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1.
International Journal of Yoga ; 15(3):195-204, 2022.
Article in English | ProQuest Central | ID: covidwho-2217249

ABSTRACT

Context: COVID-19-affected patients showed increased stress, impaired sleep quality, altered complete blood count, and increased inflammatory and oxidative parameters. Yoga is an add-on nonpharmacological treatment that is established to normalize the abovementioned parameters. Heartfulness meditation is a form of Raja yoga. Aims: The present study aimed to study the effects of 4 weeks of heartfulness meditation on the abovementioned parameters in COVID-19 patients following treatment completion. Settings and Design: The present study was a randomized controlled trial carried out in the Department of Physiology, AIIMS, Mangalagiri, Andhra Pradesh. Subjects and Methods: Out of 50 COVID-19 treatment-completed patients recruited for the study, 25 were randomly assigned to the study group who received 4-week app-based heartfulness meditation. Other 25 patients were assigned to the control group who received app-based relaxation for 4 weeks. Perceived stress score, Pittsburgh Sleep Quality Index questionnaire, baseline cardiovascular parameters, complete blood count, serum cortisol, inflammatory parameters, oxidative stress parameters, and antioxidant parameters were assessed before and after 4 weeks of intervention in both the groups. The outcome assessor was blinded in the present study. Statistical Analysis Used: The mean difference between the two groups was tested using the Student's t-test or Mann–Whitney U-test based on data distribution. Effect of intervention was analyzed using paired Student's t-test for dependent samples test or Wilcoxon signed-rank test based on data distribution. Results: The groups were comparable before intervention for all the variables. After 4 weeks of intervention, we observed a significant decrease in stress, circulating cortisol, inflammatory markers, and oxidative stress biomarker in both the groups. Further, we observed improved sleep quality and antioxidant biomarkers in both the groups. These beneficial alterations following intervention were high in the study group compared to the control group. Conclusions: Our results suggest that app-based heartfulness meditation/relaxation can be used as a nonpharmacological adjuvant to hasten the recovery process in patients who have completed the COVID-19 treatment protocol. Beneficial effects in subjects practicing heartfulness meditation were more than that observed in subjects practicing relaxation.

2.
Pharmaceuticals ; 16(1):52, 2023.
Article in English | ProQuest Central | ID: covidwho-2216693

ABSTRACT

Acute lung injury (ALI) is one of the adverse effects of the antineoplastic agent cisplatin (CIS). Oxidative stress, inflammation, and necroptosis are linked to the emergence of lung injury in various disorders. This study evaluated the effect of the macrolide antibiotic azithromycin (AZM) on oxidative stress, inflammatory response, and necroptosis in the lungs of CIS-administered rats, pinpointing the involvement of PPARγ, SIRT1, and Nrf2/HO-1 signaling. The rats received AZM for 10 days and a single dose of CIS on the 7th day. CIS provoked bronchial and alveolar injury along with increased levels of ROS, MDA, NO, MPO, NF-κB p65, TNF-α, and IL-1β, and decreased levels of GSH, SOD, GST, and IL-10, denoting oxidative and inflammatory responses. The necroptosis-related proteins RIP1, RIP3, MLKL, and caspase-8 were upregulated in CIS-treated rats. AZM effectively prevented lung tissue injury, ameliorated oxidative stress and NF-κB p65 and pro-inflammatory markers levels, boosted antioxidants and IL-10, and downregulated necroptosis-related proteins in CIS-administered rats. AZM decreased the concentration of Ang II and increased those of Ang (1-7), cytoglobin, PPARγ, SIRT1, Nrf2, and HO-1 in the lungs of CIS-treated rats. In conclusion, AZM attenuated the lung injury provoked by CIS in rats through the suppression of inflammation, oxidative stress, and necroptosis. The protective effect of AZM was associated with the upregulation of Nrf2/HO-1 signaling, cytoglobin, PPARγ, and SIRT1.

