Redox Experimental Medicine最新文献

Regulatory drugs of Glutamate Transporter 1 (EAAT2/GLT-1) expression and activity. Role in quenching oxidative damage. 谷氨酸转运体 1（EAAT2/GLT-1）表达和活性的调节药物。在淬灭氧化损伤中的作用。

Redox Experimental Medicine Pub Date : 2024-06-01 DOI: 10.1530/rem-24-0004

Davinia Domínguez-González, Blanca Romero-Llopis, Marta Roldán-Lázaro, Lorena Baquero, Rita Noverques, Federico V. Pallardó, Juan Antonio Navarro, P. González-Cabo

{"title":"Regulatory drugs of Glutamate Transporter 1 (EAAT2/GLT-1) expression and activity. Role in quenching oxidative damage.","authors":"Davinia Domínguez-González, Blanca Romero-Llopis, Marta Roldán-Lázaro, Lorena Baquero, Rita Noverques, Federico V. Pallardó, Juan Antonio Navarro, P. González-Cabo","doi":"10.1530/rem-24-0004","DOIUrl":"https://doi.org/10.1530/rem-24-0004","url":null,"abstract":"L-glutamate is one of the major neurotransmitters in the CNS, directly and indirectly involved in numerous brain functions. In several neurodegenerative diseases, it has been observed that an excess of extracellular glutamate overstimulates glutamate receptors, leading to exacerbated neuronal excitation in a process of excitotoxicity and oxidative damage that promotes neuronal death. A number of L-glutamate transporters have been identified in the membrane of neurons and astrocytes. They are responsible for the reuptake of glutamate released into the synaptic cleft after excitatory neurotransmission concomitantly regulating the extracellular concentration of glutamate, protecting neurons from its excitotoxic action. Among all of them, literature highlights Glutamate Transporter 1, known as Excitatory Amino Acid Transporter type 2 (EAAT2) in humans and Glutamate Transporter type 1 (GLT-1) in rodents, also known as solute carrier family 1 member 2 (SLC1A2). It is the predominant glutamate transporter in the brain and ensures the majority of L-glutamate reuptake. Decreased expression of this transporter along with increased levels of oxidative stress have been observed in several chronic and acute neurodegenerative disorders. For this reason, the use of drugs capable of both, increasing the expression of Glutamate Transporter 1 and mitigating oxidative damage, has been proposed as an effective therapeutic strategy for these pathologies. We present in this work an overview of the main drugs displaying such a double effect.\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141279090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metformin and its redox-related mechanisms of action in type 2 diabetes 二甲双胍及其氧化还原相关机制在2型糖尿病中的作用

Redox Experimental Medicine Pub Date : 2023-09-01 DOI: 10.1530/rem-23-0015

Teresa Vezza, C. Luna-Marco, S. Rovira-Llopis, V. M. Víctor

{"title":"Metformin and its redox-related mechanisms of action in type 2 diabetes","authors":"Teresa Vezza, C. Luna-Marco, S. Rovira-Llopis, V. M. Víctor","doi":"10.1530/rem-23-0015","DOIUrl":"https://doi.org/10.1530/rem-23-0015","url":null,"abstract":"Type 2 diabetes (T2D) is a long-term metabolic disease characterized by progressive β-cell functional decline and insulin resistance, which increases the risk of cardiovascular complications as well as associated-morbidity and mortality. Evidence suggests a strong relationship between hyperglycaemia, oxidative stress and the development and progression of T2D. Indeed, a hyperglycaemic state can reduce the activity of antioxidant enzymes and increase lipid-peroxidation and protein oxidation products, as well as DNA damage. At present, metformin is the recommended first-line glucose-lowering agent in patients with T2D. Despite the vast clinical experience gained over several decades of use, several mechanisms of action of metformin have yet to be fully elucidated. This review provides an overview of the existing literature concerning the complicated interplay between oxidative stress and T2D and the molecular mechanisms underlying the redox-related mechanisms of action of metformin, which include (but are not limited to) interaction with AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms, inhibition of gluconeogenesis, and action on leukocyte-endothelium interactions.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115955775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of Oxidative Stress, Gut Microbiota and derived metabolites in the Etiology and progression of NAFLD 氧化应激、肠道微生物群和衍生代谢物在NAFLD病因学和进展中的作用

