Free Radical Research最新文献_第3页

Oxidative imbalance linked to impaired mitochondrial bioenergetics mediates the toxicity of mesoionic compounds MI-D and MI-J in hepatocarcinoma cells (HepG2). 与线粒体生物能量受损相关的氧化失衡介导中离子化合物MI-D和MI-J对肝癌细胞（HepG2）的毒性

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-03-01 Epub Date: 2025-04-01 DOI: 10.1080/10715762.2025.2485219

Ana Paula Perbiche Neves, Fernando Diego Kaziuk, Marília Locatelli Corrêa-Ferreira, Glaucia Regina Martinez, Ester Mazepa, Danilo Sousa-Pereira, Aurea Echevarria, Sheila Maria Brochado Winnischofer, Amanda do Rocio Andrade Pires, Silvia Maria Suter Correia Cadena

{"title":"Oxidative imbalance linked to impaired mitochondrial bioenergetics mediates the toxicity of mesoionic compounds MI-D and MI-J in hepatocarcinoma cells (HepG2).","authors":"Ana Paula Perbiche Neves, Fernando Diego Kaziuk, Marília Locatelli Corrêa-Ferreira, Glaucia Regina Martinez, Ester Mazepa, Danilo Sousa-Pereira, Aurea Echevarria, Sheila Maria Brochado Winnischofer, Amanda do Rocio Andrade Pires, Silvia Maria Suter Correia Cadena","doi":"10.1080/10715762.2025.2485219","DOIUrl":"10.1080/10715762.2025.2485219","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a common and deadly form of liver cancer with limited treatment options for advanced stages. Mesoionic compounds MI-D and MI-J have shown potential for treating HCC due to their significant toxicity to these cells. This study investigated whether this toxicity is linked to their effects on oxidative balance in HepG2 cells cultured in high glucose (HG-glycolysis-dependent) and galactose plus glutamine supplemented (GAL-oxidative phosphorylation-dependent) DMEM medium. ROS levels were increased in cells cultured in both media when exposed to MI-D and MI-J (50 μM). However, MI-D at an intermediate concentration (25 μM) decreased ROS levels in the GAL medium. Superoxide dismutase (SOD) activity increased under all tested conditions by compounds (25 μM). Conversely, MI-D and MI-J decreased total peroxidase activity in both media at 25 and 50 μM, respectively. MI-D in the HG medium decreased glutathione peroxidase (GPX) activity, whereas MI-J reduced the enzyme activity at a concentration of 25 μM and increased it at 50 μM. In the GAL medium, MI-J (50 μM) increased GPx activity, while glutathione reductase (GR) activity was decreased by the compounds (50 μM) in both media. Furthermore, the P-AMPK/tAMPk ratio was increased by MI-J at 25 μM in the GAL medium. Our results show that MI-D and MI-J caused oxidative imbalance, particularly affecting cells cultured in the GAL medium. The data also support that the mesoionic effects depended on their concentration and substituent in the mesoionic ring.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"308-320"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Down-regulation of Selenoprotein K impairs the proliferation and differentiation of chicken skeletal muscle satellite cells by inhibiting the Nrf2 antioxidant signaling pathway. 硒蛋白K的下调通过抑制Nrf2抗氧化信号通路影响鸡骨骼肌卫星细胞的增殖和分化。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-03-01 Epub Date: 2025-02-26 DOI: 10.1080/10715762.2025.2470900

