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":"Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) in plants– maintenance of structural individuality and functional blend","authors":"Mamun Mandal ,&nbsp;Manisha Sarkar ,&nbsp;Azmi Khan ,&nbsp;Moumita Biswas ,&nbsp;Antonio Masi ,&nbsp;Randeep Rakwal ,&nbsp;Ganesh Kumar Agrawal ,&nbsp;Amrita Srivastava ,&nbsp;Abhijit Sarkar","doi":"10.1016/j.arres.2022.100039","DOIUrl":"10.1016/j.arres.2022.100039","url":null,"abstract":"<div><p>The free radicals along with several reactive oxygen species (ROS) and reactive nitrogen species (RNS) are known to play a dual role in the biological living system which carries a substantial importance in terms of signal networking in plants. The production of these active molecules in different cellular compartments eventually led to oxidative damage. However recent discoveries have evidenced its crucial roles as signaling molecules, activating stress responses against environmental challenges. As can be seen, the cellular organelles are considered to be the primary repository and site of action for reactive species there by later with the establishment of stress signaling concept, the underlying mechanism of ROS/RNS interaction has been elucidated properly by cellular organelle based study. These efforts led to the identification of signaling cascades generated by ROS and RNS which are not only involved with various antioxidative pathways but also correspond with other stress specific mechanisms. This study focuses on a burgeoning area of plant study, highlights the site specific generation, interplay, effect on several metabolic pathways and mode of reaction of ROS/RNS in cells. The review moreover postulates the fundamental mechanism of ROS/RNS cross talking in a lucid manner which further helps to stand out its significant importance with respect to plant survival during the course of evolution. Increasing interest in the area of plant stress and the ROS/RNS signaling, more elementary knowledge regarding their specificity, regulation, flexibility yet to be explored at molecular level by the advancement of technology.</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 100039"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266713792200011X/pdfft?md5=b48ab81d2c08236125451c9cf5eb19ec&pid=1-s2.0-S266713792200011X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44573936","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 stress and impaired insulin secretion in cystic fibrosis pig pancreas","authors":"Yunxia O'Malley ,&nbsp;Mitchell C. Coleman ,&nbsp;Xingshen Sun ,&nbsp;Junying Lei ,&nbsp;Jianrong Yao ,&nbsp;Casey F. Pulliam ,&nbsp;Paige Kluz ,&nbsp;Michael L. McCormick ,&nbsp;Yaling Yi ,&nbsp;Yumi Imai ,&nbsp;John F. Engelhardt ,&nbsp;Andrew W. Norris ,&nbsp;Douglas R. Spitz ,&nbsp;Aliye Uc","doi":"10.1016/j.arres.2022.100040","DOIUrl":"10.1016/j.arres.2022.100040","url":null,"abstract":"<div><p>Cystic fibrosis-related diabetes (CFRD) is one the most common comorbidities in cystic fibrosis (CF). Pancreatic oxidative stress has been postulated in the pathogenesis of CFRD, but no studies have been done to show an association. The main obstacle is the lack of suitable animal models and no immediate availability of pancreas tissue in humans. In the CF porcine model, we found increased pancreatic total glutathione (GSH), glutathione disulfide (GSSG), 3-nitrotyrosine- and 4-hydroxynonenal-modified proteins, and decreased copper zinc superoxide dismutase (CuZnSOD) activity, all indicative of oxidative stress. CF pig pancreas demonstrated increased DHE oxidation (as a surrogate marker of superoxide) <em>in situ</em> compared to non-CF and this was inhibited by a SOD-mimetic (GC4401). Catalase and glutathione peroxidase activities were not different between CF and non-CF pancreas. Isolated CF pig islets had significantly increased DHE oxidation, peroxide production, reduced insulin secretion in response to high glucose and diminished secretory index compared to non-CF islets. Acute treatment with apocynin or an SOD mimetic failed to restore insulin secretion. These results are consistent with the hypothesis that CF pig pancreas is under significant oxidative stress as a result of increased O₂^●− and peroxides combined with reduced antioxidant defenses against reactive oxygen species (ROS). We speculate that insulin secretory defects in CF may be due to oxidative stress.</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 100040"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c4/4d/nihms-1822502.PMC9328447.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40571734","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":"6-gingerol attenuates pulmonary inflammation and oxidative stress in mice model of house dust mite-induced asthma","authors":"Babajide O. Ajayi ,&nbsp;Temitope A. Olajide ,&nbsp;Ebenezer T. Olayinka","doi":"10.1016/j.arres.2022.100036","DOIUrl":"10.1016/j.arres.2022.100036","url":null,"abstract":"<div><p>Asthma is a chronic non-communicable inflammatory disease of the lung that affects over 300 million people worldwide. 