Redox Report最新文献_第5页

Emerging roles of hydrogen sulfide-metabolizing enzymes in cancer. 硫化氢代谢酶在癌症中的新作用。

IF 5.2 2区生物学

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-12-06 DOI: 10.1080/13510002.2024.2437338

Alyaa Dawoud, Rana A Youness, Kareem Elsayed, Heba Nafae, Hoda Allam, Hager Adel Saad, Carole Bourquin, Csaba Szabo, Reham Abdel-Kader, Mohamed Z Gad

{"title":"Emerging roles of hydrogen sulfide-metabolizing enzymes in cancer.","authors":"Alyaa Dawoud, Rana A Youness, Kareem Elsayed, Heba Nafae, Hoda Allam, Hager Adel Saad, Carole Bourquin, Csaba Szabo, Reham Abdel-Kader, Mohamed Z Gad","doi":"10.1080/13510002.2024.2437338","DOIUrl":"10.1080/13510002.2024.2437338","url":null,"abstract":"Gasotransmitters play crucial roles in regulating many physiological processes, including cell signaling, cellular proliferation, angiogenesis, mitochondrial function, antioxidant production, nervous system functions and immune responses. Hydrogen sulfide (H2S) is the most recently identified gasotransmitter, which is characterized by its biphasic behavior. At low concentrations, H2S promotes cellular bioenergetics, whereas at high concentrations, it can exert cytotoxic effects. Cystathionine β-synthetase (CBS), cystathionine-γ-lyase (CSE), 3-mercaptopyruvate sulfurtransferase (3-MST), and cysteinyl-tRNA synthetase 2 (CARS2) are pivotal players in H2S biosynthesis in mammalian cells and tissues. The focus of this review is the regulation of the various pathways involved in H2S metabolism in various forms of cancer. Key enzymes in this process include the sulfide oxidation unit (SOU), which includes sulfide:quinone oxidoreductase (SQOR), human ethylmalonic encephalopathy protein 1 (hETHE1), rhodanese, sulfite oxidase (SUOX/SO), and cytochrome c oxidase (CcO) enzymes. Furthermore, the potential role of H2S methylation processes mediated by thiol S-methyltransferase (TMT) and thioether S-methyltransferase (TEMT) is outlined in cancer biology, with potential opportunities for targeting them for clinical translation. In order to understand the role of H2S in oncogenesis and tumor progression, one must appreciate the intricate interplay between H2S-synthesizing and H2S-catabolizing enzymes.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"29 1","pages":"2437338"},"PeriodicalIF":5.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hesperidin activates Nrf2 to protect cochlear hair cells from cisplatin-induced damage 橙皮甙激活Nrf2，保护耳蜗毛细胞免受顺铂诱导的损伤

IF 3.8 2区生物学

Redox Report Pub Date : 2024-04-17 DOI: 10.1080/13510002.2024.2341470

Jintao Lou, Fan Wu, Wuhui He, Rui Hu, Ziyi Cai, Guisheng Chen, Wenji Zhao, Zhigang Zhang, Yu Si

引用次数: 0

Zinc ameliorates acrylamide-induced oxidative stress and apoptosis in testicular cells via Nrf2/HO-1/NfkB and Bax/Bcl2 signaling pathway 锌通过Nrf2/HO-1/NfkB和Bax/Bcl2信号通路改善丙烯酰胺诱导的睾丸细胞氧化应激和凋亡

IF 3.8 2区生物学

Redox Report Pub Date : 2024-04-17 DOI: 10.1080/13510002.2024.2341537

Ayodeji Johnson Ajibare, Adeyemi Fatai Odetayo, Olabode Oluwadare Akintoye, Luqman Aribidesi Olayaki

引用次数: 0

Astaxanthin prevents bone loss in osteoporotic rats with palmitic acid through suppressing oxidative stress 虾青素通过抑制氧化应激防止棕榈酸骨质疏松症大鼠的骨质流失

IF 3.8 2区生物学

Redox Report Pub Date : 2024-04-16 DOI: 10.1080/13510002.2024.2333096

Zhou-Shan Tao, Xing-Jing Wu, Min Yang, Cai-Liang Shen

引用次数: 0

Enhancing the bioavailability and activity of natural antioxidants with nanobubbles and nanoparticles 利用纳米气泡和纳米颗粒提高天然抗氧化剂的生物利用率和活性

