Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe最新文献

{"title":"Pharmacological significance of MitoQ in ameliorating mitochondria-related diseases","authors":"Lateef Adegboyega Sulaimon ,&nbsp;Lukman Olalekan Afolabi ,&nbsp;Rahmat Adetutu Adisa ,&nbsp;Akinrinade George Ayankojo ,&nbsp;Mariam Olanrewaju Afolabi ,&nbsp;Abiodun Mohammed Adewolu ,&nbsp;Xiaochun Wan","doi":"10.1016/j.arres.2022.100037","DOIUrl":"10.1016/j.arres.2022.100037","url":null,"abstract":"<div><p>The Mitochondria is a critical sub-cellular organelle that plays an integral part in a normal cellular process. Besides ATP production, the mitochondria participate in various key cellular processes such as cell signaling, epigenetic regulation leading to cell proliferation, migration, apoptosis, differentiation, and autophagy – highlighting their importance to cellular health. However, mitochondrial dysfunction has serious organismal consequences, playing critical roles in the pathophysiology of many diseases, including neurodegenerative disorders, cardiovascular diseases, cancer, pulmonary and liver diseases. In recent years, mitochondrial dysfunction has spurred a surge of interest in developing mitochondria-targeted therapies. MitoQ is a selective antioxidant that concentrates in the mitochondria and prevents oxidative damage to the mitochondria. The therapeutic relevance of MitoQ has been studied in various diseased conditions to determine its efficacy in either slowing disease progression or alleviating symptoms. In this review, we discussed mitochondrial dysfunction in selected diseases and the therapeutic benefit of MitoQ in numerous studies.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"5 ","pages":"Article 100037"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000091/pdfft?md5=306efe8688d4779000cb7d489516bd41&pid=1-s2.0-S2667137922000091-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43231768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc Homeostasis, Reactive Oxygen Species Imbalance and Bisphenol-A Exposure in the Preimplantation Mouse Embryo: a possible adverse outcome pathway","authors":"Charalampos Chatzicharalampous ,&nbsp;David Bai ,&nbsp;Olivia G Camp ,&nbsp;Narendra Joshi ,&nbsp;Husam M. Abu-Soud","doi":"10.1016/j.arres.2022.100032","DOIUrl":"https://doi.org/10.1016/j.arres.2022.100032","url":null,"abstract":"<div><p>Bisphenol-A (BPA) is a ubiquitous xenoestrogen found in plastic products used for food containers, paper products, water pipes, etc. Individuals exposed to BPA are susceptible to detrimental effects; with poor oocyte quality, sperm motility, and impaired embryo implantation observed in mouse models at levels as low as 100 µg/kg/day. To investigate the mechanism through which BPA affects embryo development, oocytes were retrieved from 8-10-week-old mice and fertilized using IVF. The embryos were divided into 4 groups and exposed to increasing BPA concentrations (10 - 200 µM) for 18 hours, then were graded daily based on morphological appearance and development. A subgroup of the treated embryos (n = 10/group) were further evaluated for induction of apoptosis, overproduction of ROS, and zinc depletion. Mouse oocytes were treated with BPA (up to 300 µΜ), then, using RT-PCR, we preformed gene expression studies for AZGP1, an important gene in zinc homeostasis. Cultured day 5 mouse embryos that were exposed to BPA concentrations &gt; 50 µM had fewer progressions to blastocysts, lower blastocyst grades, and more were arrested as compared to controls (p&lt;0.05). Enhancement of ROS production and increased apoptosis associated with zinc depletion were evident in embryos treated with increasing concentrations of BPA (p&lt;0.05). Gene expression studies showed downregulation of the AZGP1 gene in oocytes exposed to high BPA concentrations (p&lt;0.01). This work may help women experiencing infertility that were exposed to high levels of BPA, as well as women suffering from diseases associated with zinc deficiency.