6-Gingerol (6-G) is a phytocompound found in ginger rhizome that has been reported to exhibit anti-inflammatory effects. However, there is paucity of information regarding the effect of 6-G on asthma. This study was designed to evaluate the effect of 6-G on house dust mite (HDM) -induced asthma. Male mice were divided into 5 groups of 10 mice each. Group 1 served as control; group 2 received 6-G (10 mg/kg/day) for 5 weeks. Group 3 received HDM (10 µg/kg/day) for 4 weeks. Group 4 received 6-G (10 mg/kg/day) for 1 week prior to co-exposure with HDM (10 µg/kg/day) for 4 weeks, and group 5 received Dexamethasone (DEX) (1 mg/kg/day) and HDM (10 µg/kg/day) for 4 weeks. Administration of HDM significantly increased lymphocytes, leukocytes, neutrophils, eosinophils, myeloperoxidase (MPO), nitric oxide (•NO), malondialdehyde, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and decreased the activities of superoxide dismutase (SOD), catalase, glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione (GSH) and ascorbic acid (AA) levels relative to control. Administration of 6-G and DEX prior to HDM exposure significantly decreased lymphocytes, leukocytes, neutrophils, eosinophils, MPO, •NO, malondialdehyde, TNF-α, IL-6 and increased the activities of SOD, catalase, GST, GPx, and levels of GSH and AA relative to HDM group. Histopathological examination of the lungs of HDM-treated mice showed the presence of oedema and inflammation of the bronchi and alveoli. Administration of 6-G and DEX reversed these lesions. 6-G ameliorated House dust mite-induced asthma via anti-inflammatory and anti-oxidant mechanism.</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 100036"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266713792200008X/pdfft?md5=873408b9e3827c7874133fb44cdcf878&pid=1-s2.0-S266713792200008X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49243583","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":"Extracellular superoxide dismutase (EC-SOD) R213G variant reduces mitochondrial ROS and preserves mitochondrial function in bleomycin-induced lung injury","authors":"Hanan Elajaili ,&nbsp;Laura Hernandez-Lagunas ,&nbsp;Peter Harris ,&nbsp;Genevieve C. Sparagna ,&nbsp;Raleigh Jonscher ,&nbsp;Denis Ohlstrom ,&nbsp;Carmen C. Sucharov ,&nbsp;Russell P. Bowler ,&nbsp;Hagir Suliman ,&nbsp;Kristofer S. Fritz ,&nbsp;James R. Roede ,&nbsp;Eva S. Nozik","doi":"10.1016/j.arres.2022.100035","DOIUrl":"https://doi.org/10.1016/j.arres.2022.100035","url":null,"abstract":"<div><p>Extracellular superoxide dismutase (EC-SOD) is highly expressed in the lung and vasculature. A common human single nucleotide polymorphism (SNP) in the matrix binding region of EC-SOD leads to a single amino acid substitution, R213G, and alters EC-SOD tissue binding affinity. The change in tissue binding affinity redistributes EC-SOD from tissue to extracellular fluids. Mice (R213G mice) expressing a knock-in of this EC-SOD SNP exhibit elevated plasma and reduced lung EC-SOD content and activity and are protected against bleomycin-induced lung injury and inflammation. It is unknown how the redistribution of EC-SOD alters site-specific redox-regulated molecules relevant for protection. In this study, we tested the hypothesis that the change in the local EC-SOD content would influence not only the extracellular redox microenvironment where EC-SOD is localized but also protect the intracellular redox status of the lung. Mice were treated with bleomycin and harvested 7 days post-treatment. Superoxide levels, measured by electron paramagnetic resonance (EPR), were lower in plasma and Bronchoalveolar lavage fluid (BALF) cells in R213G mice compared to wild-type (WT) mice, while lung cellular superoxide levels in R213G mice were not elevated post-bleomycin compared to WT mice despite low lung EC-SOD levels. Lung glutathione redox potential (E_hGSSG), determined by HPLC and fluorescence, was more oxidized in WT compared to R213G mice. In R213G mice, lung mitochondrial oxidative stress was reduced shown by mitochondrial superoxide level measured by EPR in lung and the resistance to bleomycin-induced cardiolipin oxidation. Bleomycin treatment suppressed mitochondrial respiration in WT mice. Mitochondrial function was impaired at baseline in R213G mice but did not exhibit further suppression in respiration post-bleomycin.  Collectively, the results indicate that R213G variant preserves intracellular redox state and protects mitochondrial function in the setting of bleomycin-induced inflammation.