulness as a predictor of mortality in COVID-19 patients. Methods: Baseline characteristics and serum samples were collected from hospitalized COVID-19 patients and compared with healthy controls. The serum OS biomarkers, including malondialdehyde (MDA) and total antioxidant capacity (TAC), were assessed by spectrophotometric and oxygen radical absorbance capacity (ORAC) methods, respectively. Results: A total of 152 individuals were analyzed (COVID-19 patients vs. healthy controls). Compared with healthy controls (n = 76), patients infected with SARS-CoV-2 (n = 76) presented higher levels of MDA (p < 0.001) and decreased TAC (p < 0.001). A total of 37 (49%) patients with COVID-19 died. The area under the receiver operating characteristic (ROC) curve (AUC) estimated that the combination of the OS biomarkers (MDA+TAC) (AUC = 0.6394, p = 0.037) was a significant predictor of mortality. A higher level of MDA was associated with mortality (HR, 1.05, 95% CI, 1.00-1.10, p = 0.045). Conclusion: This study concludes that OS is increased in patients with COVID-19 and is associated with mortality. To our knowledge, this is the first evidence of the expression of OS biomarkers and their association with mortality among the Mexican population.


Subject(s)
COVID-19 , SARS-CoV-2 , Antioxidants/metabolism , Biomarkers/metabolism , Humans , Mexico/epidemiology , Oxidative Stress
2.
Methods Mol Biol ; 2511: 333-344, 2022.
Article in English | MEDLINE | ID: covidwho-1941387

ABSTRACT

Infection with SARS-CoV-2, the causative agent of COVID-19, causes numerous cellular dysfunctions. The virus enters the host cells and hijacks the cell machinery for its replication, resulting in disturbances of the oxidative, reductive balance, increased production of damaging reactive oxygen species (ROS), and mitochondrial dysfunction. This damaging cycle can make cells less resistant to infection and make the host more likely to experience a severe disease course. Treatment with antioxidants has been tested as a potential approach to reduce the effects of this disorder. Here, we present a protocol to assess the impact of treatment with a mixture of curcuminoids on physiological and molecular biomarkers, focusing on determining total antioxidant capacity. We used a cohort of diabetes patients with an imbalance in redox mechanisms as such patients are more likely to become severely ill from COVID-19 than healthy persons.


Subject(s)
COVID-19 , Antioxidants/metabolism , Antioxidants/therapeutic use , Humans , Oxidation-Reduction , Oxidative Stress/physiology , Reactive Oxygen Species/metabolism , SARS-CoV-2
3.
Int J Mol Sci ; 23(12)2022 Jun 07.
Article in English | MEDLINE | ID: covidwho-1884212

ABSTRACT

Coronavirus 2019 disease (COVID-19) is caused by different variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which emerged in December of 2019. COVID-19 pathogenesis is complex and involves a dysregulated renin angiotensin system. Severe courses of the disease are associated with a dysregulated immunological response known as cytokine storm. Many scientists have demonstrated that SARS-CoV-2 impacts oxidative homeostasis and stimulates the production of reactive oxygen species (ROS). In addition, the virus inhibits glutathione (GSH) and nuclear factor erythroid 2-related factor 2 (NRF2)-a major antioxidant which induces expression of protective proteins and prevents ROS damage. Furthermore, the virus stimulates NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes which play a significant role in inducing a cytokine storm. A variety of agents with antioxidant properties have shown beneficial effects in experimental and clinical studies of COVID-19. This review aims to present mechanisms of oxidative stress induced by SARS-CoV-2 and to discuss whether antioxidative drugs can counteract detrimental outcomes of a cytokine storm.


Subject(s)
COVID-19 , Antioxidants/metabolism , Antioxidants/therapeutic use , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Humans , Oxidative Stress , Reactive Oxygen Species , SARS-CoV-2
4.
Mar Drugs ; 20(5)2022 Apr 28.
Article in English | MEDLINE | ID: covidwho-1875691