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"4 ","pages":"Article 100032"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000042/pdfft?md5=3c3c996f31297c9886d5d2e6bc706ea4&pid=1-s2.0-S2667137922000042-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92065754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells","authors":"Azraa Ayesha ,&nbsp;Edward M Bahnson ,&nbsp;Yukako Kayashima ,&nbsp;Jennifer Wilder ,&nbsp;Phillip K Huynh ,&nbsp;Sylvia Hiller ,&nbsp;Nobuyo Maeda-Smithies ,&nbsp;Feng Li","doi":"10.1016/j.arres.2022.100029","DOIUrl":"10.1016/j.arres.2022.100029","url":null,"abstract":"<div><p>Vitamin B12 (B12) is an essential co-factor for two enzymes in mammalian metabolism and can also act as a mimetic of superoxide dismutase (SOD) converting superoxide (O₂ ^•−) to hydrogen peroxide (H₂O₂). High oral dose B12 decreases renal O₂ ^•− and post-ischemia/reperfusion injury in mice and protects against damage induced by hypoxia/reperfusion in mouse kidney proximal tubular cells (BU.MPT). O₂ ^•− is unstable and rapidly converted to H₂O₂. H₂O₂ mediates oxidative stress associated with O₂ ^•−. Whether B12 protects against damage induced by H₂O₂ is unknown. Both BU.MPT cells and mouse brain endothelial cells (bEdn.3) were applied to test the effects of B12 on H₂O₂-induced cytotoxicity. Both types of cells were treated with different doses of H₂O₂ with or without different doses of B12. Cell viability was analyzed 24 h later. H₂O₂ caused cell death only at a very high dose, and high pharmacological dose of B12 did not prevent this detrimental effect in either cell type. In bEnd.3 cells, transcriptional levels of heme oxygenase-1 (HO-1) increased, while nuclear factor erythroid 2-related factor 2 (Nrf2) decreased by H₂O₂. The levels of transcripts were not affected by the B12 treatment. We conclude that the cytotoxic effects of exogenous H₂O₂ in BU.MPT and bEdn.3 cells are not prevented by B12.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"4 ","pages":"Article 100029"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/80/69/nihms-1797049.PMC9067605.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10615622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antimicrobial seleno-organic coatings and compounds acting primarily on the plasma membrane: A review","authors":"Phat Tran ,&nbsp;Jonathan Kopel ,&nbsp;Bojana Ristic ,&nbsp;Harrison Marsh ,&nbsp;Joe Fralick ,&nbsp;Ted Reid","doi":"10.1016/j.arres.2022.100031","DOIUrl":"10.1016/j.arres.2022.100031","url":null,"abstract":"<div><h3>Introduction</h3><p>Bacterial infections have been the major cause of disease throughout history. However, some bacteria have evolved to attain multi-drug resistance (MDR) against a wide range of antibiotics. Today, the acquisition and spread of antibiotic resistance among pathogenic bacteria constitute a major threat to modern medicine. One approach to overcoming MDR bacteria has been the use of elemental selenium to generate reactive oxygen species (ROS) which damage the cell membrane and intracellular proteins. In this review, we will discuss the underlying antibacterial mechanisms of selenium-coated devices, selenium conjugated peptides, antibodies, and nanoparticles against MDR bacteria.</p></div><div><h3>Methods</h3><p>We conducted a literature review of the characteristics of selenium and recent developments of its utilization as an effective treatment strategy.</p></div><div><h3>Results</h3><p>One of the proposed solutions to this problem was the attachment of elemental selenium to different materials to kill bacteria through the catalytic generation of superoxide radicals. Superoxide anion, along with hydrogen peroxide and hydroxyl radical, are the noxious byproducts of partial oxygen reduction that perform lethal cellular oxidative damage. Due to the short half-life of the superoxide radical (≤1 milliseconds) only bacteria localized near selenium are destroyed.</p></div><div><h3>Conclusion</h3><p>Therefore, due to this antimicrobial mechanism, surface coatings of a plethora of devices containing elemental selenium have been demonstrated as an effective method against pathogenic and antibiotic resistant bacteria. Furthermore, utilization of selenium conjugated peptides, antibodies, and nanoparticles have been investigated as both antimicrobial and anti-cancer therapeutics.