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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 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-17 DOI: 10.1080/13510002.2024.2341537
Ayodeji Johnson Ajibare, Adeyemi Fatai Odetayo, Olabode Oluwadare Akintoye, Luqman Aribidesi Olayaki
Acrylamide is a toxic substance formed in some foods that require high-temperature cooking processes and has been implicated as a gonadotoxic agent. Zinc, on the other hand, is a known antioxidant ...
丙烯酰胺是一种有毒物质,在一些需要高温烹饪的食物中会形成丙烯酰胺,并被认为是一种性腺毒素。另一方面,锌是一种已知的抗氧化剂 ...
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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 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-16 DOI: 10.1080/13510002.2024.2333096
Zhou-Shan Tao, Xing-Jing Wu, Min Yang, Cai-Liang Shen
The study aimed to assess the role of Astaxanthin (ATX) in palmitic acid(PA) -induced bone loss in Ovariectomized(OVX) rats.In the OVX rat model, we observed that PA affects bone metabolism and acc...
该研究旨在评估虾青素(ATX)在棕榈酸(PA)诱导的卵巢切除(OVX)大鼠骨质流失中的作用。
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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 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-05 DOI: 10.1080/13510002.2024.2333619
Miroslav Čolić, Sandra Kraljević Pavelić, Željka Peršurić, Andrea Agaj, Aleksandar Bulog, Krešimir Pavelić
Objectives: Many polyphenols such as EGCG from green tea, curcumin, apigenin, resveratrol or the alkaloid berberine show in-vitro activity that is much higher than FDA and EU approved drugs. And ye...
目的:许多多酚类物质,如绿茶中的 EGCG、姜黄素、芹菜素、白藜芦醇或生物碱小檗碱,在体外显示出的活性远远高于美国 FDA 和欧盟批准的药物。而且...
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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 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-03-05 DOI: 10.1080/13510002.2024.2324234
Yanmin Jiang, Lan Xu, Xue Zhu, Xiaowei Zhu, Xiang Xu, Jianbo Li
Diabetic gastrointestinal dysfunction (DGD) is a serious complication of diabetic mellitus (DM), affecting the enteric nervous system (ENS), particular enteric glial cells (EGCs). This study aimed ...
糖尿病胃肠功能紊乱(DGD)是糖尿病(DM)的一种严重并发症,会影响肠神经系统(ENS),尤其是肠神经胶质细胞(EGCs)。本研究旨在 ...
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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 Q2 Biochemistry, Genetics and Molecular Biology 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
Increased life expectancy, attributed to improved access to healthcare and drug development, has led to an increase in multimorbidity, a key contributor to polypharmacy. Polypharmacy is characteris...
预期寿命的延长归因于医疗保健服务的改善和药物的开发,这导致了多病症的增加,而多病症是导致多重用药的一个关键因素。多药治疗的特点是...
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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 Q2 Biochemistry, Genetics and Molecular Biology 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

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.

目的:阻塞性睡眠呼吸暂停(OSA)与肺炎严重程度相关;然而,阻塞性睡眠呼吸暂停促进肺癌进展的机制尚不清楚。方法:招募25例肺癌患者,探讨OSA与癌症相关成纤维细胞(CAFs)活化的关系。采用qPCR、Western blot和ELISA检测肺癌细胞(A549)和WI38成纤维细胞缺氧诱导tgf - β的表达。伤口愈合和transwell试验评估癌细胞的迁移和侵袭。建立A549或A549- luc + WI38异种移植小鼠模型,检测体内与肺肿瘤生长和上皮间质转化(EMT)相关的间歇性缺氧(IH)。结果:OSA促进肺癌患者CAF的活化和富集。缺氧(osa样治疗)激活了肺癌细胞和成纤维细胞中的tgf - β信号,促进了癌细胞的迁移和侵袭,并富集了CAFs。IH促进肺癌异种移植瘤的进展和EMT过程。肺癌细胞与成纤维细胞共接种可进一步促进肺癌的进展。结论:IH通过上调tgf - β信号,促进肺癌细胞迁移,增加CAF激活和肺癌肿瘤比例,从而促进肺癌进展。
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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 Q2 Biochemistry, Genetics and Molecular Biology 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

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.

