Reactive oxygen species (Apex, N.C.)最新文献

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Reactive Oxygen Species: Methods and Protocols 活性氧:方法和方案
Reactive oxygen species (Apex, N.C.) Pub Date : 2021-01-01 DOI: 10.1007/978-1-0716-0896-8
J. Espada
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引用次数: 1
Reactive Oxygen Species: Network Pharmacology and Therapeutic Applications 活性氧:网络药理学和治疗应用
Reactive oxygen species (Apex, N.C.) Pub Date : 2021-01-01 DOI: 10.1007/978-3-030-68510-2
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引用次数: 9
ROS in 2021: New Look, Same Mission 2021年的ROS:新面貌,同样的使命
Reactive oxygen species (Apex, N.C.) Pub Date : 2021-01-01 DOI: 10.20455/ros.2021.e.801
E. Ros
{"title":"ROS in 2021: New Look, Same Mission","authors":"E. Ros","doi":"10.20455/ros.2021.e.801","DOIUrl":"https://doi.org/10.20455/ros.2021.e.801","url":null,"abstract":"This ROS Editorial outlines several changes and improvements regarding Reactive Oxygen Species (Apex) (ISSN 2380-2367). These include: (1) the Journal’s migration to a new url—rosj.org for improved performance; (2) adoption of a continuous publishing model for timely publishing; and (3) addition of a new section on “Education and Resources” for young ROS researchers.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42985384","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
5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats. 5-甲氧基吲哚-2-羧酸(MICA)不能延缓ZSF1型糖尿病大鼠II型糖尿病的发生和进展
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-05-01 DOI: 10.20455/ros.2020.821
Chun-Yan Li, Wei-Xing Ma, Liang-Jun Yan
{"title":"5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats.","authors":"Chun-Yan Li, Wei-Xing Ma, Liang-Jun Yan","doi":"10.20455/ros.2020.821","DOIUrl":"https://doi.org/10.20455/ros.2020.821","url":null,"abstract":"5-Methoxyindole-2-carboxylic acid (MICA) is a well-established reversible inhibitor of mitochondrial dihydrolipoamide dehydrogenase (DLDH). This chemical, as an indole derivative, has been shown to be neuroprotective against ischemic stroke injury when administered either before or after ischemic stroke in animal models. MICA has also been studied as a potential antidiabetic agent by numerous investigators, though the underlying mechanisms remain sketchy. To attempt to elucidate the mechanisms of its antidiabetic action, we tested the effect of MICA on ZSF1 rat, a widely used rodent model of type 2 diabetes. ZSF1 rats as well as its healthy controls were fed with control diet or MICA-containing diet (200 mg/kg/day) for 9 weeks. Unexpectedly, comparison of body weight changes and blood glucose levels at the end of the 9-week's feeding period indicated that MICA failed to show any anti-diabetic effect in the ZSF1 diabetic rats. The reasons for this failure were discussed.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"9 27 1","pages":"144-147"},"PeriodicalIF":0.0,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42224611","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
5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats. 5-甲氧基吲哚-2-羧酸(MICA)不能延缓ZSF1型糖尿病大鼠II型糖尿病的发生和进展
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-05-01
Chun-Yan Li, Wei-Xing Ma, Liang-Jun Yan
{"title":"5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats.","authors":"Chun-Yan Li,&nbsp;Wei-Xing Ma,&nbsp;Liang-Jun Yan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>5-Methoxyindole-2-carboxylic acid (MICA) is a well-established reversible inhibitor of mitochondrial dihydrolipoamide dehydrogenase (DLDH). This chemical, as an indole derivative, has been shown to be neuroprotective against ischemic stroke injury when administered either before or after ischemic stroke in animal models. MICA has also been studied as a potential antidiabetic agent by numerous investigators, though the underlying mechanisms remain sketchy. To attempt to elucidate the mechanisms of its antidiabetic action, we tested the effect of MICA on ZSF1 rat, a widely used rodent model of type 2 diabetes. ZSF1 rats as well as its healthy controls were fed with control diet or MICA-containing diet (200 mg/kg/day) for 9 weeks. Unexpectedly, comparison of body weight changes and blood glucose levels at the end of the 9-week's feeding period indicated that MICA failed to show any anti-diabetic effect in the ZSF1 diabetic rats. The reasons for this failure were discussed.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"9 27","pages":"144-147"},"PeriodicalIF":0.0,"publicationDate":"2020-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301685/pdf/nihms-1592935.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38055470","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}
引用次数: 0
Relationship between Optical Redox Status and Reactive Oxygen Species in Cancer Cells. 肿瘤细胞光氧化还原状态与活性氧的关系
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-03-01