Redox Experimental Medicine Pub Date : 2023-08-01 DOI: 10.1530/rem-23-0016

Ankita Das, Arka De, Tanuja Mohanty, P. Aich

{"title":"Role of Oxidative Stress, Gut Microbiota and derived metabolites in the Etiology and progression of NAFLD","authors":"Ankita Das, Arka De, Tanuja Mohanty, P. Aich","doi":"10.1530/rem-23-0016","DOIUrl":"https://doi.org/10.1530/rem-23-0016","url":null,"abstract":"Non-alcoholic fatty liver disease or NAFLD is a complex and multifactorial liver disease that is affecting a majority of the world's population now more than ever. The review focuses on two major contributing factors in the etiology of the disease - oxidative stress and the gut microbiota. There is a complex interplay between oxidative stress and the gut microbiota in the pathogenesis of NAFLD. Oxidative stress in NAFLD can result from both the accumulation of lipids in the liver and the interactions between gut-derived metabolites and the liver. Dysbiosis in the gut microbiota can contribute to oxidative stress by promoting the production of ROS and altering the balance of antioxidant systems. This interplay between oxidative stress and the gut microbiota can create a vicious cycle, where dysbiosis contributes to oxidative stress, and oxidative stress further promotes dysbiosis, exacerbating liver damage in NAFLD. \u0000\u0000Understanding the intricate relationship between oxidative stress, the gut microbiota, and NAFLD is essential for developing targeted therapeutic strategies. This understanding requires more scientific research to unravel the complex and interconnecting pathways underlying NAFLD pathogenesis and progression. Modulating the gut microbiota through dietary interventions, prebiotics, probiotics, and change in lifestyle may help restore microbial balance and reduce oxidative stress in NAFLD. \u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"58 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116689263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Scavenger Receptor B1 involvement in COPD pathogenesis 清道夫受体B1参与COPD发病机制

Redox Experimental Medicine Pub Date : 2023-08-01 DOI: 10.1530/rem-23-0012

C. Cervellati, P. Casolari, A. Pecorelli, C. Sticozzi, F. Nucera, A. Papi, G. Caramori, G. Valacchi

{"title":"Scavenger Receptor B1 involvement in COPD pathogenesis","authors":"C. Cervellati, P. Casolari, A. Pecorelli, C. Sticozzi, F. Nucera, A. Papi, G. Caramori, G. Valacchi","doi":"10.1530/rem-23-0012","DOIUrl":"https://doi.org/10.1530/rem-23-0012","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is one of the main causes of morbidity and mortality in the United States. In 2020, almost 150,000 people died from COPD, making it the sixth leading cause of death and the fifth disease-related cause of death, behind heart disease, cancer, COVID-19, accidents, and stroke. \u0000\u0000Although exposure to cigarette smoke has been shown to be the main risk factor for COPD, the mechanisms underlying this association remain unclear as many smokers do not develop COPD.\u0000\u0000Several mechanisms contribute to the pathogenesis of COPD, such as pulmonary influx of inflammatory cells, imbalance between proteolytic and antiproteolytic molecules, alteration of the redox homeostasis. Among them, oxidative stress has been suggested to be the major driving mechanism in COPD pathogenesis. There is increased oxidative stress in the lungs of COPD patients due to exogenous oxidants in cigarette smoke and as a consequence of endogenous generation of reactive oxygen species by inflammatory cells and the consequent decrease in antioxidants content. The scavenger receptor BI (SRB1), beside playing a key role in mediating the uptake of high-density lipoprotein (HDL)-derived cholesterol and cholesteryl ester in tissues, it is also involved in the tissue antioxidant uptake for tocopherol. Loss of SRB1 significantly decreases tocopherol lung content making lung tissue more susceptible to oxidative damage. Therefore, because of its role in modulating the antioxidant defense in lung tissues, the loss of SRB1 may contribute to the development of COPD by preventing the tissue uptake of antioxidants molecules such as tocopherol.\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128408465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Untargeted metabolomics reveal sex specific and nonspecific redox modulating metabolites in kidneys following binge drinking 非靶向代谢组学揭示了酗酒后肾脏中性别特异性和非特异性氧化还原调节代谢物