Xue-Wei Chen, Yue Li, Yi-Tong Fu, Wan-Xue Xu, Jie Yang, Xue Wen, Rui-Feng Fan

{"title":"Down-regulation of Selenoprotein K impairs the proliferation and differentiation of chicken skeletal muscle satellite cells by inhibiting the Nrf2 antioxidant signaling pathway.","authors":"Xue-Wei Chen, Yue Li, Yi-Tong Fu, Wan-Xue Xu, Jie Yang, Xue Wen, Rui-Feng Fan","doi":"10.1080/10715762.2025.2470900","DOIUrl":"10.1080/10715762.2025.2470900","url":null,"abstract":"Skeletal muscle satellite cells (SMSCs) are pivotal for skeletal muscle regeneration post-injury, and their development is intricately influenced by regulatory factors. Selenoprotein K (SELENOK), an endoplasmic reticulum resident selenoprotein, is known for its crucial role in maintaining skeletal muscle redox sensing. However, the specific molecular mechanism of SELENOK in SMSCs remains unclear. In this study, a SELENOK knockdown model was established to delve into its role in SMSCs. The results revealed that SELENOK knockdown hindered SMSCs proliferation and differentiation, as evidenced by the regulation of key proteins such as Pax7, Myf5, CyclinD1, MyoD, and Myf6, and the inhibitory effects were mitigated by N-Acetyl-l-cysteine (NAC). SELENOK knockdown induced oxidative stress, further analyses uncovered that SELENOK knockdown downregulated nuclear transcription factor nuclear erythroid factor 2-like 2 (Nrf2) protein expression while upregulating cytoplasmic kelch-like ECH-associated protein 1 (Keap1) protein expression. SELENOK knockdown impeded Nestin and sequestosome 1/p62 (p62) interaction with Keap1, leading to increased Nrf2 ubiquitination. This prevented Nrf2 transportation from cytoplasm to nucleus mediated by Keap1, ultimately resulting in the downregulation of catalase (CAT), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (GPX4) protein expression. Notably, SELENOK knockdown-induced inhibition of SMSCs proliferation and differentiation was alleviated by Oltipraz, an activator of the Nrf2 pathway. This study provided novel insights, demonstrating that SELENOK is a key player in SMSCs proliferation and differentiation by influencing the Nrf2 antioxidant signaling pathway.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"215-225"},"PeriodicalIF":3.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Involvement of iron ions in 6-hydroxydopamine-induced disruption of intracellular copper metabolism. 铁离子参与6-羟多巴胺诱导的细胞内铜代谢的破坏。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-15 DOI: 10.1080/10715762.2025.2465276

Ami Kato, Ayano Tani, Fuka Kamijo, Tomohiro Otsuka, Tetsuro Kamiya, Hirokazu Hara

{"title":"Involvement of iron ions in 6-hydroxydopamine-induced disruption of intracellular copper metabolism.","authors":"Ami Kato, Ayano Tani, Fuka Kamijo, Tomohiro Otsuka, Tetsuro Kamiya, Hirokazu Hara","doi":"10.1080/10715762.2025.2465276","DOIUrl":"10.1080/10715762.2025.2465276","url":null,"abstract":"Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. Recently, disorders in metabolism of metals, including copper (Cu) and iron (Fe), have been reported to be linked to the pathogenesis of PD. We previously demonstrated that 6-hydoroxydopamine (6-OHDA), a neurotoxin used for the production of PD model animals, decreases Atox1, a Cu chaperone, and ATP7A, a Cu transporter, and disrupts intracellular Cu metabolism in human neuroblastoma SH-SY5Y cells. However, the exact mechanisms remain unclear. Meanwhile, intracellular Fe modulates 6-OHDA-induced cellular responses. In this study, we investigated whether Fe participates in 6-OHDA-induced abnormality in Cu metabolism. 6-OHDA-induced reactive oxygen species (ROS) production and cellular injury were suppressed by Fe chelators, deferoxamine and 2,2'-bipyridyl (BIP). These chelators also restored 6-OHDA-induced degradation of Atox1 and ATP7A proteins and subsequent Cu accumulation, indicating that intracellular Fe is involved in the disruption of Cu homeostasis associated with 6-OHDA. Atox1 has redox-sensitive cysteine (Cys) residues in its Cu-binding site. The Cys residues of Atox1 were oxidized by 6-OHDA, and BIP suppressed their oxidation. Moreover, the replacement of Cys with histidine in the Cu-binding site conferred resistance to 6-OHDA-induced Atox1 degradation. These results suggest that oxidized modification of Atox1 by 6-OHDA is likely to accelerate its degradation. Thus, we conclude that Fe and Cu metabolisms are closely related to each other in the pathogenesis of PD.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"129-137"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metformin ameliorates gestational diabetes mellitus via inhibiting ferroptosis of trophoblasts through the Nrf2/HO-1 signaling pathway. 二甲双胍通过Nrf2/HO-1信号通路抑制滋养细胞铁下垂，改善妊娠期糖尿病。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-19 DOI: 10.1080/10715762.2025.2468737