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"4 ","pages":"Article 100031"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000030/pdfft?md5=dcea710b9ddca5ade733019b64cadf99&pid=1-s2.0-S2667137922000030-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43885756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring mitochondrial hydrogen sulfide signalling for therapeutic interventions in vascular diseases","authors":"Lorena Diaz Sanchez ,&nbsp;Lissette Sanchez-Aranguren ,&nbsp;Mandeep Marwah ,&nbsp;Keqing Wang ,&nbsp;Corinne M Spickett ,&nbsp;Helen R Griffiths ,&nbsp;Irundika HK Dias","doi":"10.1016/j.arres.2022.100030","DOIUrl":"10.1016/j.arres.2022.100030","url":null,"abstract":"<div><p>Hydrogen sulfide (H₂S), a gaseous signalling molecule, is important in numerous physiological and pathophysiological processes. Despite its initial identification as an environmental toxin, H₂S is now well described as an essential physiological molecule that is finely balanced to maintain cellular functions, especially in modulating mitochondrial activity. Mitochondria are responsible for the oxidation of H₂S and its safe elimination while maintaining mitochondrial biogenesis. H₂S oxidation in mitochondria generates various reactive sulfur species that could post-translationally modify proteins by sulfhydration. Sulfhydrated proteins participate in many regulatory activities either by direct interactions in the electron transport chain or indirect regulation by epigenetics. These investigations explain the importance of research of H₂S as a therapeutic molecule beyond the traditional understanding as a protective role through its anti-inflammatory and antioxidant properties. This review focuses on highlighting the significant involvement of the H₂S pathway in vascular diseases and current H₂S donors for therapeutic use under development.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"4 ","pages":"Article 100030"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000029/pdfft?md5=0a2b1a634567bc18b69b031b26e6ea6b&pid=1-s2.0-S2667137922000029-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46071063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences and effects of aerobic capacity on redox stress resilience in older men and women","authors":"Savannah R. Berry,&nbsp;Ethan L. Ostrom,&nbsp;Tinna Traustadóttir","doi":"10.1016/j.arres.2021.100022","DOIUrl":"10.1016/j.arres.2021.100022","url":null,"abstract":"<div><p>Resistance to oxidative stress is reduced with age but there is lack of data regarding sex differences. In general, many sex differences are driven by sex hormones and thus might be expected to be lessened after menopause and at older ages. Aerobic fitness has been shown to increase redox capacity in older adults but whether adaptations differ between men and women is unknown. The aim of this study was to investigate sex differences and the association between redox capacity and aerobic fitness. Healthy men (n=20 and women (n=17) ages 60-86y participated in this study. Maximal oxygen consumption was measured with a graded exercise test on a cycle ergometer. Resistance to oxidative stress was measured by F₂-isoprostane (F₂-isoP) response to forearm ischemia/reperfusion (I/R) trial. The I/R trial elicited a significant F₂-isoP response in the cohort as a whole (<em>p</em>&lt;0.05). Women had higher F₂-isoP levels across time compared to men and an earlier peak (<em>p</em>&lt;0.05). When the data were analyzed as percent change from baseline, the time-by-sex interaction remained significant (<em>p</em>&lt;0.01) but the group difference was no longer significant. Fitness levels were negatively correlated with both the overall F₂-isoP levels (AUC; r=-0.490) and the response with respect to baseline (AURC; r=-0.476) in women (<em>p</em>&lt;0.05) but not in men. These data suggest that age and menopause-related increases in oxidative stress are greater in women relative to the expected age-related increase in men. Furthermore, women are more responsive to the effects of physical fitness on attenuating oxidative stress, possibly mediated by body composition.