ABSTRACT

Nowadays, the logarithmic production of existing well-known food materials is unable to keep up with the demand caused by the exponential growth of the human population in terms of the equality of access to food materials. Famous local food materials with treasury properties such as mangrove fruits are an excellent source to be listed as emerging food candidates with ethnomedicinal properties. Thus, this study reviews the nutrition content of several edible mangrove fruits and the innovation to improve the fruit into a highly economic food product. Within the mangrove fruit, the levels of primary metabolites such as carbohydrates, protein, and fat are acceptable for daily intake. The mangrove fruits, seeds, and endophytic fungi are rich in phenolic compounds, limonoids, and their derivatives as the compounds present a multitude of bioactivities such as antimicrobial, anticancer, and antioxidant. In the intermediary process, the flour of mangrove fruit stands as a supplementation for the existing flour with antidiabetic or antioxidant properties. The mangrove fruit is successfully transformed into many processed food products. However, limited fruits from species such as Bruguiera gymnorrhiza, Rhizophora mucronata, Sonneratia caseolaris, and Avicennia marina are commonly upgraded into traditional food, though many more species demonstrate ethnomedicinal properties. In the Middle East, A. marina is the dominant species, and the study of the phytochemicals and fruit development is limited. Therefore, studies on the development of mangrove fruits to functional for other mangrove species are demanding. The locally accepted mangrove fruit is coveted as an alternate food material to support the sustainable development goal of eliminating world hunger in sustainable ways.


Subject(s)
Fruit , Rhizophoraceae , Antioxidants/metabolism , Functional Food , Humans , Phytochemicals/analysis , Rhizophoraceae/metabolism
5.
Int J Mol Sci ; 22(19)2021 Sep 25.
Article in English | MEDLINE | ID: covidwho-1855648

ABSTRACT

Being one of the main proteins in the human body and many animal species, albumin plays a decisive role in the transport of various ions-electrically neutral and charged molecules-and in maintaining the colloidal osmotic pressure of the blood. Albumin is able to bind to almost all known drugs, as well as many nutraceuticals and toxic substances, largely determining their pharmaco- and toxicokinetics. Albumin of humans and respective representatives in cattle and rodents have their own structural features that determine species differences in functional properties. However, albumin is not only passive, but also an active participant of pharmacokinetic and toxicokinetic processes, possessing a number of enzymatic activities. Numerous experiments have shown esterase or pseudoesterase activity of albumin towards a number of endogeneous and exogeneous esters. Due to the free thiol group of Cys34, albumin can serve as a trap for reactive oxygen and nitrogen species, thus participating in redox processes. Glycated albumin makes a significant contribution to the pathogenesis of diabetes and other diseases. The interaction of albumin with blood cells, blood vessels and tissue cells outside the vascular bed is of great importance. Interactions with endothelial glycocalyx and vascular endothelial cells largely determine the integrative role of albumin. This review considers the esterase, antioxidant, transporting and signaling properties of albumin, as well as its structural and functional modifications and their significance in the pathogenesis of certain diseases.


Subject(s)
Antioxidants/metabolism , Esterases/metabolism , Protein Transport/physiology , Serum Albumin/metabolism , Signal Transduction/physiology , Animals , Humans , Oxidation-Reduction
6.
Cells ; 11(8)2022 04 11.
Article in English | MEDLINE | ID: covidwho-1785541

ABSTRACT

The novel coronavirus (2019-nCoVCOVID-19) belongs to the Beta coronavirus family, which contains MERS-CoV (Middle East respiratory syndrome coronavirus) and SARS-CoV (severe acute respiratory syndrome coronavirus). SARS-CoV-2 activates the innate immune system, thereby activating the inflammatory mechanism, causing the release of inflammatory cytokines. Moreover, it has been suggested that COVID-19 may penetrate the central nervous system, and release inflammatory cytokines in the brains, inducing neuroinflammation and neurodegeneration. Several links connect COVID-19 with Alzheimer's disease (AD), such as elevated oxidative stress, uncontrolled release of the inflammatory cytokines, and mitochondrial apoptosis. There are severe concerns that excessive immune cell activation in COVID-19 may aggravate the neurodegeneration and amyloid-beta pathology of AD. Here, we have collected the evidence, showing the links between the two diseases. The focus has been made to collect the information on the activation of the inflammation, its contributors, and shared therapeutic targets. Furthermore, we have given future perspectives, research gaps, and overlapping pathological bases of the two diseases. Lastly, we have given the short touch to the drugs that have equally shown rescuing effects against both diseases. Although there is limited information available regarding the exact links between COVID-19 and neuroinflammation, we have insight into the pathological contributors of the diseases. Based on the shared pathological features and therapeutic targets, we hypothesize that the activation of the immune system may induce neurological disorders by triggering oxidative stress and neuroinflammation.