Lingya Fang, Sha Lu, Liuyuan Fang, Junxin Yu, Nisile Kakongma, Wensheng Hu

{"title":"Metformin ameliorates gestational diabetes mellitus via inhibiting ferroptosis of trophoblasts through the Nrf2/HO-1 signaling pathway.","authors":"Lingya Fang, Sha Lu, Liuyuan Fang, Junxin Yu, Nisile Kakongma, Wensheng Hu","doi":"10.1080/10715762.2025.2468737","DOIUrl":"10.1080/10715762.2025.2468737","url":null,"abstract":"Both mothers and infants experience oxidative stress due to gestational diabetes mellitus (GDM), which is strongly associated with adverse pregnancy outcomes. Ferroptosis, a novel form of programmed cell death characterized by iron-dependent lipid peroxidation, is believed to play a critical role in the pathogenesis and progression of GDM. Metformin (MET) has shown potential in alleviating oxidative stress; however, research on its specific mechanisms of action in GDM remains limited. We collected placental tissues from GDM patients and healthy controls and established an in vitro GDM cell model. We measured markers of ferroptosis including malondialdehyde (MDA), glutathione (GSH), and glutathione peroxidase 4 (GPX4) activity. Additionally, we evaluated reactive oxygen species (ROS) levels, apoptosis, cell viability, and migration in the cell model. Our findings revealed significant changes in the GDM group compared to controls, including increased MDA and GSSG levels, decreased GSH levels, and reduced expression of GPX4 protein in the GDM placenta. High-glucose (HG) conditions were shown to reduce trophoblast cell viability and migration, accompanied by elevated ROS and MDA levels, as well as reduced expression of GSH, GPX4, Nrf2, and HO-1 proteins. Importantly, treatment with MET reversed these effects, similar to the action of deferoxamine mesylate (DFOM), a known ferroptosis inhibitor. These results confirm the occurrence of ferroptosis in the placentas of GDM patients and demonstrate that MET mitigates high-glucose-induced ferroptosis in trophoblasts through the Nrf2/HO-1 signaling pathway. This study provides novel insights into the protective mechanisms of MET, offering potential therapeutic strategies for GDM. management.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"190-203"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gold nanoparticles-supported iron oxide particles endows bone scaffolds with anti-tumor function. 金纳米颗粒-氧化铁颗粒赋予骨支架抗肿瘤功能。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-18 DOI: 10.1080/10715762.2025.2466246

Tiantian He, Wenjing Yang, Youwen Yang, Shuping Peng, Cijun Shuai

{"title":"Gold nanoparticles-supported iron oxide particles endows bone scaffolds with anti-tumor function.","authors":"Tiantian He, Wenjing Yang, Youwen Yang, Shuping Peng, Cijun Shuai","doi":"10.1080/10715762.2025.2466246","DOIUrl":"10.1080/10715762.2025.2466246","url":null,"abstract":"Iron oxide (Fe-O) has anti-tumor properties, due to its ability of catalyzing hydrogen peroxide (H2O2) of tumor cells to generate reactive oxygen species (ROS) and then cause ferroptosis. Its anti-tumor performance is restricted due to insufficient H2O2 in tumor cells. A nanomedicine, Au nanoparticles (NPs) grown on Fe-O, was integrated into poly-l-lactide (PLLA) scaffolds. Results indicated that Au NPs could consume glucose of tumor cells to produce H2O2, which supplemented reaction substrate. PLLA/Au@Fe-O scaffold showed enhanced anti-tumor activities against MG63, including increased mortality, decreased migration and colony formation. PLLA/Au@Fe-O scaffold promoted ferroptosis in MG63, including up-regulation of COX-2 protein, down-regulation of FTH1 protein and GPX4 protein. PLLA/Au@Fe-O scaffold also promoted autophagy in MG63, including down-regulation of P62 protein, and up-regulation of LC3BII/I. Mechanistically, PLLA/Au@Fe-O scaffold possessed enhanced anti-tumor activities through promoting ferroptosis and autophagy.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"169-182"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hyper-energy metabolism of oxidative phosphorylation and enhanced glycolysis contributes to radioresistance in glioma cells. 氧化磷酸化的高能量代谢和糖酵解的增强有助于胶质瘤细胞的辐射抗性。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-01-28 DOI: 10.1080/10715762.2025.2456740

Yogesh Rai, Ankit Kumar Tiwari, Rakesh Pandey, B S Dwarakanath, Anant Narayan Bhatt