Redox Experimental Medicine Pub Date : 2023-05-01 DOI: 10.1530/rem-23-0005

Daniel Rafferty, Luana C de Carvalho, Mason Sutter, Katlyn Heneghan, Victoria Nelson, Megan Leitner, Charlotte Bolch, A. Lasek, P. Puthanveetil

{"title":"Untargeted metabolomics reveal sex specific and nonspecific redox modulating metabolites in kidneys following binge drinking","authors":"Daniel Rafferty, Luana C de Carvalho, Mason Sutter, Katlyn Heneghan, Victoria Nelson, Megan Leitner, Charlotte Bolch, A. Lasek, P. Puthanveetil","doi":"10.1530/rem-23-0005","DOIUrl":"https://doi.org/10.1530/rem-23-0005","url":null,"abstract":"Binge drinking is a growing health concern among all age groups. The ability of individuals to handle ethanol in their systems differs not due to differences in enzyme expression but also due to other factors. Vital organs including brain, liver, heart and kidneys are at high risk following repeated exposure to high concentrations of ethanol from binge drinking. The impact of chronic binge drinking on kidneys is not well studied. Using a mouse model of chronic binge drinking, we have identified major metabolic alterations that could set the stage for detrimental effects in the kidneys of male and female mice. We have deciphered that even though there are pathway overlaps, the different sexes exhibited unique and divergent metabolic pathway dysregulations as per the metabolite panels following binge drinking. We have reported that binge drinking could negatively influence renal redox homeostasis in both sexes through regulation of different metabolite clusters. In male mice by downregulation of pantothenic acid and riboflavin synthesis, and female mice by upregulation of α-aminoadipic acid and formyl kynurenine level. Interestingly, uric acid biosynthesis pathway has been upregulated independent of the sex specific effects, portraying the significance of uric acid as a potential marker for binge drinking induced injury in both the sexes. Thus, by altering renal metabolome binge drinking sets the stage for renal damage by disturbing renal redox balance. Our data has high translational potential and will aid in finding ideal therapeutics in a sex-specific manner for subjects exposed to binge drinking induced renal injury.\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128547698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of heme oxygenase-1 in tumor immune escape 血红素加氧酶-1在肿瘤免疫逃逸中的作用

Redox Experimental Medicine Pub Date : 2023-05-01 DOI: 10.1530/rem-23-0006

M. Nitti, Jasmin Ortolan, A. Furfaro

引用次数: 0

Mitochondrial dysfunction, iron accumulation, and ferroptosis in parkinson’s disease 帕金森病的线粒体功能障碍、铁积累和铁下垂

Redox Experimental Medicine Pub Date : 2023-05-01 DOI: 10.1530/rem-23-0004

Nahom Teferi, Meron Challa, Timothy R Woodiwiss, B. Allen, Michael Petronek

引用次数: 0

Protection of C2C12 skeletal muscle cells towards oxidation by a polyphenol rich plant extract 富含多酚的植物提取物对C2C12骨骼肌细胞氧化的保护作用

Redox Experimental Medicine Pub Date : 2023-03-01 DOI: 10.1530/rem-23-0002

Jacques Kaminski, M. Haumont, Emmanuelle Prost-Camus, P. Durand, M. Prost, G. Lizard, N. Latruffe