3.
International Journal of Molecular Sciences ; 24(1):558, 2023.
Article in English | Academic Search Complete | ID: covidwho-2216313

ABSTRACT

The mechanistic interplay between SARS-CoV-2 infection, inflammation, and oxygen homeostasis is not well defined. Here, we show that the hypoxia-inducible factor (HIF-1α) transcriptional pathway is activated, perhaps due to a lack of oxygen or an accumulation of mitochondrial reactive oxygen species (ROS) in the lungs of adult Syrian hamsters infected with SARS-CoV-2. Prominent nuclear localization of HIF-1α and increased expression of HIF-1α target proteins, including glucose transporter 1 (Glut1), lactate dehydrogenase (LDH), and pyruvate dehydrogenase kinase-1 (PDK1), were observed in areas of lung consolidation filled with infiltrating monocytes/macrophages. Upregulation of these HIF-1α target proteins was accompanied by a rise in glycolysis as measured by extracellular acidification rate (ECAR) in lung homogenates. A concomitant reduction in mitochondrial respiration was also observed as indicated by a partial loss of oxygen consumption rates (OCR) in isolated mitochondrial fractions of SARS-CoV-2-infected hamster lungs. Proteomic analysis further revealed specific deficits in the mitochondrial ATP synthase (Atp5a1) within complex V and in the ATP/ADP translocase (Slc25a4). The activation of HIF-1α in inflammatory macrophages may also drive proinflammatory cytokine production and complement activation and oxidative stress in infected lungs. Together, these findings support a role for HIF-1α as a central mediator of the metabolic reprogramming, inflammation, and bioenergetic dysfunction associated with SARS-CoV-2 infection. [ FROM AUTHOR]

4.
Antioxidants ; 12(1):172, 2023.
Article in English | ProQuest Central | ID: covidwho-2215511

ABSTRACT

The term "cytokine storm” describes an acute pathophysiologic state of the immune system characterized by a burst of cytokine release, systemic inflammatory response, and multiple organ failure, which are crucial determinants of many disease outcomes. In light of the complexity of cytokine storms, specific strategies are needed to prevent and alleviate their occurrence and deterioration. Nuclear factor erythroid 2-related factor 2 (NRF2) is a CNC-basic region-leucine zipper protein that serves as a master transcription factor in maintaining cellular redox homeostasis by orchestrating the expression of many antioxidant and phase II detoxification enzymes. Given that inflammatory response is intertwined with oxidative stress, it is reasonable to assume that NRF2 activation limits inflammation and thus cytokine storms. As NRF2 can mitigate inflammation at many levels, it has emerged as a potential target to prevent and treat cytokine storms. In this review, we summarized the cytokine storms caused by different etiologies and the rationale of interventions, focusing mainly on NRF2 as a potential therapeutic target.

5.
Oral & Maxillofacial Pathology Journal ; 14(1):66-69, 2023.
Article in English | Web of Science | ID: covidwho-2208030

ABSTRACT

Introduction: COVID-19 pandemic has been the most challenging global health concern that the world has ever seen and is the focus of active research around the world. The interaction of the SARS CoV2 virus with the target cells, their action on the immune system and the subsequent reaction has all been linked to the inflammatory processes that are taking place in the human body mainly the oxidative stress.Objective: Through this article we aim to analyse the effect of oxidative stress in the pathogenesis of COVID-19, highlighting the role of the same in the oral manifestations that are being reported in literature and its subsequent impact in the transmission and propagation of SARS-CoV2. The role of antioxidants in the control of the SARS-CoV2 infection has also been explored.Materials and Methods: Four reviewers independently collected the data pertaining to the topic from case reports and review articles published in electronic databases like PubMed, Scopus, Science Direct and Research gate.Conclusion: Increased release of cytokines known as cytokine storm has been associated with disease progression, oral manifestation as well as adverse effects in patients with COVID 19. However, as this is an ongoing pandemic with new mu-tations occurring frequently, further clinical trials are required to evaluate the exact mechanisms that may be at play in the pathogenesis of SARS-CoV2 infection.