Allison Podsednik, Annemarie Jacob, Lin Z Li, He N Xu
{"title":"Relationship between Optical Redox Status and Reactive Oxygen Species in Cancer Cells.","authors":"Allison Podsednik,&nbsp;Annemarie Jacob,&nbsp;Lin Z Li,&nbsp;He N Xu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Shifted NAD(H) redox status and enhanced reactive oxygen species (ROS) scavenging systems have been observed in cancers. However, how such redox shift is related to the ROS level in cancer cells is less clear. Based on collecting the intrinsic fluorescence of oxidized flavoproteins (Fp containing flavin adenine dinucleotide) and reduced nicotinamide adenine dinucleotide (NADH), optical redox imaging (ORI) provides a quantitative measure of the mitochondrial redox state by the optical redox ratio, Fp/(NADH+Fp), a surrogate marker of the NAD<sup>+</sup>-coupled redox state NAD<sup>+</sup>/NADH. Our study aims to explore the relationship between NAD(H) redox status and ROS by imaging NADH, Fp, and ROS levels using cultured breast cancer cell models. By manipulating either ROS levels via application of exogenous H<sub>2</sub>O<sub>2</sub> or redox status via metabolic perturbation compounds, we found that: (1) oxidation of NAD(H) redox status correlates with ROS levels at lower H<sub>2</sub>O<sub>2</sub> concentrations (up to ~700 μM), but not necessarily at higher concentrations; (2) an elevated ROS level diminishes NADH and reduces redox ratio plasticity; (3) either more oxidized or more reduced status can correlate to an increased ROS level; and (4) sometimes, a more oxidized status can correlate to a decreased ROS level depending on cell lines. These observations indicated that cellular NAD(H) redox state and ROS are intricately related but can also change separately. This study can benefit cancer research as both NAD(H) redox status and ROS have been implicated in cancer transformation and progression.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"9 26","pages":"95-108"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025870/pdf/nihms-1553211.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37651592","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}
引用次数: 0
Relationship between Optical Redox Status and Reactive Oxygen Species in Cancer Cells. 癌症细胞光学氧化还原状态与活性氧的关系。
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-03-01 DOI: 10.20455/ROS.2020.815
Allison Podsednik, Annemarie Jacob, Lin Z. Li, He N. Xu
{"title":"Relationship between Optical Redox Status and Reactive Oxygen Species in Cancer Cells.","authors":"Allison Podsednik, Annemarie Jacob, Lin Z. Li, He N. Xu","doi":"10.20455/ROS.2020.815","DOIUrl":"https://doi.org/10.20455/ROS.2020.815","url":null,"abstract":"Shifted NAD(H) redox status and enhanced reactive oxygen species (ROS) scavenging systems have been observed in cancers. However, how such redox shift is related to the ROS level in cancer cells is less clear. Based on collecting the intrinsic fluorescence of oxidized flavoproteins (Fp containing flavin adenine dinucleotide) and reduced nicotinamide adenine dinucleotide (NADH), optical redox imaging (ORI) provides a quantitative measure of the mitochondrial redox state by the optical redox ratio, Fp/(NADH+Fp), a surrogate marker of the NAD+-coupled redox state NAD+/NADH. Our study aims to explore the relationship between NAD(H) redox status and ROS by imaging NADH, Fp, and ROS levels using cultured breast cancer cell models. By manipulating either ROS levels via application of exogenous H2O2 or redox status via metabolic perturbation compounds, we found that: (1) oxidation of NAD(H) redox status correlates with ROS levels at lower H2O2 concentrations (up to ~700 μM), but not necessarily at higher concentrations; (2) an elevated ROS level diminishes NADH and reduces redox ratio plasticity; (3) either more oxidized or more reduced status can correlate to an increased ROS level; and (4) sometimes, a more oxidized status can correlate to a decreased ROS level depending on cell lines. These observations indicated that cellular NAD(H) redox state and ROS are intricately related but can also change separately. This study can benefit cancer research as both NAD(H) redox status and ROS have been implicated in cancer transformation and progression.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"9 26 1","pages":"95-108"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49490607","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: 13
Role of Reactive Oxygen Species in the Cytotoxicity of Arsenic Trioxide and Pamidronate for Human Prostate Cancer Cells. 活性氧在三氧化二砷和帕米膦酸钠对人前列腺癌细胞的细胞毒性中的作用。
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-03-01 DOI: 10.20455/ros.2020.811
J. Doroshow, S. Gaur