Subject(s)
COVID-19 , Neuroinflammatory Diseases , Alzheimer Disease/virology , Antioxidants/metabolism , COVID-19/complications , COVID-19/physiopathology , Cytokines , Humans , Neuroinflammatory Diseases/virology , Oxidative Stress , SARS-CoV-2
7.
Int J Mol Sci ; 23(7)2022 Apr 02.
Article in English | MEDLINE | ID: covidwho-1776249

ABSTRACT

The quantity of high-density lipoproteins (HDL) is represented as the serum HDL-C concentration (mg/dL), while the HDL quality manifests as the diverse features of protein and lipid content, extent of oxidation, and extent of glycation. The HDL functionality represents several performance metrics of HDL, such as antioxidant, anti-inflammatory, and cholesterol efflux activities. The quantity and quality of HDL can change during one's lifetime, depending on infection, disease, and lifestyle, such as dietary habits, exercise, and smoking. The quantity of HDL can change according to age and gender, such as puberty, middle-aged symptoms, climacteric, and the menopause. HDL-C can decrease during disease states, such as acute infection, chronic inflammation, and autoimmune disease, while it can be increased by regular aerobic exercise and healthy food consumption. Generally, high HDL-C at the normal level is associated with good HDL quality and functionality. Nevertheless, high HDL quantity is not always accompanied by good HDL quality or functionality. The HDL quality concerns the morphology of the HDL, such as particle size, shape, and number. The HDL quality also depends on the composition of the HDL, such as apolipoproteins (apoA-I, apoA-II, apoC-III, serum amyloid A, and α-synuclein), cholesterol, and triglyceride. The HDL quality is also associated with the extent of HDL modification, such as glycation and oxidation, resulting in the multimerization of apoA-I, and the aggregation leads to amyloidogenesis. The HDL quality frequently determines the HDL functionality, which depends on the attached antioxidant enzyme activity, such as the paraoxonase and cholesterol efflux activity. Conventional HDL functionality is regression, the removal of cholesterol from atherosclerotic lesions, and the removal of oxidized species in low-density lipoproteins (LDL). Recently, HDL functionality was reported to expand the removal of ß-amyloid plaque and inhibit α-synuclein aggregation in the brain to attenuate Alzheimer's disease and Parkinson's disease, respectively. More recently, HDL functionality has been associated with the susceptibility and recovery ability of coronavirus disease 2019 (COVID-19) by inhibiting the activity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The appearance of dysfunctional HDL is frequently associated with many acute infectious diseases and chronic aging-related diseases. An HDL can be a suitable biomarker to diagnose many diseases and their progression by monitoring the changes in its quantity and quality in terms of the antioxidant and anti-inflammatory abilities. An HDL can be a protein drug used for the removal of plaque and as a delivery vehicle for non-soluble drugs and genes. A dysfunctional HDL has poor HDL quality, such as a lower apoA-I content, lower antioxidant ability, smaller size, and ambiguous shape. The current review analyzes the recent advances in HDL quantity, quality, and functionality, depending on the health and disease state during one's lifetime.


Subject(s)
COVID-19 , Lipoproteins, HDL , Anti-Inflammatory Agents , Antioxidants/metabolism , Apolipoprotein A-I/metabolism , Cholesterol/metabolism , Cholesterol, HDL , Female , Humans , Lipoproteins, HDL/metabolism , Lipoproteins, LDL/metabolism , Middle Aged , SARS-CoV-2 , alpha-Synuclein
8.
Mol Biol Rep ; 49(7): 5863-5874, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1772970

ABSTRACT

BACKGROUND: Acetaminophen (APAP) is a worldwide antipyretic as well as an analgesic medication. It has been extensively utilized during the outbreak of coronavirus 2019 (COVID-19). APAP misuse would lead to liver injury. Diacerein (DIA), an anthraquinone derivative, has antioxidant and inflammatory properties. Hence, this study attempted to evaluate the impact of DIA treatment on liver injury induced by APAP and its influence on nuclear factor-κB (NF-κB) /toll-like receptor 4 (TLR4)/high mobility group box-1(HMGB-1) signaling as well as the expression of peroxisome proliferator-activated receptor-gamma (PPAR-γ) expression. METHODS: Male albino rats received 25 as well as 50 mg/kg/day DIA orally for seven days. One hour after the last administration, rats received APAP (1gm/kg, orally). For histopathological analysis, liver tissues and blood were collected, immunohistochemical (IHC) assay, biochemical assay, as well as quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: DIA markedly reduced liver injury markers and ameliorated histopathological changes. Moreover, DIA dose-dependently alleviated oxidative stress status caused by APAP administration along with inflammatory markers, including the level of interleukin-1 beta (IL-1ß), myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6). Furthermore, DIA downregulated protein levels as well as mRNA of HMGB-1, TLR4, NF-κB p65 expression, and enhanced PPAR-γ expression. Moreover, DIA ameliorated apoptotic (Bax) and caspase-3 expressions and increased the anti-apoptotic (Bcl2) expression. CONCLUSIONS: This study demonstrated that DIA exerts anti-apoptotic, anti-inflammatory, and antioxidant properties against liver injury induced by APAP that is attributed to inhibition of the HMGB1/TLR4/NF-κB pathway, besides upregulation of the expression of PPAR-γ.