IF 3.8 2区生物学

Redox Report Pub Date : 2024-04-05 DOI: 10.1080/13510002.2024.2333619

Miroslav Čolić, Sandra Kraljević Pavelić, Željka Peršurić, Andrea Agaj, Aleksandar Bulog, Krešimir Pavelić

引用次数: 0

Hyperglycemic stress induces oxidative damage of enteric glial cells by triggering redoxosomes/p66SHC activation 高血糖应激通过触发氧化还原体/p66SHC 激活诱导肠胶质细胞氧化损伤

IF 3.8 2区生物学

Redox Report Pub Date : 2024-03-05 DOI: 10.1080/13510002.2024.2324234

Yanmin Jiang, Lan Xu, Xue Zhu, Xiaowei Zhu, Xiang Xu, Jianbo Li

引用次数: 0

Integrated approach to reducing polypharmacy in older people: exploring the role of oxidative stress and antioxidant potential therapy 减少老年人多重药物治疗的综合方法：探索氧化应激和抗氧化潜能疗法的作用

IF 3.8 2区生物学

Redox Report Pub Date : 2023-12-18 DOI: 10.1080/13510002.2023.2289740

Catalina Rojas-Solé, Víctor Pinilla-González, José Lillo-Moya, Tommy González-Fernández, Luciano Saso, Ramón Rodrigo

引用次数: 0

Evaluation of oxidative stress level: reactive oxygen species, reduced glutathione, and D-dimer in patients hospitalized due to COVID-19. COVID-19住院患者氧化应激水平评价:活性氧、还原性谷胱甘肽和d -二聚体

IF 3.8 2区生物学

Redox Report Pub Date : 2023-12-01 Epub Date: 2023-12-02 DOI: 10.1080/13510002.2023.2272384

Claudionei Roessler, Karen Cristine Silva de Oliveira, Auricélia Xavier de Oliveira Portella, Paulo Cezar Nunes Fortes, Franciéle Romero Machado, Stífani Machado Araujo, Marina Prigol, Léia Carolina Lucio, Dalila Moter Benvegnú, Lirane Elize Defante Ferreto

{"title":"Evaluation of oxidative stress level: reactive oxygen species, reduced glutathione, and D-dimer in patients hospitalized due to COVID-19.","authors":"Claudionei Roessler, Karen Cristine Silva de Oliveira, Auricélia Xavier de Oliveira Portella, Paulo Cezar Nunes Fortes, Franciéle Romero Machado, Stífani Machado Araujo, Marina Prigol, Léia Carolina Lucio, Dalila Moter Benvegnú, Lirane Elize Defante Ferreto","doi":"10.1080/13510002.2023.2272384","DOIUrl":"10.1080/13510002.2023.2272384","url":null,"abstract":"Elevated D-dimer levels at hospital admission may also indicate a higher likelihood of progressing to a severe or critical state. This study aimed to assess reactive oxygen species (ROS), non-enzymatic antioxidant reduced glutathione (GSH), and D-dimer levels in COVID-19 patients upon admission, examining their association with mortality outcomes. Data was collected from the medical records of 170 patients hospitalized in a referral hospital unit between March 2020 and December 2021. Patients were divided into two groups: the ward bed group (n = 87), comprising 51% with moderate clinical conditions, and the intensive care unit (ICU) group (n = 83), comprising 49% with severe conditions. The mean age was 59.4 years, with a male predominance of 52.4%. The overall death rate was 43%, with 30.6% in the moderate group and 69.4% in the severe group. The average time from symptom onset to hospitalization was 6.42 days. Results showed that non-survivors had high D-dimer and ROS counts, longer ICU stays, and worse saturation levels at admission. In conclusion, elevated ROS and D-dimer levels may contribute to worse outcomes in critically ill patients, potentially serving as specific and sensitive predictors of poor outcomes upon admission.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"1-6"},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Melittin kills A549 cells by targeting mitochondria and blocking mitophagy flux. 蜂毒素通过靶向线粒体和阻断线粒体自噬通量杀死A549细胞。

IF 3.8 2区生物学

Redox Report Pub Date : 2023-12-01 Epub Date: 2023-12-02 DOI: 10.1080/13510002.2023.2284517

Xuan Li, Zheng Li, Yu-Qi Meng, Hui Qiao, Ke-Rong Zhai, Zhen-Qing Li, Shi-Lin Wei, Bin Li

