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":"Oxidative stress is inhibited by plant-based supplements: A quantitative lipidomic analysis of antioxidant activity and lipid compositional change","authors":"Julia Bahja,&nbsp;Nicolas A. Stewart,&nbsp;Marcus K. Dymond","doi":"10.1016/j.arres.2022.100054","DOIUrl":"https://doi.org/10.1016/j.arres.2022.100054","url":null,"abstract":"<div><p>Dietary supplements containing plant extracts are often marketed as having antioxidant properties. Using complex lipid mixtures derived from cellular tissue, we perform a targeted lipidomic assessment of the antioxidant activity of five plant extract supplements. Formulations derived from grape seed, milk thistle, pine bark, turmeric and hawthorn extract were evaluated. Overall, we find evidence to suggest that all supplements suppressed <em>in vitro</em> lipid oxidation to some degree. Suppression of oxidation was most effective in the dominant lipid classes, phosphatidylcholine (PC) and phosphatidylethanolamine (PE), which contain significant numbers of polyunsaturated lipids. Under the conditions of study, grape seed extract supplement was the most effective antioxidant showing statistically significant suppression of lipid oxidation in 11 of the 15 lipid classes quantified. Lipid compositional changes and metrics such as the PC: PE ratio and the double bond index were determined to provide an insight into the effect of oxidative stress and antioxidants on collective membrane properties. Finally, the likely stress that <em>in vivo</em> lipid oxidation could cause to cells, and the mitigating effects of supplements in this context, is also discussed.</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":"6 ","pages":"Article 100054"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000261/pdfft?md5=d42f2f4da9e0a445fd162a5757f9ab3e&pid=1-s2.0-S2667137922000261-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137115640","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":"Structure and biological evaluation of Caenorhabditis elegans CISD-1/mitoNEET, a KLP-17 tail domain homologue, supports attenuation of paraquat-induced oxidative stress through a p38 MAPK-mediated antioxidant defense response","authors":"Jacob R. Boos ,&nbsp;Hanna N. Jandrain ,&nbsp;Emi Hagiuda ,&nbsp;Alexander T. Taguchi ,&nbsp;Kazuya Hasegawa ,&nbsp;Bailey L. Fedun ,&nbsp;Sarah J. Taylor ,&nbsp;Sofhia M. Elad ,&nbsp;Sarah E. Faber ,&nbsp;Takashi Kumasaka ,&nbsp;Toshio Iwasaki ,&nbsp;Werner J. Geldenhuys","doi":"10.1016/j.arres.2022.100048","DOIUrl":"10.1016/j.arres.2022.100048","url":null,"abstract":"<div><p>CISD-1/mitoNEET is an evolutionarily conserved outer mitochondrial membrane [2Fe-2S] protein that regulates mitochondrial function and morphology. The [2Fe-2S] clusters are redox reactive and shown to mediate oxidative stress <em>in vitro</em> and <em>in vivo</em>. However, there is limited research studying CISD-1/mitoNEET mediation of oxidative stress in response to environmental stressors. In this study, we have determined the X-ray crystal structure of <em>Caenorhabditis elegans</em> CISD-1/mitoNEET homologue and evaluated the mechanisms of oxidative stress resistance to the pro-oxidant paraquat in age-synchronized populations by generating <em>C. elegans</em> gain and loss of function CISD-1 models. The structure of the <em>C. elegans</em> CISD-1/mitoNEET soluble domain refined at 1.70-Å resolution uniquely shows a reversible disulfide linkage at the homo-dimeric interface and also represents the N-terminal tail domain for dimerization of the cognate kinesin motor protein KLP-17 involved in chromosome segregation dynamics and germline development of the nematode. Moreover, overexpression of CISD-1/mitoNEET in <em>C. elegans</em> has revealed beneficial effects on oxidative stress resistance against paraquat-induced reactive oxygen species generation, corroborated by increased activation of the p38 mitogen-activated protein kinase (MAPK) signaling cascade.</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":"6 ","pages":"Article 100048"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a8/b5/nihms-1855856.PMC9757825.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10401541","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 in patients with pulmonary hypertension","authors":"Tammy O. Wichman ,&nbsp;Galo Martin Sanchez Palacios ,&nbsp;Ross Davidson ,&nbsp;Christopher S. Wichman ,&nbsp;Matthew C. Zimmerman","doi":"10.1016/j.arres.2022.100053","DOIUrl":"10.1016/j.arres.2022.100053","url":null,"abstract":"<div><h3>Rationale</h3><p>Pulmonary arterial hypertension is a devastating cardiovascular disease that is progressive and fatal despite advances in therapy. Animal models have shown that oxidative stress may be pathogenic in pulmonary hypertension.</p></div><div><h3>Objectives</h3><p>We hypothesized that oxidative stress, as measured by increased levels of oxidants, including superoxide, may play a role in pulmonary arterial hypertension in humans. We also hypothesized that oxidants are elevated in patients with pulmonary arterial hypertension compared with normal controls and that they correlate with measures of pulmonary arterial hypertension severity.</p></div><div><h3>Methods and Measurements</h3><p>Using a novel application of electron paramagnetic resonance spectroscopy to measure free radical oxidants, we initially evaluated whether levels of oxidants from whole blood collected from the pulmonary artery obtained during right heart catheterization would correlate with oxidant levels in peripheral venous blood. We then measured oxidants in peripheral venous blood in patients with pulmonary arterial hypertension and normal controls.</p></div><div><h3>Main Results</h3><p>Results showed a significant correlation between oxidant levels in blood collected from the pulmonary artery and peripheral vein but no significant elevation of oxidants in pulmonary hypertension patients versus control subjects. Furthermore, there were no correlations between levels of oxidants and severity of pulmonary arterial hypertension, as assessed by symptoms, functional capacity, hemodynamics, and the REVEAL risk score.</p></div><div><h3>Conclusions</h3><p>Contrary to previous animal studies and indirect measures of oxidative stress, we were unable to confirm an oxidative environment in patients with pulmonary arterial hypertension, at least when assessed by levels of free radical oxidants, such as superoxide, in whole blood via electron paramagnetic resonance spectroscopy.</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":"6 ","pages":"Article 100053"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266713792200025X/pdfft?md5=8cc7af36fc2dc0a9035f848b938a6006&pid=1-s2.0-S266713792200025X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49035473","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":"Corrigendum to ‘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.2022.100052","DOIUrl":"10.1016/j.arres.2022.100052","url":null,"abstract":"","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":"6 ","pages":"Article 100052"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137922000248/pdfft?md5=0eae6c9e5c057a43f27f91be25fbbc27&pid=1-s2.0-S2667137922000248-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43343939","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":"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}