6.
Int J Mol Sci ; 23(7)2022 Mar 25.
Article in English | MEDLINE | ID: covidwho-2200271

ABSTRACT

The genomic activity of vitamin D is associated with metabolic effects, and the hormone has a strong impact on several physiological functions and, therefore, on health. Among its renowned functions, vitamin D is an immunomodulator and a molecule with an anti-inflammatory effect, and, recently, it has been much studied in relation to its response against viral infections, especially against COVID-19. This review aims to take stock of the correlation studies between vitamin D deficiency and increased risks of severe COVID-19 disease and, similarly, between vitamin D deficiency and acute respiratory distress syndrome. Based on this evidence, supplementation with vitamin D has been tested in clinical trials, and the results are discussed. Finally, this study includes a biochemical analysis on the effects of vitamin D in the body's defense mechanisms against viral infection. In particular, the antioxidant and anti-inflammatory functions are considered in relation to energy metabolism, and the potential, beneficial effect of vitamin D in COVID-19 is described, with discussion of its influence on different biochemical pathways. The proposed, broader view of vitamin D activity could support a better-integrated approach in supplementation strategies against severe COVID-19, which could be valuable in a near future of living with an infection becoming endemic.


Subject(s)
COVID-19 , Vitamin D Deficiency , COVID-19/drug therapy , Humans , SARS-CoV-2 , Vitamin D/metabolism , Vitamin D Deficiency/complications , Vitamin D Deficiency/drug therapy , Vitamin D Deficiency/epidemiology , Vitamins/therapeutic use
7.
J Allergy Clin Immunol ; 150(3): 594-603.e2, 2022 09.
Article in English | MEDLINE | ID: covidwho-2179904

ABSTRACT

BACKGROUND: Lymphopenia is predictive of survival in patients with coronavirus disease 2019 (COVID-19). OBJECTIVE: The aim of this study was to understand the cause of the lymphocyte count drop in severe forms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. METHODS: Monocytic production of reactive oxygen species (ROSs) and T-cell apoptosis were measured by flow cytometry, DNA damage in PBMCs was measured by immunofluorescence, and angiotensin II (AngII) was measured by ELISA in patients infected with SARS-CoV-2 at admission to an intensive care unit (ICU) (n = 29) or not admitted to an ICU (n = 29) and in age- and sex-matched healthy controls. RESULTS: We showed that the monocytes of certain patients with COVID-19 spontaneously released ROSs able to induce DNA damage and apoptosis in neighboring cells. Of note, high ROS production was predictive of death in ICU patients. Accordingly, in most patients, we observed the presence of DNA damage in up to 50% of their PBMCs and T-cell apoptosis. Moreover, the intensity of this DNA damage was linked to lymphopenia. SARS-CoV-2 is known to induce the internalization of its receptor, angiotensin-converting enzyme 2, which is a protease capable of catabolizing AngII. Accordingly, in certain patients with COVID-19 we observed high plasma levels of AngII. When looking for the stimulus responsible for their monocytic ROS production, we revealed that AngII triggers ROS production by monocytes via angiotensin receptor I. ROSs released by AngII-activated monocytes induced DNA damage and apoptosis in neighboring lymphocytes. CONCLUSION: We conclude that T-cell apoptosis provoked via DNA damage due to the release of monocytic ROSs could play a major role in COVID-19 pathogenesis.