{"title":"Protection of C2C12 skeletal muscle cells towards oxidation by a polyphenol rich plant extract","authors":"Jacques Kaminski, M. Haumont, Emmanuelle Prost-Camus, P. Durand, M. Prost, G. Lizard, N. Latruffe","doi":"10.1530/rem-23-0002","DOIUrl":"https://doi.org/10.1530/rem-23-0002","url":null,"abstract":"Sarcopenia is a very disabling age-related disease which affects the mass and the strenght of skelettal muscles. This syndrome has no efficient treatment and is associated with an important oxidative stress which could play important roles in skelettal muscle degeneration. In this context, the cytoprotective activity and the antioxidant properties of a polyphenol-rich plant extract (PRPE) was evaluated in undifferentiated C2C12 murine skeletal muscle cells (myoblasts). PRPE is a potent antioxidant mixture as shown by its Reactive Oxygen Species (ROS) scavenging properties by using the KRL (Kit Radicaux Libres) method and the dihydroethidium (DHE) scavening assay. In addition, PRPE has significant protecting properties in C2C12 cells towards oxidative stress triggered by 2, 2′-azobis (2-amidinopropane) dihydrochloride (AAPH) which is a ROS generator, as measured by different complementary approaches. PRPE counteracts several AAPH-induced cytotoxic effects. PRPE prevents morphological changes evaluated by phase contrast microscopy, decreases the number of dying cells determined by counting in the presence of trypan blue and the intracellular ROS overproduction evaluated by flow cytometry after staining with dihydroethidium (DHE). In addition, PRPE tends to normalize the expression of genes (peroxiredoxin 1 (Pdrx1), nuclear factor erythroid 2-related factor 2 (Nrf2), peroxisome proliferator-activator receptor gamma coactivator 1-alpha (Pgc1α)) involved in the oxidant stress defense under ROS exposure. Altogether; our data show that PRPE has potent antioxidant properties and protects C2C12 skeletal muscle cells towards AAPH-induced oxidative stress. These cytoprotective properties of PRPE in skeletal muscle cells submitted to a pro-oxidant environment deserve further investigation in the context of sarcopenia.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"68 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116973590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

HISTOMORPHOLOGICAL RESPONSE OF D-RIBOSE L-CYSTEINE ON KETAMINE-INDUCED TESTICULAR TOXICITY IN ADULT MALE WISTAR RATS d -核糖l -半胱氨酸对氯胺酮致成年雄性wistar大鼠睾丸毒性的组织形态学反应

Redox Experimental Medicine Pub Date : 2023-02-01 DOI: 10.1530/rem-22-0025

O. A. Adedotun, Chidi Chinazo Chukwunenye, Adebanke Faith Balogun, Mojisola Ajoke Olawale, John Olaitan Babatunde, B. Ogunlade