Subject(s)
COVID-19 , Chemical and Drug Induced Liver Injury , HMGB1 Protein , Acetaminophen , Animals , Anthraquinones/metabolism , Anthraquinones/pharmacology , Anthraquinones/therapeutic use , Antioxidants/metabolism , Antioxidants/pharmacology , Chemical and Drug Induced Liver Injury/metabolism , HMGB1 Protein/metabolism , Humans , Liver/metabolism , Male , NF-kappa B/metabolism , PPAR gamma/metabolism , Rats , Toll-Like Receptor 4/genetics
9.
Cells ; 11(6)2022 03 09.
Article in English | MEDLINE | ID: covidwho-1731953

ABSTRACT

The infection with SARS-CoV-2 impairs the glucose-insulin axis and this contributes to oxidative (OS) and nitrosative (NSS) stress. Here, we evaluated changes in glucose metabolism that could promote the loss of redox homeostasis in COVID-19 patients. This was comparative cohort and analytical study that compared COVID-19 patients and healthy subjects. The study population consisted of 61 COVID-19 patients with and without comorbidities and 25 healthy subjects (HS). In all subjects the plasma glucose, insulin, 8-isoprostane, Vitamin D, H2S and 3-nitrotyrosine were determined by ELISA. The nitrites (NO2-), lipid-peroxidation (LPO), total-antioxidant-capacity (TAC), thiols, glutathione (GSH) and selenium (Se) were determined by spectrophotometry. The glucose, insulin and HOMA-IR (p < 0.001), 8-isoprostanes, 3-nitrotyrosine (p < 0.001) and LPO were increased (p = 0.02) while Vitamin D (p = 0.01), H2S, thiols, TAC, GSH and Se (p < 0.001) decreased in COVID-19 patients in comparison to HS. The SARS-CoV-2 infection resulted in alterations in the glucose-insulin axis that led to hyperglycemia, hyperinsulinemia and IR in patients with and without comorbidities. These alterations increase OS and NSS reflected in increases or decreases in some oxidative markers in plasma with major impact or fatal consequences in patients that course with metabolic syndrome. Moreover, subjects without comorbidities could have long-term alterations in the redox homeostasis after infection.


Subject(s)
COVID-19 , Hyperglycemia , Insulin Resistance , Selenium , Antioxidants/metabolism , Glucose , Glutathione/metabolism , Homeostasis , Humans , Hyperglycemia/complications , Insulin/metabolism , Oxidation-Reduction , Oxidative Stress , SARS-CoV-2 , Sulfhydryl Compounds , Vitamin D , Vitamins
10.
J Med Virol ; 94(4): 1558-1565, 2022 04.
Article in English | MEDLINE | ID: covidwho-1718402

ABSTRACT

The pathogenesis of SARS-CoV-2 infection, causative pathogen of the known COVID-19 pandemic is not well clarified. In this regard oxidative stress is one of the topics that need to be investigated. Therefore, the present research was performed to explore the relationship between the oxidant/antioxidant system and COVID-19 exacerbation. Sera were collected from 120 patients with COVID-19 infection and 60 healthy volunteers as the control group. The patient group consisted of 60 cases with mild disease and 60 severely ill patients. Serum levels of total antioxidant capacity (TAC) and nitric oxide (NO) as well as serum activities of the two main antioxidant defense enzymes, superoxide dismutase (SOD) and catalase (CAT), were measured. TAC levels were considerably lower in patients compared with healthy individuals (p < 0.05) and also between patients with mild and severe diseases (p < 0.05). A rather decreasing trend was also found in NO concentration as well as SOD and CAT activity, though, the observed differences were not statistically significant (p > 0.05). These findings suggest that COVID-19 patients may be susceptible to depleted total antioxidant capacity. Moreover, showing such variations in blood samples of infected individuals could be considered as a predictive marker of COVID-19 severity.