Subject(s)
Angiotensin II , COVID-19 , Lymphopenia , Angiotensin II/blood , Apoptosis , COVID-19/diagnosis , COVID-19/pathology , DNA Damage , Humans , Reactive Oxygen Species , SARS-CoV-2 , T-Lymphocytes
8.
Mol Biol Rep ; 49(11): 11169-11176, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2174666

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a current global illness triggered by severe acute respiratory coronavirus 2 (SARS-CoV-2) leading to acute viral pneumonia, acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and cytokine storm in severe cases. In the COVID-19 era, different unexpected old drugs are repurposed to find out effective and cheap therapies against SARS-CoV-2. One of these elected drugs is nitazoxanide (NTZ) which is an anti-parasitic drug with potent antiviral activity. It is effectively used in the treatment of protozoa and various types of helminths in addition to various viral infections. Thus, we aimed to elucidate the probable effect of NTZ on SARS-CoV-2 infections. Findings of the present study illustrated that NTZ can reduce SARS-CoV-2-induced inflammatory reactions through activation of interferon (IFN), restoration of innate immunity, inhibition of the release of pro-inflammatory cytokines, suppression of the mammalian target of rapamycin (mTOR), and induction of autophagic cell death. Moreover, it can inhibit the induction of oxidative stress which causes cytokine storm and is associated with ALI, ARDS, and multi-organ damage (MOD). This study concluded that NTZ has important anti-inflammatory and immunological properties that may mitigate SARS-CoV-2 infection-induced inflammatory disorders. Despite broad-spectrum antiviral properties of NTZ, the direct anti-SARS-CoV-2 effect was not evident and documented in recent studies. Then, in silico and in vitro studies in addition to clinical trials and prospective studies are needed to confirm the beneficial impact of NTZ on the pathogenesis of SARS-CoV-2 infection.


Subject(s)
Acute Lung Injury , COVID-19 , Respiratory Distress Syndrome , Humans , COVID-19/drug therapy , Cytokine Release Syndrome , SARS-CoV-2 , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , Cytokines/metabolism , Acute Lung Injury/drug therapy
9.
Biochimica et Biophysica Acta - Bioenergetics ; Conference: EBEC2022, 2022.
Article in English | EMBASE | ID: covidwho-2176722

ABSTRACT

Molecular hydrogen H2 has been reported to be an antioxidative, anti-inflammatory, and antiapoptotic agent with therapeutic potential for various diseases such as cardiac arrest, asthma, chronic obstructive pulmonary disease (COPD), and, most recently, COVID-19 [1]. In previous studies, H2 is typically administered repeatedly or over longer periods of time (hours to days) via inhalation of H2 gas, drinking H2-rich water, or injection of H2 saline, wherefore the observed effects, e.g. on mitochondrial metabolism [2], might be either directly or indirectly related to H2. To investigate a direct short-term effect of H2 on mitochondrial function, we measured mitochondrial respiration and H2O2 production in permeabilized HEK 293T cells upon sequential changes of H2 concentration cH2 in the experimental medium. O2 and H2O2 flux were measured simultaneously in the O2k with the Fluo-Module (Oroboros Instruments). Increase of cH2 was accomplished by injecting H2 into the gas phase of the open O2k-chamber. This causes not only an increase of cH2 but also a decrease of oxygen concentration cO2. As mitochondrial ROS production is a continuous function of cO2, we used the conventionally applied N2 gas as a control to distinguish between cO2- and cH2-dependent effects. Measurements were started near air saturation (~160 muM of oxygen). The plasma membrane was permeabilized with digitonin and the NADH-linked substrates pyruvate & malate were titrated to measure O2 and H2O2 flux in the LEAK state (without ADP). Upon transition of cO2 from ~160 to ~25 muM, a decrease in O2 and H2O2 flux was observed. This was comparable between regimes with increased cH2 or cN2. Further transitions by re-oxygenation and injection of H2 or N2 yielded the same results. Similarly, cO2-dependent changes in mitochondrial respiration and H2O2 production in the OXPHOS state (kinetically saturating [ADP]) were independent of the increase in cH2 or cN2. These results indicate that short-term exposure to increased cH2 does not affect mitochondrial respiration or H2O2 production. [1] Y. Tian, Y. Zhang, Y. Wang, Y. Chen, Hydrogen, a Novel Therapeutic Molecule, Regulates Oxidative Stress, Inflammation, and Apoptosis, Frontiers in Physiology, 12 (2021) 1-14 [2] A. Gvozdjakova, J. Kucharska, B. Kura, O. Vancova O, A new insight into the molecular hydrogen effect on coenzyme Q and mitochondrial function of rats, J Physiol Pharmacol., 1 (2020) 29-34 Copyright © 2022