入院时d -二聚体水平升高也可能表明进展到严重或危重状态的可能性更高。本研究旨在评估COVID-19患者入院时的活性氧(ROS)、非酶促抗氧化剂还原性谷胱甘肽(GSH)和d -二聚体水平,并研究它们与死亡率结果的关系。数据收集自2020年3月至2021年12月期间在转诊医院住院的170名患者的医疗记录。患者分为两组:病房组(n = 87),占临床病情中度的51%;重症监护病房(ICU)组(n = 83),占重症的49%。平均年龄59.4岁,男性占52.4%。总死亡率为43%,其中中度组30.6%,重度组69.4%。从出现症状到住院平均时间为6.42 d。结果显示,非幸存者d -二聚体和ROS计数较高,ICU住院时间较长,入院时饱和度较差。总之,ROS和d -二聚体水平升高可能导致危重患者预后较差,可能作为入院时不良预后的特异性和敏感性预测指标。
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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 Q2 Biochemistry, Genetics and Molecular Biology 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

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.

蜂毒素是一种在蜂毒中发现的天然多肽,具有潜在的抗肿瘤作用,特别是在肺癌方面。我们前期的研究主要关注其对人肺腺癌细胞A549的影响,发现蜂毒素可诱导细胞内活性氧(ROS)爆发和氧化损伤,导致细胞死亡。考虑到线粒体在维持细胞内氧化还原水平和ROS中的重要作用,我们进一步研究了线粒体损伤在蜂毒素诱导的肺癌细胞凋亡中的作用。我们的研究结果表明,melittin通过直接靶向A549细胞的线粒体,引起线粒体膜电位(MMP)的变化,触发线粒体ROS爆发(图1),激活线粒体相关凋亡通路Bax/Bcl-2(图2)。此外,我们使用一种表达melittin- myc的慢病毒感染A549细胞,证实了melittin可以直接靶向结合线粒体,引起上述生物学效应(图2)。melittin在抑制自噬的同时诱导线粒体损伤,导致受损线粒体的异常降解(图5)。综上所述,我们的研究揭示了melittin以线粒体为靶点,导致线粒体损伤,抑制自噬-溶酶体降解途径。该过程触发mitoROS破裂,最终激活A549细胞线粒体相关的Bax/Bcl-2凋亡信号通路。
{"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":"<p><p>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.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"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
Investigation of serum ischemic-modified albumin, galectin-3, paraoxonase-1, and myeloperoxidase activity levels in patients with acute brucellosis. 急性布鲁氏菌病患者血清缺血修饰白蛋白、galectin-3、paraoxonase-1 和髓过氧化物酶活性水平的研究。
IF 3.8 2区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-12-01 Epub Date: 2023-12-06 DOI: 10.1080/13510002.2023.2289727
Ahmet Dündar

Objectives: Infection remains current as an important discussion topic in the etiological factors of atherosclerosis. Ischemic-modified albumin (IMA), galectin-3 (gal-3), paraoxonase-1 (PON-1), and myeloperoxidase (MPO) are biomolecules that play an important role in the pathogenesis of atherosclerosis. Our aim is to investigate serum IMA, gal-3, PON-1, and MPO activity in acute brucellosis infection.

Materials and methods: Forty patients with acute brucellosis and 40 healthy individuals were included in the study. Serum IMA, gal-3, PON-1, and MPO activity were analyzed by the ELISA method.

Results: In acute brucellosis infection, serum gal-3, IMA, and MPO activities were found to be significantly increased compared to the control group, and PON-1 activity was found to be significantly decreased compared to the control group (p < 0.001). There was a positive correlation between serum IMA, and MPO activity (r = 0.707 p = 0.000) and a negative correlation (r = -0.943, p = 0.000) between PON-1 activity. There was a positive correlation between serum gal-3 and MPO activity (r = 0.683, p = 0.000) and IMA level (r = 0.927, p = 0.000) and a negative correlation between PON-1 activity (r = -0.951, p = 0.000).Conclusion, it was found that serum gal-3, IMA levels and MPO activity increased, while PON-1 activity decreased. These results showed that the oxidant-anti-oxidant balance is impaired in acute brucellosis infection. In addition, these results indicate that brucella infection may be increase the risk of atherosclerosis. Further studies are needed to support our findings.