Subject(s)
Antioxidants/metabolism , Biomarkers/blood , COVID-19/blood , Adult , COVID-19/physiopathology , Case-Control Studies , Catalase/blood , Cross-Sectional Studies , Female , Humans , Logistic Models , Male , Middle Aged , Nitric Oxide/blood , Oxidative Stress/physiology , Predictive Value of Tests , Severity of Illness Index , Superoxide Dismutase/blood
11.
Bull Exp Biol Med ; 172(4): 423-429, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1696762

ABSTRACT

We studied the lung-protective effect and mechanisms of the anti-inflammatory and antioxidant effects of ultra-short-wave diathermy (USWD) in a rat model of LPS-induced acute lung injury. Histological examination of the lung tissues was performed and the levels of oxidative stress-related factors and inflammatory cytokines were measured. It was shown that the lung injury score, the lung wet-to-dry weight ratio (W/D), oxidative stress-related factors malondialdehyde and acyl-CoA synthetase long-chain family member 4 (ACSL4), and inflammatory cytokines were increased after LPS administration, while USWD treatment reduced these parameters. In addition, superoxide dismutase and glutathione peroxidase 4 were decreased in rats with LPS-induced acute lung injury, while USWD therapy up-regulated the expression of these enzymes. Thus, USWD could antagonize lung injury by inhibiting oxidative stress and inflammatory response in rats with acute lung injury. USWD can be a promising adjunctive treatment to counter oxidative stress and inflammation and a potential therapeutic candidate for the treatment of patients with this pathology.


Subject(s)
Acute Lung Injury , Diathermy , Acute Lung Injury/drug therapy , Acute Lung Injury/therapy , Animals , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Antioxidants/metabolism , Humans , Lipopolysaccharides/pharmacology , Lung , Oxidative Stress , Radio Waves , Rats
12.
Int J Mol Sci ; 22(16)2021 Aug 05.
Article in English | MEDLINE | ID: covidwho-1662662

ABSTRACT

Nuclear factor erythroid 2-related factor (Nrf2) is a transcriptional activator of the cell protection gene that binds to the antioxidant response element (ARE). Therefore, Nrf2 protects cells and tissues from oxidative stress. Normally, Kelch-like ECH-associated protein 1 (Keap1) inhibits the activation of Nrf2 by binding to Nrf2 and contributes to Nrf2 break down by ubiquitin proteasomes. In moderate oxidative stress, Keap1 is inhibited, allowing Nrf2 to be translocated to the nucleus, which acts as an antioxidant. However, under unusually severe oxidative stress, the Keap1-Nrf2 mechanism becomes disrupted and results in cell and tissue damage. Oxide-containing atmospheric environment generally contributes to the development of respiratory diseases, possibly leading to the failure of the Keap1-Nrf2 pathway. Until now, several studies have identified changes in Keap1-Nrf2 signaling in models of respiratory diseases, such as acute respiratory distress syndrome (ARDS)/acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and asthma. These studies have confirmed that several Nrf2 activators can alleviate symptoms of respiratory diseases. Thus, this review describes how the expression of Keap1-Nrf2 functions in different respiratory diseases and explains the protective effects of reversing this expression.


Subject(s)
NF-E2-Related Factor 2/metabolism , Respiratory Tract Diseases/metabolism , Animals , Antioxidants/metabolism , Humans , Oxidative Stress/physiology , Signal Transduction/physiology
13.
Front Immunol ; 12: 769011, 2021.
Article in English | MEDLINE | ID: covidwho-1650341

ABSTRACT

Asthma patients may increase their susceptibility to SARS-CoV-2 infection and the poor prognosis of coronavirus disease 2019 (COVID-19). However, anti-COVID-19/asthma comorbidity approaches are restricted on condition. Existing evidence indicates that luteolin has antiviral, anti-inflammatory, and immune regulation capabilities. We aimed to evaluate the possibility of luteolin evolving into an ideal drug and explore the underlying molecular mechanisms of luteolin against COVID-19/asthma comorbidity. We used system pharmacology and bioinformatics analysis to assess the physicochemical properties and biological activities of luteolin and further analyze the binding activities, targets, biological functions, and mechanisms of luteolin against COVID-19/asthma comorbidity. We found that luteolin may exert ideal physicochemical properties and bioactivity, and molecular docking analysis confirmed that luteolin performed effective binding activities in COVID-19/asthma comorbidity. Furthermore, a protein-protein interaction network of 538 common targets between drug and disease was constructed and 264 hub targets were obtained. Then, the top 6 hub targets of luteolin against COVID-19/asthma comorbidity were identified, namely, TP53, AKT1, ALB, IL-6, TNF, and VEGFA. Furthermore, the enrichment analysis suggested that luteolin may exert effects on virus defense, regulation of inflammation, cell growth and cell replication, and immune responses, reducing oxidative stress and regulating blood circulation through the Toll-like receptor; MAPK, TNF, AGE/RAGE, EGFR, ErbB, HIF-1, and PI3K-AKT signaling pathways; PD-L1 expression; and PD-1 checkpoint pathway in cancer. The possible "dangerous liaison" between COVID-19 and asthma is still a potential threat to world health. This research is the first to explore whether luteolin could evolve into a drug candidate for COVID-19/asthma comorbidity. This study indicated that luteolin with superior drug likeness and bioactivity has great potential to be used for treating COVID-19/asthma comorbidity, but the predicted results still need to be rigorously verified by experiments.