{"title":"Melittin kills A549 cells by targeting mitochondria and blocking mitophagy flux.","authors":"Xuan Li, Zheng Li, Yu-Qi Meng, Hui Qiao, Ke-Rong Zhai, Zhen-Qing Li, Shi-Lin Wei, Bin Li","doi":"10.1080/13510002.2023.2284517","DOIUrl":"10.1080/13510002.2023.2284517","url":null,"abstract":"Melittin, a naturally occurring polypeptide found in bee venom, has been recognized for its potential anti-tumor effects, particularly in the context of lung cancer. Our previous study focused on its impact on human lung adenocarcinoma cells A549, revealing that melittin induces intracellular reactive oxygen species (ROS) burst and oxidative damage, resulting in cell death. Considering the significant role of mitochondria in maintaining intracellular redox levels and ROS, we further examined the involvement of mitochondrial damage in melittin-induced apoptosis in lung cancer cells. Our findings demonstrated that melittin caused changes in mitochondrial membrane potential (MMP), triggered mitochondrial ROS burst (Figure 1), and activated the mitochondria-related apoptosis pathway Bax/Bcl-2 by directly targeting mitochondria in A549 cells (Figure 2). Further, we infected A549 cells using a lentivirus that can express melittin-Myc and confirmed that melittin can directly target binding to mitochondria, causing the biological effects described above (Figure 2). Notably, melittin induced mitochondrial damage while inhibiting autophagy, resulting in abnormal degradation of damaged mitochondria (Figure 5). To summarize, our study unveils that melittin targets mitochondria, causing mitochondrial damage, and inhibits the autophagy-lysosomal degradation pathway. This process triggers mitoROS burst and ultimately activates the mitochondria-associated Bax/Bcl-2 apoptotic signaling pathways in A549 cells.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"2284517"},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Obstructive sleep apnea promotes the progression of lung cancer by modulating cancer cell invasion and cancer-associated fibroblast activation via TGFβ signaling. 阻塞性睡眠呼吸暂停通过TGFβ信号调节癌细胞侵袭和癌症相关成纤维细胞激活，从而促进肺癌的进展。

IF 3.8 2区生物学

Redox Report Pub Date : 2023-12-01 Epub Date: 2023-11-27 DOI: 10.1080/13510002.2023.2279813

Zhilei Cui, Zhengshang Ruan, Meigui Li, Rongrong Ren, Yizong Ma, Junxiang Zeng, Jinyuan Sun, Wenjing Ye, Weiguo Xu, Xuejun Guo, Dengfei Xu, Linlin Zhang

{"title":"Obstructive sleep apnea promotes the progression of lung cancer by modulating cancer cell invasion and cancer-associated fibroblast activation via TGFβ signaling.","authors":"Zhilei Cui, Zhengshang Ruan, Meigui Li, Rongrong Ren, Yizong Ma, Junxiang Zeng, Jinyuan Sun, Wenjing Ye, Weiguo Xu, Xuejun Guo, Dengfei Xu, Linlin Zhang","doi":"10.1080/13510002.2023.2279813","DOIUrl":"10.1080/13510002.2023.2279813","url":null,"abstract":"Objective: Obstructive sleep apnea (OSA) is associated with severity of pneumonia; however, the mechanism by which OSA promotes lung cancer progression is unclear.Methods: Twenty-five lung cancer patients were recruited to investigate the relationship between OSA and cancer-associated fibroblast (CAFs) activation. Lung cancer cells (A549) and WI38 fibroblast cells were used to explore the hypoxia-induced TGFβ expression using qPCR, Western blot, and ELISA. Wound healing and transwell assays were performed to evaluate cancer cell migration and invasion. A549 or A549-Luc + WI38 xenograft mouse models were established to detect the intermittent hypoxia (IH) associated with lung tumor growth and epithelial-mesenchymal transition (EMT) in vivo.Results: OSA promotes CAF activation and enrichment in lung cancer patients. Hypoxia (OSA-like treatment) activated TGFβ signaling in both lung cancer cells and fibroblasts, which promoted cancer cell migration and invasion, and enriched CAFs. IH promoted the progression and EMT process of lung cancer xenograft tumor. Co-inoculation of lung cancer cells and fibroblast cells could further promote lung cancer progression.Conclusions: IH promotes lung cancer progression by upregulating TGFβ signaling, promoting lung cancer cell migration, and increasing the CAF activation and proportion of lung tumors.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"2279813"},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138446072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0