目的:目前,感染仍是动脉粥样硬化病因学研究的一个重要课题。缺血修饰白蛋白(IMA)、凝血酶原-3(gal-3)、副氧自由基酶-1(PON-1)和髓过氧化物酶(MPO)是在动脉粥样硬化发病机制中起重要作用的生物大分子。我们的目的是研究急性布鲁氏菌病感染者血清中 IMA、gal-3、PON-1 和 MPO 的活性:研究对象包括 40 名急性布鲁氏菌病患者和 40 名健康人。采用 ELISA 方法分析血清 IMA、gal-3、PON-1 和 MPO 活性:结果:与对照组相比,急性布鲁氏菌病感染者的血清 gal-3、IMA 和 MPO 活性明显升高,而 PON-1 活性则明显降低(p r = 0.707 p = 0.000),且 PON-1 活性与对照组呈负相关(r = -0.943,p = 0.000)。血清 gal-3 与 MPO 活性呈正相关(r = 0.683,p = 0.000),与 IMA 水平呈正相关(r = 0.927,p = 0.000),与 PON-1 活性呈负相关(r = -0.951,p = 0.000)。这些结果表明,急性布鲁氏菌病感染时,氧化-抗氧化平衡受损。此外,这些结果还表明,布鲁氏菌感染可能会增加动脉粥样硬化的风险。我们还需要进一步的研究来支持我们的发现。
{"title":"Investigation of serum ischemic-modified albumin, galectin-3, paraoxonase-1, and myeloperoxidase activity levels in patients with acute brucellosis.","authors":"Ahmet Dündar","doi":"10.1080/13510002.2023.2289727","DOIUrl":"10.1080/13510002.2023.2289727","url":null,"abstract":"<p><strong>Objectives: </strong>Infection remains current as an important discussion topic in the etiological factors of atherosclerosis. Ischemic-modified albumin (IMA), galectin-3 (gal-3), paraoxonase-1 (PON-1), and myeloperoxidase (MPO) are biomolecules that play an important role in the pathogenesis of atherosclerosis. Our aim is to investigate serum IMA, gal-3, PON-1, and MPO activity in acute brucellosis infection.</p><p><strong>Materials and methods: </strong>Forty patients with acute brucellosis and 40 healthy individuals were included in the study. Serum IMA, gal-3, PON-1, and MPO activity were analyzed by the ELISA method.</p><p><strong>Results: </strong>In acute brucellosis infection, serum gal-3, IMA, and MPO activities were found to be significantly increased compared to the control group, and PON-1 activity was found to be significantly decreased compared to the control group (<i>p</i> < 0.001). There was a positive correlation between serum IMA, and MPO activity (<i>r</i> = 0.707 <i>p</i> = 0.000) and a negative correlation (<i>r</i> = -0.943, <i>p</i> = 0.000) between PON-1 activity. There was a positive correlation between serum gal-3 and MPO activity (<i>r</i> = 0.683, <i>p</i> = 0.000) and IMA level (<i>r</i> = 0.927, <i>p</i> = 0.000) and a negative correlation between PON-1 activity (<i>r</i> = -0.951, <i>p</i> = 0.000).Conclusion, it was found that serum gal-3, IMA levels and MPO activity increased, while PON-1 activity decreased. These results showed that the oxidant-anti-oxidant balance is impaired in acute brucellosis infection. In addition, these results indicate that brucella infection may be increase the risk of atherosclerosis. Further studies are needed to support our findings.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138488388","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
Deeper insight into ferroptosis: association with Alzheimer's, Parkinson's disease, and brain tumors and their possible treatment by nanomaterials induced ferroptosis. 更深入地了解铁下垂:与阿尔茨海默病、帕金森病和脑肿瘤的关系,以及纳米材料诱导铁下垂的可能治疗方法。
IF 3.8 2区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-12-01 Epub Date: 2023-11-27 DOI: 10.1080/13510002.2023.2269331
Virendra Kumar Yadav, Nisha Choudhary, Amel Gacem, Rakesh Kumar Verma, Mohd Abul Hasan, Mohammad Tarique Imam, Ziyad Saeed Almalki, Krishna Kumar Yadav, Hyun-Kyung Park, Tathagata Ghosh, Pankaj Kumar, Ashish Patel, Haresh Kalasariya, Byong-Hun Jeon, Hassan Ali AlMubarak