Subject(s)
Anti-Inflammatory Agents/metabolism , Antioxidants/metabolism , Antiviral Agents/metabolism , Asthma/epidemiology , Asthma/metabolism , COVID-19/epidemiology , COVID-19/metabolism , Immunologic Factors/metabolism , Luteolin/metabolism , SARS-CoV-2/metabolism , Anti-Inflammatory Agents/chemistry , Antioxidants/chemistry , Antiviral Agents/chemistry , Comorbidity , Computational Biology/methods , Drug Discovery/methods , Humans , Immunologic Factors/chemistry , Interleukin-6/metabolism , Luteolin/chemistry , Molecular Docking Simulation , Protein Interaction Maps/drug effects , Proto-Oncogene Proteins c-akt/metabolism , Serum Albumin, Human/metabolism , Signal Transduction/drug effects , Tumor Necrosis Factor-alpha/metabolism , Tumor Suppressor Protein p53/metabolism , Vascular Endothelial Growth Factor A/metabolism
14.
Arch Med Res ; 52(8): 843-849, 2021 11.
Article in English | MEDLINE | ID: covidwho-1635366

ABSTRACT

AIM AND BACKGROUND: Covid-19 has been as an important human infectious disease that has affected several countries. Cytokine storm has major role is Covid-19 pathogenesis. The association between inflammation and oxidative stress is well stablished. In this article, we aim to assess oxidative stress markers in Covid-19 patients compare to the healthy subjects. METHOD: A total of 48 persons (24 with Covid-19 and 24 controls) were evaluated in this research. Serum oxidative stress markers including Malondialdehyde (MDA), total oxidant status (TOS), activity of catalase (CAT) and super oxide dismutase (SOD) were measured alongside routine laboratory tests. RESULTS: Patients group were divided into ICU and Non-ICU groups. ESR, CRP and serum level of ferritin were significantly higher in case group. Serum level of albumin was significantly lower in Covid-19 patients. Serum MDA and TOS was significantly increased in Covid-19 patients. Also, Covid-19 patients had higher serum activity of CAT and GPX. CONCLUSION: Oxidative stress markers are significantly elevated in Covid-19 patients. This may have significant role in mechanism of disease development. In the fight against Covid-19, as a global struggle, all possible treatments demand more attention. So, Covid-19 patients may benefit from strategies for reducing or preventing oxidative stress.


Subject(s)
COVID-19 , Antioxidants/metabolism , Catalase/metabolism , Humans , Malondialdehyde , Oxidative Stress , SARS-CoV-2 , Superoxide Dismutase/metabolism
15.
Inflammopharmacology ; 29(5): 1347-1355, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1557643

ABSTRACT

The natural pathway of antioxidant production is mediated through Kelch-like erythroid cell-derived protein with Cap and collar homology [ECH]-associated protein 1 (Keap1)-Nuclear factor erythroid 2-related factor 2 (Nrf2) system. Keap1 maintains a low level of Nrf2 by holding it in its protein complex. Also, Keap1 facilitates the degradation of Nrf2 by ubiquitination. In other words, Keap1 is a down-regulator of Nrf2. To boost the production of biological antioxidants, Keap1 has to be inhibited and Nrf2 has to be released. Liberated Nrf2 is in an unbound state, so it travels to the nucleus to stimulate the antioxidant response element (ARE) present on the antioxidant genes. AREs activate biosynthesis of biological antioxidants through genes responsible for the production of antioxidants. In some cases of coronavirus disease 2019 (COVID-19), there is an enormous release of cytokines. The antioxidant defense mechanism in the body helps in counteracting symptoms induced by the cytokine storm in COVID-19. So, boosting the production of antioxidants is highly desirable in such a condition. In this review article, we have compiled the role of Keap1-Nrf2 system in antioxidant production. We further propose its potential therapeutic use in managing cytokine storm in COVID-19.