</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 100035"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000078/pdfft?md5=7249a1dbf304d14cff0d9b9bb24befcb&pid=1-s2.0-S2667137922000078-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137243259","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":"Identification of severity and passive measurement of oxidative stress biomarkers for β–thalassemia patients: K-means, random forest, XGBoost, decision tree, neural network based novel framework","authors":"Debleena Basu ,&nbsp;Rupal Sinha ,&nbsp;Saswata Sahu ,&nbsp;Jyotsna Malla ,&nbsp;Nishant Chakravorty ,&nbsp;Partha Sarathi Ghosal","doi":"10.1016/j.arres.2022.100034","DOIUrl":"10.1016/j.arres.2022.100034","url":null,"abstract":"<div><p>Iron-overload induced oxidative stress in β–thalassemia patients is one of the major challenges in the associated treatment protocol. The severity and accurate prognosis of the disease is largely dependent on several clinical parameters, and different hormones also provide passive indication in this context. The present study focused on clinical implication of iron overload, tropic hormones, and oxidative stress biomarkers on severity of β–thalassemia patients as well as understating their interactive effects. Extensive blood serum samples were collected from group of case and control and statistical analysis was performed on the analyzed study parameters from the serum samples. The oxidative stress biomarkers, Malondialdehyde (MDA) and protein carbonyl level showed significant positive correlation with ferritin levels in case. A novel framework was developed to categorize the severity of the disease through K-means clustering and several classification algorithms, such as XGBoost, random forest, and decision tree. Furthermore, a neural network model was used for predicting the oxidative stress biomarker, MDA and protein carbonyl from measured value of ferritin and trophic hormones. The results of clustering depicted that ferritin and the oxidative stress biomarkers were conclusive parameters in determining the severity of the disease. Among the classifiers, XGBoost showed the highest accuracy after k-cross validation (100%). The neural network model exhibited high accuracy in predicting MDA and protein carbonyl. The proposed technique can be chosen as a real life decision tool for medical professionals in the diagnosis and treatment of β–thalassemia. Furthermore, the approach of passive determination of some critical blood parameters may be attributed from the developed prediction model, which can also be instrumental in the similar area of medical research.</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 100034"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000066/pdfft?md5=062dc45ef78109b619481feafa18d410&pid=1-s2.0-S2667137922000066-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48275075","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":"Potential roles of oxidative stress and insulin resistance in diisononyl phthalate induced dyslipidemia and hepatosteatosis in BALB/c mice","authors":"Ayokanmi Ore ,&nbsp;Adenike Adebola Adewale ,&nbsp;Samuel Abiodun Kehinde ,&nbsp;Tolulope Oreoluwa Faniyi ,&nbsp;Abolade Deborah Oladeji ,&nbsp;Precious Chinenye Rufus ,&nbsp;Ayoade Ajibola Akande ,&nbsp;Ifunanya Emmanuella Chukwuemeka","doi":"10.1016/j.arres.2022.100038","DOIUrl":"https://doi.org/10.1016/j.arres.2022.100038","url":null,"abstract":"<div><p>Exposure to plastic-derived endocrine disrupting chemicals (EDCs) such as phthalates have become a source of concern to human health. Phthalates are applied industrially as plasticizers in the production of various plastic products. They have been reported for the various forms of toxic responses in both human and animal studies. Diisononyl phthalate (DiNP) was recently used to replace di(2-ethylhexyl) phthalate (DEHP) due to some toxicity concerns. However, recent evidences suggest that DiNP may disrupt the endocrine system, alter lipid metabolism and induce hepatic steatosis. Hence, this work was designed to probe the potential impacts of DiNP on oxidative stress biomarkers and insulin resistance as a possible link to dyslipidemia and development of hepatic steatosis. To achieve these, twenty seven (27) male BALB/c mice were distributed into three (3) experimental groups of nine (9) mice each. Group I was the control while mice in groups II and III were exposed to 20 and 200 mg/kg body weight, (bw) DiNP respectively orally (per os, p.o.) for 28 days. Thereafter, plasma insulin, glucose, plasma lipid levels as well as insulin resistance (IR) index were determined. The effects of DiNP on hepatic biomarker of inflammation (tumor necrosis factor alpha, TNF-α), oxidative stress (malondialdehyde, MDA), antioxidants (glutathione peroxidase, reduced glutathione and catalase) were also investigated in addition to liver histopathology. Data obtained show that DiNP especially at 200 mg/kg bw significantly (<em>p</em> &lt; 0.05) alter plasma glucose and lipid profile and induced IR. Other responses observed at this dose level include significant inflammation, oxidative stress and hepatic fatty degeneration (as shown in hematoxylin and eosin stained liver sections). Current findings suggest that insulin resistance and oxidative stress may influence DiNP-induced dyslipidemia and hepatic steatosis in mice.</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 100038"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000108/pdfft?md5=1a59a4463e3d49c756b26963f91e79e7&pid=1-s2.0-S2667137922000108-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137243258","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":"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}