Ferroptosis is an emerging and novel type of iron-dependent programmed cell death which is mainly caused by the excessive deposition of free intracellular iron in the brain cells. This deposited free iron exerts a ferroptosis pathway, resulting in lipid peroxidation (LiPr). There are mainly three ferroptosis pathways viz. iron metabolism-mediated cysteine/glutamate, and LiPr-mediated. Iron is required by the brain as a redox metal for several physiological activities. Due to the iron homeostasis balance disruption, the brain gets adversely affected which further causes neurodegenerative diseases (NDDs) like Parkinson's and Alzheimer's disease, strokes, and brain tumors like glioblastoma (GBS), and glioma. Nanotechnology has played an important role in the prevention and treatment of these NDDs. A synergistic effect of nanomaterials and ferroptosis could prove to be an effective and efficient approach in the field of nanomedicine. In the current review, the authors have highlighted all the latest research in the field of ferroptosis, specifically emphasizing on the role of major molecular key players and various mechanisms involved in the ferroptosis pathway. Moreover, here the authors have also addressed the correlation of ferroptosis with the pathophysiology of NDDs and theragnostic effect of ferroptosis and nanomaterials for the prevention and treatment of NDDs.

铁凋亡是一种新型的铁依赖性程序性细胞死亡,主要是由脑细胞内游离铁的过度沉积引起的。这种沉积的游离铁发挥铁下垂途径,导致脂质过氧化(LiPr)。铁下垂途径主要有铁代谢介导的半胱氨酸/谷氨酸和脂质酶介导的三种。铁作为一种氧化还原金属是大脑进行多种生理活动所必需的。由于铁体内平衡的破坏,大脑受到不利影响,进一步导致神经退行性疾病(ndd),如帕金森病和阿尔茨海默病,中风,脑肿瘤,如胶质母细胞瘤(GBS)和胶质瘤。纳米技术在这些ndd的预防和治疗中发挥了重要作用。纳米材料与铁下垂的协同效应可能是纳米医学领域的一种有效途径。在本文中,作者对铁下垂领域的最新研究进行了综述,重点介绍了铁下垂途径中主要关键分子的作用和各种机制。此外,作者还讨论了铁下垂与ndd的病理生理关系以及铁下垂和纳米材料在ndd预防和治疗中的诊断作用。
{"title":"Deeper insight into ferroptosis: association with Alzheimer's, Parkinson's disease, and brain tumors and their possible treatment by nanomaterials induced ferroptosis.","authors":"Virendra Kumar Yadav, Nisha Choudhary, Amel Gacem, Rakesh Kumar Verma, Mohd Abul Hasan, Mohammad Tarique Imam, Ziyad Saeed Almalki, Krishna Kumar Yadav, Hyun-Kyung Park, Tathagata Ghosh, Pankaj Kumar, Ashish Patel, Haresh Kalasariya, Byong-Hun Jeon, Hassan Ali AlMubarak","doi":"10.1080/13510002.2023.2269331","DOIUrl":"10.1080/13510002.2023.2269331","url":null,"abstract":"<p><p>Ferroptosis is an emerging and novel type of iron-dependent programmed cell death which is mainly caused by the excessive deposition of free intracellular iron in the brain cells. This deposited free iron exerts a ferroptosis pathway, resulting in lipid peroxidation (LiPr). There are mainly three ferroptosis pathways viz. iron metabolism-mediated cysteine/glutamate, and LiPr-mediated. Iron is required by the brain as a redox metal for several physiological activities. Due to the iron homeostasis balance disruption, the brain gets adversely affected which further causes neurodegenerative diseases (NDDs) like Parkinson's and Alzheimer's disease, strokes, and brain tumors like glioblastoma (GBS), and glioma. Nanotechnology has played an important role in the prevention and treatment of these NDDs. A synergistic effect of nanomaterials and ferroptosis could prove to be an effective and efficient approach in the field of nanomedicine. In the current review, the authors have highlighted all the latest research in the field of ferroptosis, specifically emphasizing on the role of major molecular key players and various mechanisms involved in the ferroptosis pathway. Moreover, here the authors have also addressed the correlation of ferroptosis with the pathophysiology of NDDs and theragnostic effect of ferroptosis and nanomaterials for the prevention and treatment of NDDs.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138446071","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
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Redox Report
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