Subject(s)
COVID-19/metabolism , COVID-19/therapy , Cytokine Release Syndrome/metabolism , Cytokine Release Syndrome/therapy , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , Animals , Antioxidants/metabolism , Antioxidants/pharmacology , Antioxidants/therapeutic use , Disease Management , Humans , Kelch-Like ECH-Associated Protein 1/antagonists & inhibitors , NF-E2-Related Factor 2/agonists , Oxidative Stress/drug effects , Oxidative Stress/physiology
16.
Arch Med Res ; 52(8): 843-849, 2021 11.
Article in English | MEDLINE | ID: covidwho-1527582

ABSTRACT

AIM AND BACKGROUND: Covid-19 has been as an important human infectious disease that has affected several countries. Cytokine storm has major role is Covid-19 pathogenesis. The association between inflammation and oxidative stress is well stablished. In this article, we aim to assess oxidative stress markers in Covid-19 patients compare to the healthy subjects. METHOD: A total of 48 persons (24 with Covid-19 and 24 controls) were evaluated in this research. Serum oxidative stress markers including Malondialdehyde (MDA), total oxidant status (TOS), activity of catalase (CAT) and super oxide dismutase (SOD) were measured alongside routine laboratory tests. RESULTS: Patients group were divided into ICU and Non-ICU groups. ESR, CRP and serum level of ferritin were significantly higher in case group. Serum level of albumin was significantly lower in Covid-19 patients. Serum MDA and TOS was significantly increased in Covid-19 patients. Also, Covid-19 patients had higher serum activity of CAT and GPX. CONCLUSION: Oxidative stress markers are significantly elevated in Covid-19 patients. This may have significant role in mechanism of disease development. In the fight against Covid-19, as a global struggle, all possible treatments demand more attention. So, Covid-19 patients may benefit from strategies for reducing or preventing oxidative stress.


Subject(s)
COVID-19 , Antioxidants/metabolism , Catalase/metabolism , Humans , Malondialdehyde , Oxidative Stress , SARS-CoV-2 , Superoxide Dismutase/metabolism
17.
Sci Rep ; 11(1): 21075, 2021 10 26.
Article in English | MEDLINE | ID: covidwho-1493212

ABSTRACT

Bats are potential natural reservoirs for emerging viruses, causing deadly human diseases, such as COVID-19, MERS, SARS, Nipah, Hendra, and Ebola infections. The fundamental mechanisms by which bats are considered "living bioreactors" for emerging viruses are not fully understood. Some studies suggest that tolerance to viruses is linked to suppressing antiviral immune and inflammatory responses due to DNA damage by energy generated to fly. Our study reveals that bats' gut bacteria could also be involved in the host and its microbiota's DNA damage. We performed screening of lactic acid bacteria and bacilli isolated from bats' feces for mutagenic and oxidative activity by lux-biosensors. The pro-mutagenic activity was determined when expression of recA increased with the appearance of double-strand breaks in the cell DNA, while an increase of katG expression in the presence of hydroxyl radicals indicated antioxidant activity. We identified that most of the isolated bacteria have pro-mutagenic and antioxidant properties at the same time. This study reveals new insights into bat gut microbiota's potential involvement in antiviral response and opens new frontiers in preventing emerging diseases originating from bats.


Subject(s)
Chiroptera/virology , Gastrointestinal Microbiome , Mutagens , Animals , Antioxidants/metabolism , Antiviral Agents , Bacillus , Bacterial Proteins/genetics , Biosensing Techniques , COVID-19 , DNA , DNA Damage , Disease Reservoirs/virology , Escherichia coli/metabolism , Feces , Immune System , Inflammation , Lactic Acid/metabolism , Mass Spectrometry , Mutagenesis , Oxidative Stress , Rec A Recombinases/metabolism , SARS-CoV-2 , Viruses/isolation & purification , Zoonoses/virology
18.
Int J Biol Macromol ; 189: 802-818, 2021 Oct 31.
Article in English | MEDLINE | ID: covidwho-1364074