10.
Salus ; 25(3):25-31, 2021.
Article in Spanish | EMBASE | ID: covidwho-2207151

ABSTRACT

Background: SARS-CoV-2, the etiological agent responsible for COVID-19, is an RNA virus belonging to the Coronaviridae family. During the virus replication, viral components interact with the cellular machinery, inducing alterations in cell physiology, which contributes to viral pathogenesis. Method(s): A bibliographical research about cellular stress and SARS-CoV-2 was performed at NCBI/Pubmed. Result(s): In response to the infection, signaling pathways are activated in the host cell, the goal of these pathways being to restore homeostasis. If homeostasis is not recovered, the signaling leads to cell death activation. Among the best-characterized signaling pathways, the cellular stress pathways such as oxidative stress, UPR, and autophagy stand out, which are evolutionarily conserved and are also interconnected with each other. There is strong theoretical and experimental evidence of various interactions of some components of these pathways with different viral proteins of coronavirus, and some studies with SARS-CoV-2 have already been performed. In this review, we highlight some of the cellular pathways-virus characterized to date. Conclusion(s): The cellular pathways and their relationship to viral infections remains unclear. The study of these relationships might constitute an important target for new research and the development of antiviral therapies. Copyright © 2021, Revista Salus. All rights reserved.

11.
Pharmacophore ; 13(5):72-77, 2022.
Article in English | Web of Science | ID: covidwho-2206963

ABSTRACT

Regular exercise can increase the sensitivity of endogenous antioxidants so that it can increase the immune system against viral infections. Antioxidants like bioflavonoids, which are found in lemon peel essential oil, help shield the body from the damaging effects of free radicals and immunomodulators. The goal of this research was to find out whether or not frequent moderate -intensity exercise and the lemon peel essential oil can boost immunity during the Covid-19 Pandemic. The experimental animals were separated into two groups at random, with ten white rats in each group: group P1 consisted of rats that participated in swimming activities of moderate intensity for forty minutes;group P2 consisted of rats that participated in swimming activities of moderate intensity for forty minutes, but also received 0.05 milliliters of lemon peel essential oil every hour for the preceding hour before the rats participated in swimming activities. The average TAC level in the RDF group (pre-test 320.34 +/- 44.05 mu mol;post-test 353.01 +/- 70.22 mu mol) and average CRP level (pre-test 0.54 +/- 0.11 ng/ml;post-test 0.49 +/- 0.04 ng/ml). The average TAC level in the RE groups (pre-test 338.15 +/- 29.14 mu mol;post-test 356.48 +/- 44.34 mu mol) and average CRP level (pre-test 0.56 +/- 0.04 ng/ml;post-test 0.53 +/- 0.09 ng/ml). There were no significantly increased TAC (p>0.05) and decreased CRP (p>0.05) after the exercise test compared to before. There were no substantial differences between the two groups (p>0.05).