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"3 ","pages":"Article 100022"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137921000229/pdfft?md5=5fd4db83d6f4e0e302ab7d8121715a21&pid=1-s2.0-S2667137921000229-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45270042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of circadian and redox rhythms in cancer hypoxia","authors":"Sonal Omer,&nbsp;D. Karunagaran,&nbsp;G.K. Suraishkumar","doi":"10.1016/j.arres.2021.100018","DOIUrl":"10.1016/j.arres.2021.100018","url":null,"abstract":"<div><p>Cancer therapy faces considerable challenges due to the gaps in the understanding of the interlinked aspects of the relevant modalities. Hypoxia, altered circadian rhythms, and altered redox rhythms are some of the central and therapeutically targetable, relevant modalities. Recent studies suggest the existence of bi-directional crosstalk between hypoxia-circadian rhythm, hypoxia-redox rhythm, and redox-circadian rhythms. However, the interconnections between the three modalities are not yet established in cancer pathophysiology. This work reviews the recent investigations on the interconnected roles of circadian clock oscillations, redox oscillations, and hypoxia in cancer. Based on the available data, we highlight the gating of the hypoxic signaling pathway by the two oscillatory systems. An understanding of the molecular coupling is expected to result in better cancer therapies through drugs that modify circadian rhythm, redox rhythm, and hypoxia.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"3 ","pages":"Article 100018"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.arres.2021.100018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44635668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative cleavage of polyunsaturated fatty acid chains via dioxygenation/pseudoperoxidation by 15-lipoxygenase","authors":"Ichiro Koshiishi,&nbsp;Yuta Takigawa","doi":"10.1016/j.arres.2021.100023","DOIUrl":"10.1016/j.arres.2021.100023","url":null,"abstract":"<div><p>Aberrant progression of one-electron reduction of fatty acid hydroperoxides in cells is thought to be responsible for cell death, such as ferroptosis caused by reactive carbonyl compounds and hydrocarbon radicals generated through the cleavage of C-C bonds of fatty acid alkoxyl radicals belonging to oxygen-centered radicals. In the present study, we investigated the mechanism underlying the oxidative cleavage of polyunsaturated fatty acid chains by 15-lipoxygenase under anaerobic conditions using soybean 15-lipoxygenase as a model enzyme. The apparent reaction rate constant of lipoxygenase(Fe²⁺) with 13-hydroperoxyoctadecadienoic acid (13-HpODE) was approximately 7.3 times higher than that with 9-HpODE. The production of 13-oxo-tridecadienoic acid (13-OTA) in this reaction was remarkably inhibited in the presence of a five-membered nitroxyl radical, 3-carbamoyl-2,2,5,5-tetramethyl-3-pyrroline-N-oxyl (CmΔP), which is a specific spin-trapping agent for carbon-centered radicals. The trapped adduct appeared to be a CmΔP adduct with a linoleate epoxyallyl radical, which was derived from the linoleate alkoxyl radical through intramolecular rearrangement at the reaction site on the enzyme. Furthermore, 13-OTA production in the α-linolenate hydroperoxide/lipoxygenase(Fe²⁺) system was six times higher than that in the linoleate hydroperoxide/lipoxygenase(Fe²⁺) system. Based on these facts, we hypothesized that under anaerobic conditions, the fatty acid epoxyallyl radical at the reaction site on the enzyme spontaneously degrades into reactive carbonyl compounds and hydrocarbon radicals through the cleavage of C-C bonds. In conclusion, radical scavengers against carbon-centered radicals should inhibit the lipoxygenase-inducing cell death through preventing the cleavage of C-C bond of fatty acid epoxyallyl radicals.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"3 ","pages":"Article 100023"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137921000230/pdfft?md5=ff2d70145953bc8105337840895f90c7&pid=1-s2.0-S2667137921000230-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48439878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitoquinol mesylate alleviates oxidative damage in cirrhotic and advanced hepatocellular carcinogenic rats through mitochondrial protection and antioxidative effects","authors":"Lateef A. Sulaimon ,&nbsp;Rahmat A. Adisa ,&nbsp;Titilola A. Samuel ,&nbsp;Fatimah B. Abdulkareem ,&nbsp;Akinrinade G. Ayankojo","doi":"10.1016/j.arres.2021.100014","DOIUrl":"https://doi.org/10.1016/j.arres.2021.100014","url":null,"abstract":"<div><p>Mitochondrial dysfunction due to oxidative stress is usually implicated in pathological conditions such as cirrhosis and hepatocellular carcinoma (HCC). This study investigated the chemopreventive and