ABSTRACT

COVID-19 disease has put life of people in stress worldwide from many aspects. Since the virus has mutated in absolutely short period of time the challenge to find a suitable vaccine has become harder. Infection to COVID-19, especially at severe life threatening states is highly dependent on the strength of the host immune system. This system is partially dependent on the balance between oxidative stress and antioxidant. Besides, this virus still has unknown mechanism of action companied by a probable commune period. From another hand, some reactive oxygen species (ROS) levels can be helpful on the state determination of the disease. Thus it could be possible to use modern bioanalytical techniques for their detection and determination, which could indicate the disease state at the golden time window since they have the potential to show whether specific DNA, RNA, enzymes and proteins are affected. This also could be used as a preclude study or a reliable pathway to define the best optimized time of cure beside effective medical actions. Herein, some ROS and their relation with SARS-CoV-2 virus have been considered. In addition, modern bioelectroanalytical techniques on this approach from quantitative and qualitative points of view have been reviewed.


Subject(s)
Antioxidants/metabolism , COVID-19/metabolism , Oxidative Stress , Reactive Oxygen Species/metabolism , SARS-CoV-2/metabolism , COVID-19/therapy , Humans
19.
Inflammopharmacology ; 29(5): 1347-1355, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1349298

ABSTRACT

The natural pathway of antioxidant production is mediated through Kelch-like erythroid cell-derived protein with Cap and collar homology [ECH]-associated protein 1 (Keap1)-Nuclear factor erythroid 2-related factor 2 (Nrf2) system. Keap1 maintains a low level of Nrf2 by holding it in its protein complex. Also, Keap1 facilitates the degradation of Nrf2 by ubiquitination. In other words, Keap1 is a down-regulator of Nrf2. To boost the production of biological antioxidants, Keap1 has to be inhibited and Nrf2 has to be released. Liberated Nrf2 is in an unbound state, so it travels to the nucleus to stimulate the antioxidant response element (ARE) present on the antioxidant genes. AREs activate biosynthesis of biological antioxidants through genes responsible for the production of antioxidants. In some cases of coronavirus disease 2019 (COVID-19), there is an enormous release of cytokines. The antioxidant defense mechanism in the body helps in counteracting symptoms induced by the cytokine storm in COVID-19. So, boosting the production of antioxidants is highly desirable in such a condition. In this review article, we have compiled the role of Keap1-Nrf2 system in antioxidant production. We further propose its potential therapeutic use in managing cytokine storm in COVID-19.


Subject(s)
COVID-19/metabolism , COVID-19/therapy , Cytokine Release Syndrome/metabolism , Cytokine Release Syndrome/therapy , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , Animals , Antioxidants/metabolism , Antioxidants/pharmacology , Antioxidants/therapeutic use , Disease Management , Humans , Kelch-Like ECH-Associated Protein 1/antagonists & inhibitors , NF-E2-Related Factor 2/agonists , Oxidative Stress/drug effects , Oxidative Stress/physiology
20.
Int J Mol Sci ; 22(15)2021 Jul 26.
Article in English | MEDLINE | ID: covidwho-1325685

ABSTRACT

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a well-known transcription factor best recognised as one of the main regulators of the oxidative stress response. Beyond playing a crucial role in cell defence by transactivating cytoprotective genes encoding antioxidant and detoxifying enzymes, Nrf2 is also implicated in a wide network regulating anti-inflammatory response and metabolic reprogramming. Such a broad spectrum of actions renders the factor a key regulator of cell fate and a strategic player in the control of cell transformation and response to viral infections. The Nrf2 protective roles in normal cells account for its anti-tumour and anti-viral functions. However, Nrf2 overstimulation often occurs in tumour cells and a complex correlation of Nrf2 with cancer initiation and progression has been widely described. Therefore, if on one hand, Nrf2 has a dual role in cancer, on the other hand, the factor seems to display a univocal function in preventing inflammation and cytokine storm that occur under viral infections, specifically in coronavirus disease 19 (COVID-19). In such a variegate context, the present review aims to dissect the roles of Nrf2 in both cancer and COVID-19, two widespread diseases that represent a cause of major concern today. In particular, the review describes the molecular aspects of Nrf2 signalling in both pathological situations and the most recent findings about the advantages of Nrf2 inhibition or activation as possible strategies for cancer and COVID-19 treatment respectively.


Subject(s)
COVID-19/metabolism , NF-E2-Related Factor 2/metabolism , Neoplasms/metabolism , Animals , Anti-Inflammatory Agents/chemistry , Anti-Inflammatory Agents/metabolism , Antioxidants/chemistry , Antioxidants/metabolism , COVID-19/drug therapy , Humans , NF-E2-Related Factor 2/chemistry , Neoplasms/drug therapy , Signal Transduction
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