12.
Physiological Reports ; 10(24) (no pagination), 2022.
Article in English | EMBASE | ID: covidwho-2204042

ABSTRACT

SARS-CoV-2 infection is known to instigate a range of physiologic perturbations, including vascular dysfunction. However, little work has concluded how long these effects may last, especially among young adults with mild symptoms. To determine potential recovery from acute vascular dysfunction in young adults (8 M/8F, 21 +/- 1 yr, 23.5 +/- 3.1 kgm-2), we longitudinally tracked brachial artery flow-mediated dilation (FMD) and reactive hyperemia (RH) in the arm and hyperemic response to passive limb movement (PLM) in the leg, with Doppler ultrasound, as well as circulating biomarkers of inflammation (interleukin-6, C-reactive protein), oxidative stress (thiobarbituric acid reactive substances, protein carbonyl), antioxidant capacity (superoxide dismutase), and nitric oxide bioavailability (nitrite) monthly for a 6-month period post-SARS-CoV-2 infection. FMD, as a marker of macrovascular function, improved from month 1 (3.06 +/- 1.39%) to month 6 (6.60 +/- 2.07%;p < 0.001). FMD/Shear improved from month one (0.10 +/- 0.06 AU) to month six (0.18 +/- 0.70 AU;p = 0.002). RH in the arm and PLM in the leg, as markers of microvascular function, did not change during the 6 months (p > 0.05). Circulating markers of inflammation, oxidative stress, antioxidant capacity, and nitric oxide bioavailability did not change during the 6 months (p > 0.05). Together, these results suggest some improvements in macrovascular, but not microvascular function, over 6 months following SARS-CoV-2 infection. The data also suggest persistent ramifications for cardiovascular health among those recovering from mild illness and among young, otherwise healthy adults with SARS-CoV-2. Copyright © 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

13.
Biomolecules ; 12(12) (no pagination), 2022.
Article in English | EMBASE | ID: covidwho-2199740

ABSTRACT

Atopic dermatitis is a chronic inflammatory skin disease in which the overproduction of reactive oxygen species plays a pivotal role in the pathogenesis and persistence of inflammatory lesions. Phototherapy represents one of the most used therapeutic options, with benefits in the clinical picture. Studies have demonstrated the immunomodulatory effect of phototherapy and its role in reducing molecule hallmarks of oxidative stress. In this review, we report the data present in literature dealing with the main signaling molecular pathways involved in oxidative stress after phototherapy to target atopic dermatitis-affected cells. Since oxidative stress plays a pivotal role in the pathogenesis of atopic dermatitis and its flare-up, new research lines could be opened to study new drugs that act on this mechanism, perhaps in concert with phototherapy. Copyright © 2022 by the authors.

14.
Free Radic Res ; : 1-18, 2023.
Article in English | PubMed | ID: covidwho-2187328

ABSTRACT

Drug repurposing allows searching for new biological targets, especially against emerging diseases such as Covid-19. Drug colchicine (COL) presents recognized anti-inflammatory action, while the nanotechnology purpose therapies with low doses, efficacy, and decrease the drug's side-effects. This study aims to evaluate the effects of COL and colchicine nanocapsules (NCCOL) on survival, LC50, activity locomotor, and oxidative stress parameters, elucidating the toxicity profile in acute and chronic exposure in Drosophila melanogaster. Three-day-old flies were investigated into groups: Control, 0.001, 0.0025, 0.005, and 0.010 mg/mL of COL or NCCOL. The survival rate, open field test, LC50, oxidative stress markers (reactive species (RS) production, thiobarbituric acid reactive substances), antioxidant enzyme activity (catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase), protein thiols, nonprotein thiols, acetylcholinesterase activity, and cell viability were measured. As a result, acute exposure to the COL decreases the number of crosses in the open field and increases CAT activity. NCCOL reduced RS levels, increased lipoperoxidation and SOD activity. Chronic exposure to the COL and NCCOL in high concentrations implied high mortality and enzymatic inhibition of the CAT and AChE, and only the COL caused locomotor damage in the open field test. Thus, NCCOL again reduced the formation of RS while COL increased. In this comparative study, NCCOL was less toxic to the antioxidant system than COL and showed notable involvement of oxidative stress as one of their toxicity mechanisms. Future studies are needed to elucidate all aspects of nanosafety related to the NCCOL.