therapeutic effects of mitochondrial targeted antioxidant, Mitoquinol Mesylate (MitoQ) in a model of diethylnitrosamine (DEN)-induced cirrhosis and advanced HCC. Liver cirrhosis and advanced HCC were induced in Wistar rats by diethylnitrosamine administration (10 mg/Kg/day, oral gavage) for 12 and 20 weeks, respectively. The cirrhotic and advanced HCC rats were treated with mitoQ (10 mg/Kg/day, oral gavage) as intervention therapy for 12-20 weeks (pre-treatment) and 4-12 weeks (post-treatment), respectively. Both MitoQ interventions improved body weight, survival index and hepatic function while reducing hepatosomatic index and nodular incidence in cirrhotic and advanced HCC rats. Pre-treatment with mitoQ suppressed the transformation of cirrhotic cells to malignancy and decreased the level of cirrhosis and HCC biomarkers. Also, pre-treatment restored the perturbations in lipid profile, mitochondrial dysfunction and oxidative stress induced by DEN-administration. MitoQ achieved these by modulating the activities of cytosolic and mitochondrial antioxidant enzymes as well as the expression of mitochondrial SOD2, GPX1 and CAT genes at both stages of cirrhosis and advanced HCC. Oral administration of MitoQ for 12 and 20 weeks further increased F₁F₀ATPase activity, suggesting mitochondrial respiratory chain uncoupling as one of its mechanisms of action. Therefore, MitoQ administration may represent a promising strategy for the prevention and treatment of liver cirrhosis and HCC by reducing hepatic oxidative stress and promoting removal of dysfunctional mitochondria.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"3 ","pages":"Article 100014"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.arres.2021.100014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91986419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nebulization of glutathione and N-Acetylcysteine as an adjuvant therapy for COVID-19 onset","authors":"José Fábio Santos Duarte Lana ,&nbsp;Anna Vitória Santos Duarte Lana ,&nbsp;Quézia Souza Rodrigues ,&nbsp;Gabriel Silva Santos ,&nbsp;Riya Navani ,&nbsp;Annu Navani ,&nbsp;Lucas Furtado da Fonseca ,&nbsp;Gabriel Ohana Marques Azzini ,&nbsp;Thiago Setti ,&nbsp;Tomas Mosaner ,&nbsp;Claudio Lopes Simplicio ,&nbsp;Taís Mazzini Setti","doi":"10.1016/j.arres.2021.100015","DOIUrl":"10.1016/j.arres.2021.100015","url":null,"abstract":"<div><p>Ever since its emergence, the highly transmissible and debilitating coronavirus disease spread at an incredibly fast rate, causing global devastation in a matter of months. SARS-CoV-2, the novel coronavirus responsible for COVID-19, infects hosts after binding to ACE2 receptors present on cells from many structures pertaining to the respiratory, cardiac, hematological, neurological, renal and gastrointestinal systems. COVID-19, however, appears to trigger a severe cytokine storm syndrome in pulmonary structures, resulting in oxidative stress, exacerbated inflammation and alveolar injury. Due to the recent nature of this disease no treatments have shown complete efficacy and safety. More recently, however, researchers have begun to direct some attention towards GSH and NAC. These natural antioxidants play an essential role in several biological processes in the body, especially the maintenance of the redox equilibrium. In fact, many diseases appear to be strongly related to severe oxidative stress and deficiency of endogenous GSH. The high ratios of ROS over GSH, in particular, appear to reflect severity of symptoms and prolonged hospitalization of COVID-19 patients. This imbalance interferes with the body's ability to detoxify the cellular microenvironment, fold proteins, replenish antioxidant levels, maintain healthy immune responses and even modulate apoptotic events. Oral administration of GSH and NAC is convenient and safe, but they are susceptible to degradation in the digestive tract. Considering this drawback, nebulization of GSH and NAC as an adjuvant therapy may therefore be a viable alternative for the management of the early stages of COVID-19.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"3 ","pages":"Article 100015"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.arres.2021.100015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48396641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}