{"title":"Role of Reactive Oxygen Species in the Cytotoxicity of Arsenic Trioxide and Pamidronate for Human Prostate Cancer Cells.","authors":"J. Doroshow, S. Gaur","doi":"10.20455/ros.2020.811","DOIUrl":"https://doi.org/10.20455/ros.2020.811","url":null,"abstract":"To examine whether combining arsenic trioxide (ARS) and pamidronate (PAM), anticancer drugs that generate reactive oxygen species (ROS), enhanced targeting of redox sensitive growth signals, we studied cloning efficiency, protein tyrosine phosphatase (PTPase) activity, and epidermal growth factor receptor (EGFR) phosphorylation in DU-145 and PC-3 human prostate cancer cells in response to treatment with ARS and/or PAM for 24 h. IC50 concentrations in a clonogenic assay for ARS and PAM were 9 and 20 μM, respectively, in DU-145 cells; and 2 and 12 μM, in PC-3 cells. When combined, ARS and PAM demonstrated additive cytotoxicity in the DU-145 line (combination index [CI] of 1.10) and synergy for PC-3 cells (CI of 0.86). ARS (20 μM for 24 h) inhibited PTPase activity by 36 ± 7 %, p < 0.05 vs. untreated controls, in DU-145 cells; and by 58 ± 8%, p < 0.05, in the PC-3 line. PAM (20 μM for 24 h) decreased PTPase activity by 24 ± 9%, p = 0.06, and 8 ± 1%, p < 0.01, in DU-145 and PC-3 cells, respectively. Combining ARS and PAM significantly inhibited PTPase activity in both cell lines at lower concentrations of each drug. Pretreatment with N-acetyl-L-cysteine reversed ARS- and PAM-induced inhibition of PTPase activity. PTPase inhibition by ARS and/or PAM treatment in both DU-145 and PC-3 cells was associated with prolonged EGFR activation. These experiments demonstrate additive or synergistic cell killing by the ARS/PAM combination in DU-145 or PC-3 cells and suggest that enhanced antitumor activity may be related to alterations in receptor tyrosine kinase signaling that occur, in part, due to ROS-mediated PTPase inhibition.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"9 26 1","pages":"81-94"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46283223","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
Role of Reactive Oxygen Species in the Cytotoxicity of Arsenic Trioxide and Pamidronate for Human Prostate Cancer Cells. 活性氧在三氧化二砷和帕米膦酸钠对人前列腺癌细胞的细胞毒性中的作用。
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-03-01
James H Doroshow, Shikha Gaur
{"title":"Role of Reactive Oxygen Species in the Cytotoxicity of Arsenic Trioxide and Pamidronate for Human Prostate Cancer Cells.","authors":"James H Doroshow, Shikha Gaur","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To examine whether combining arsenic trioxide (ARS) and pamidronate (PAM), anticancer drugs that generate reactive oxygen species (ROS), enhanced targeting of redox sensitive growth signals, we studied cloning efficiency, protein tyrosine phosphatase (PTPase) activity, and epidermal growth factor receptor (EGFR) phosphorylation in DU-145 and PC-3 human prostate cancer cells in response to treatment with ARS and/or PAM for 24 h. IC<sub>50</sub> concentrations in a clonogenic assay for ARS and PAM were 9 and 20 μM, respectively, in DU-145 cells; and 2 and 12 μM, in PC-3 cells. When combined, ARS and PAM demonstrated additive cytotoxicity in the DU-145 line (combination index [CI] of 1.10) and synergy for PC-3 cells (CI of 0.86). ARS (20 μM for 24 h) inhibited PTPase activity by 36 ± 7 %, p < 0.05 vs. untreated controls, in DU-145 cells; and by 58 ± 8%, p < 0.05, in the PC-3 line. PAM (20 μM for 24 h) decreased PTPase activity by 24 ± 9%, p = 0.06, and 8 ± 1%, p < 0.01, in DU-145 and PC-3 cells, respectively. Combining ARS and PAM significantly inhibited PTPase activity in both cell lines at lower concentrations of each drug. Pretreatment with <i>N</i>-acetyl-L-cysteine reversed ARS- and PAM-induced inhibition of PTPase activity. PTPase inhibition by ARS and/or PAM treatment in both DU-145 and PC-3 cells was associated with prolonged EGFR activation. These experiments demonstrate additive or synergistic cell killing by the ARS/PAM combination in DU-145 or PC-3 cells and suggest that enhanced antitumor activity may be related to alterations in receptor tyrosine kinase signaling that occur, in part, due to ROS-mediated PTPase inhibition.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"9 26","pages":"81-94"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182339/pdf/nihms-1580902.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37874809","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}
引用次数: 0
High-Dose Vitamin C for Mortality Reduction in Patients with Sepsis and ARDS 高剂量维生素C对脓毒症和ARDS患者死亡率的降低
Reactive oxygen species (Apex, N.C.) Pub Date : 2020-01-01 DOI: 10.20455/ros.2020.831
{"title":"High-Dose Vitamin C for Mortality Reduction in Patients with Sepsis and ARDS","authors":"","doi":"10.20455/ros.2020.831","DOIUrl":"https://doi.org/10.20455/ros.2020.831","url":null,"abstract":"","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67595290","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
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