15.
Journal of Allergy and Clinical Immunology ; 150(3):594-+, 2022.
Article in English | Web of Science | ID: covidwho-2168824

ABSTRACT

Background: Lymphopenia is predictive of survival in patients with coronavirus disease 2019 (COVID-19). Objective: The aim of this study was to understand the cause of the lymphocyte count drop in severe forms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Methods: Monocytic production of reactive oxygen species (ROSs) and T-cell apoptosis were measured by flow cytometry, DNA damage in PBMCs was measured by immunofluorescence, and angiotensin II (AngII) was measured by ELISA in patients infected with SARS-CoV-2 at admission to an intensive care unit (ICU) (n = 29) or not admitted to an ICU (n = 29) and in age- and sex-matched healthy controls. Results: We showed that the monocytes of certain patients with COVID-19 spontaneously released ROSs able to induce DNA damage and apoptosis in neighboring cells. Of note, high ROS production was predictive of death in ICU patients. Accordingly, in most patients, we observed the presence of DNA damage in up to 50% of their PBMCs and T-cell apoptosis. Moreover, the intensity of this DNA damage was linked to lymphopenia. SARS-CoV-2 is known to induce the internalization of its receptor, angiotensin-converting enzyme 2, which is a protease capable of catabolizing AngII. Accordingly, in certain patients with COVID-19 we observed high plasma levels of AngII. When looking for the stimulus responsible for their monocytic ROS production, we revealed that AngII triggers ROS production by monocytes via angiotensin receptor I. ROSs released by AngII-activated monocytes induced DNA damage and apoptosis in neighboring lymphocytes. Conclusion: We conclude that T-cell apoptosis provoked via DNA damage due to the release of monocytic ROSs could play a major role in COVID-19 pathogenesis.

16.
Diagnostic Microbiology and Infectious Disease ; : 115886, 2022.
Article in English | ScienceDirect | ID: covidwho-2165212

ABSTRACT

This study aimed to profile the clinical progression, demographics, and oxidative status of COVID-19 patients, correlating with disease severity. The study included 143 participants: 93 patients with COVID-19 (28 outpatients, 65 inpatients), and 50 control participants. Thiobarbituric acid reactive substance (TBARS) was used as an oxidative damage marker. Antioxidant activity was assessed via quantification of Vitamin C, sulfhydryl groups, ferric reduction ability of plasma (FRAP), Uric acid (UA) and evaluation of delta-aminolevulinate dehydratase (δ-ALA-D) enzymatic activity. Geriatric patients, especially men, with comorbidities such as obesity and/or chronic diseases were more likely to develop the most severe form of COVID-19. The activity of the δ-ALA-D was lower in inpatients, and there was no significant difference with the outpatient. Antioxidants decreased in COVID-19 groups, while lipid peroxidation increased. FRAP and Vitamin C decreased with evolution of the disease. Oxidative stress could be used as a predictor of worsening clinical condition.

17.
Front Cell Infect Microbiol ; 12: 924832, 2022.
Article in English | MEDLINE | ID: covidwho-2162976

ABSTRACT

The molecular footprints of COVID-19 occur everywhere, even reaching the family of biologically active gases and gasotransmitters. Besides nitric oxide and hydrogen sulfide, COVID-19 might also alter the homeostasis of dihydrogen (H2), another gaseous bioactive molecule produced endogenously by the human gut bacteria. Many studies have shown various alterations of the gut microbiota in patients with coronavirus disease 2019, including the lower abundance of hydrogen-producing bacteria that could instigate the shortage of hydrogen output. Since dihydrogen has many important bioactivities, including cytoprotective, antioxidant, anti-inflammatory, and antiapoptotic, its malproduction in COVID-19 might contribute to the disease progression and severity. On the other hand, replenishing dihydrogen by exogenous administration could be beneficial in COVID-19 for both patient- and clinical-reported outcomes. Assessing low dihydrogen along with H2 supplementation to restore normal levels could be thus combined via theranostic approaches to aid COVID-19 diagnosis and treatment.