{"title":"HISTOMORPHOLOGICAL RESPONSE OF D-RIBOSE L-CYSTEINE ON KETAMINE-INDUCED TESTICULAR TOXICITY IN ADULT MALE WISTAR RATS","authors":"O. A. Adedotun, Chidi Chinazo Chukwunenye, Adebanke Faith Balogun, Mojisola Ajoke Olawale, John Olaitan Babatunde, B. Ogunlade","doi":"10.1530/rem-22-0025","DOIUrl":"https://doi.org/10.1530/rem-22-0025","url":null,"abstract":"Background: This study aims to study the histomorphological response of D-Ribose-L-Cysteine (DRLC) on ketamine-induced testicular damage in adult male Wistar rats.\u0000\u0000Methods: A total of twenty (20) adult male Wistar rats were used for this experiment. The animals were randomly divided into four groups (A-D) (n=5). Group A served as the control, receiving distilled water as placebo; Group B were administered with 50 mg/ kg bw of Ketamine only; Group C were administered with 50 mg/ kg bw of Ketamine and 30 mg/ kg bw of DRLC; Group D were administered with 30 mg/ kg bw of DRLC only. At the end of the experiment, blood was taken from the heart via cardiac puncture and stored, semen was collected from the caudal epididymis for immediate sperm analysis, while the testes were excised and preserved for histological examination and biochemical analysis.\u0000\u0000Results: The results showed abnormalities marked by a significant decrease in the weights, sperm parameters, as well as antioxidants, serum hormonal levels and abnormal testicular microarchitecture in the rats as a result of Ketamine treatment. However, DRLC exhibits significant quenching effects and attenuating activities on the Ketamine-induced abnormalities by increasing the rats' weights, restoring the sperm parameters, as well as increasing the antioxidants and serum hormonal levels with restored testicular histoarchitecture.\u0000\u0000Conclusion: D-Ribose-L-Cysteine in the current study attenuated the toxic effects of ketamine on the testes, therefore, it could be used as adjuvant therapy for reproductive toxicant-induced testicular toxicity due to its potent antioxidant property.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124849532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Triglyceride peroxidation progression in lipid droplets of hepatocytes in nonalcoholic steatohepatitis 非酒精性脂肪性肝炎肝细胞脂滴甘油三酯过氧化进展

Redox Experimental Medicine Pub Date : 2023-01-23 DOI: 10.1530/rem-22-0024

K. Saito, Y. Matsuoka, M. Abe, Nao Kato, Kazushi Morimoto, Ken‐ichi Yamada

{"title":"Triglyceride peroxidation progression in lipid droplets of hepatocytes in nonalcoholic steatohepatitis","authors":"K. Saito, Y. Matsuoka, M. Abe, Nao Kato, Kazushi Morimoto, Ken‐ichi Yamada","doi":"10.1530/rem-22-0024","DOIUrl":"https://doi.org/10.1530/rem-22-0024","url":null,"abstract":"\u0000\u0000\u0000\u0000\u0000\u0000\u0000\u0000Nonalcoholic steatohepatitis is a chronic liver disease caused by the progression of hepatocellular death and inflammation from simple steatosis. However, the pathogenesis of this disease remains unclear. Lipid peroxidation is one of the most critical factors in the development of nonalcoholic steatohepatitis; however, oxidised lipids – the products of lipid peroxidation – are insufficiently analysed. Here, we comprehensively analysed oxidised lipids in the liver during nonalcoholic steatohepatitis development in a choline-deficient, l-amino acid-defined, high-fat diet-fed mouse model.\u0000\u0000\u0000\u0000Liver from C57BL/6J mice, fed a standard diet or a choline-deficient l-amino acid-defined high-fat diet for 1, 3, or 6 weeks, were collected to evaluate fibrosis, steatosis, inflammation, liver injury, and oxidised lipid production and to observe the suppression of these parameters upon vitamin E administration. In addition, organellar localisation of lipid peroxidation was assessed using fluorescence imaging. Finally, a mitochondria-targeted antioxidant was administered to model mice to investigate the mechanism underlying lipid peroxidation.\u0000\u0000\u0000\u0000We found an accumulation of oxidised triglycerides in the early stages of nonalcoholic steatohepatitis. Furthermore, our data indicate that oxidised triglycerides are generated by lipid peroxidation in lipid droplets due to mitochondria-derived reactive oxygen species.\u0000\u0000\u0000\u0000These results suggest the importance of lipid droplet peroxidation in the progression of nonalcoholic steatohepatitis and may contribute to the development of therapeutic methods for nonalcoholic steatohepatitis in the future.\u0000\u0000\u0000\u0000We demonstrate the specific and early occurrence of lipid peroxidation in nonalcoholic steatohepatitis pathogenesis and propose a previously unknown mechanism of disease progression.\u0000\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126031520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0