Subject(s)
COVID-19 , Gasotransmitters , Bacteria , COVID-19 Testing , Gases , Humans , Hydrogen
18.
Electronic Journal of General Medicine ; 20(1), 2023.
Article in English | Web of Science | ID: covidwho-2164612

ABSTRACT

Introduction: In the context of SARS-CoV-2 infection, it has been proposed that oxidative stress may contribute to the management of COVID-19 severity. The impact on the well-being of patients with COVID-19 using cysteine-providing supplements has not yet been evaluated and there is a need to understand the benefits and limitations they may offer.Aim: The aim of this study is to understand the experiences of improved well-being with cysteine-rich whey protein supplementation (Immunocal (R)) in patients with COVID-19.Methods: A qualitative study was conducted by conducting semi-structured interviews with four participants taking Immunocal (R) while they had COVID-19. Participants were randomly recruited through internet networking. Ethical approval was obtained from the University ethics committee. Participants were informed of the study objectives two days in advance and consent was obtained before interviews began. We used the 16-item "Use of Immunocal supplement for COVID-19" (USIC-19) questionnaire to inquire about COVID-19 behavior (time of illness, symptoms, and severity of illness) and the experience of using the supplement during illness. Confidentiality was maintained throughout this study.Results: All participants presented mild discomfort such as headache, weakness, and tiredness when they had COVID-19 impacting most of them emotionally. The use of Immunocal (R) produced a partial improvement in all patients as only two continued to experience fatigue. Immunocal (R) improved the mood (50%) and physical health of the participants. In addition, participants reported that the supplement was recommended and dosed primarily by a consultant and that they did not feel hesitant to use it because of previous experiences of friends and family. The daily dosage of half of the participants was two sachets and all felt the need to consume the supplement which resulted in daily use.Conclusion: Following the daily dosage indications of the consultants, the participants who have consumed Inmunocal (R) have presented a partial improvement of the symptoms related to COVID-19, however, they feel the need to consume the supplement daily to improve their quality of life.

19.
Int J Mol Sci ; 23(23), 2022.
Article in English | PubMed | ID: covidwho-2163436

ABSTRACT

Recent works have demonstrated a significant reduction in cholesterol levels and increased oxidative stress in patients with coronavirus disease 2019 (COVID-19). The cause of this alteration is not well known. This study aimed to comprehensively evaluate their possible association during the evolution of COVID-19. This is an observational prospective study. The primary endpoint was to analyze the association between lipid peroxidation, lipid, and inflammatory profiles in COVID-19 patients. A multivariate regression analysis was employed. The secondary endpoint included the long-term follow-up of lipid profiles. COVID-19 patients presented significantly lower values in their lipid profile (total, low, and high-density lipoprotein cholesterol) with greater oxidative stress and inflammatory response compared to the healthy controls. Lipid peroxidation was the unique oxidative parameter with a significant association with the total cholesterol (OR: 0.982;95% CI: 0.969-0.996;p = 0.012), IL1-RA (OR: 0.999;95% CI: 0.998-0.999;p = 0.021) IL-6 (OR: 1.062;95% CI: 1.017-1.110;p = 0.007), IL-7 (OR: 0.653;95% CI: 0.433-0.986;p = 0.042) and IL-17 (OR: 1.098;95% CI: 1.010-1.193;p = 0.028). Lipid abnormalities recovered after the initial insult during long-term follow-up (IQR 514 days);however, those with high LPO levels at hospital admission had, during long-term follow-up, an atherogenic lipid profile. Our study suggests that oxidative stress in COVID-19 is associated with derangements of the lipid profile and inflammation. Survivors experienced a recovery in their lipid profiles during long-term follow-up, but those with stronger oxidative responses had an atherogenic lipid profile.

20.
Redox Biology ; : 102580, 2022.
Article in English | ScienceDirect | ID: covidwho-2159756

ABSTRACT

Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM the lungs. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure.

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