{"title":"Hyper-energy metabolism of oxidative phosphorylation and enhanced glycolysis contributes to radioresistance in glioma cells.","authors":"Yogesh Rai, Ankit Kumar Tiwari, Rakesh Pandey, B S Dwarakanath, Anant Narayan Bhatt","doi":"10.1080/10715762.2025.2456740","DOIUrl":"10.1080/10715762.2025.2456740","url":null,"abstract":"The concept of dual-state hyper-energy metabolism characterized by elevated glycolysis and OxPhos has gained considerable attention during tumor growth and metastasis in different malignancies. However, it is largely unknown how such metabolic phenotypes influence the radiation response in aggressive cancers. Therefore, the present study aimed to investigate the impact of hyper-energy metabolism (increased glycolysis and OxPhos) on the radiation response of a human glioma cell line. Modulation of the mitochondrial electron transport chain was carried out using a 2,4-dinitrophenol (DNP). Metabolic characterization was carried out by assessing glucose uptake, lactate production, mitochondrial mass, membrane potential, and ATP production. The radiation response was examined by cell growth, clonogenic survival, and cell death assays. Macromolecular oxidation was assessed by DNA damage, lipid peroxidation, and protein carbonylation assay. Hypermetabolic OPM-BMG cells exhibited a significant increase in glycolysis and OxPhos following irradiation as compared to the parental BMG-1 cells. Enhanced radioresistance of OPM-BMG cells was evidenced by the increase in α/β ratio (9.58) and D1 dose (4.18 Gy) as compared to 4.36 and 2.19 Gy in BMG-1 cells respectively. Moreover, OPM-BMG cells were found to exhibit increased resistance against radiation-induced cell death, and macromolecular oxidation as compared to BMG-1 cells. Inhibition of glycolysis and mitochondrial complex-II significantly enhanced the radiosensitivity of OPM-BMG cells compared to BMG-1 cells. Our results demonstrate that the hyper-energy metabolism of increased glycolysis and OxPhos confer radioresistance. Consequently targeting glycolysis and OxPhos in combination with radiation may overcome therapeutic resistance in aggressive cancers like glioma.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"117-128"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nitric oxide is an irreversible human diamine oxidase inhibitor. 一氧化氮是一种不可逆的人二胺氧化酶抑制剂。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-03-08 DOI: 10.1080/10715762.2025.2465277

Felix Kosta, Elisabeth Gludovacz, Rudolf Figl, Nicole Borth, Bernd Jilma, Thomas Boehm

{"title":"Nitric oxide is an irreversible human diamine oxidase inhibitor.","authors":"Felix Kosta, Elisabeth Gludovacz, Rudolf Figl, Nicole Borth, Bernd Jilma, Thomas Boehm","doi":"10.1080/10715762.2025.2465277","DOIUrl":"10.1080/10715762.2025.2465277","url":null,"abstract":"Diamine oxidase (DAO) histamine-degradation rates are compromised in plasma of mastocytosis patients during severe mast cell activation events. Mast cell-liberated histamine induces the release of nitric oxide (NO) close to DAO extracellular storage sites. We hypothesized that NO inhibits DAO activity. Recombinant human DAO activity was measured after incubation with NO-releasing NONOates (R1R2N-(NO-)-N = O). Topaquinone reactivity was quantified by absorption measurements and by mass spectrometry. Several murine models of NO-production were assessed for DAO activity inhibition in vivo. Nitric oxide released from NONOates dose dependently and irreversibly inhibited DAO activity. The NO scavengers Trolox (Vitamin E derivative) and 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (C-PTIO), the reversible DAO inhibitors diminazene and ciproxifan, the substrates histamine (EC50 = 32 µM) and putrescine (EC50 = 39 µM), heparin whole blood and plasma protected DAO from inhibition. Nitric oxide reduced the reactivity of topaquinone to phenylhydrazine by 90%. None of the NO producing in vivo models showed DAO inhibition in plasma or tissue. Nitric oxide is a potent irreversible DAO inhibitor in vitro representing the first discovered natural inhibitor for this enzyme. Endogenous mouse DAO inhibition in vivo could not be demonstrated. The true nature of human DAO activity inhibition during severe mastocytosis events remains unknown.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"138-151"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tetrahydrocurcumin exhibits neuroprotective effects by inhibiting neuron ferroptosis via activity of iPLA2β/p38 MAPK phosphorylation in rat TBI model. 在大鼠TBI模型中，四氢姜黄素通过iPLA2β/p38 MAPK磷酸化活性抑制神经元铁凋亡，显示出神经保护作用。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-19 DOI: 10.1080/10715762.2025.2465282

Yonghong Bi, Lan Luo, Pengyu Duan, Zhehao Jin, Xiaoqian Zhang, Guanghui He, Xiaoyan Li, Weiyu Feng, Bing Zhang

{"title":"Tetrahydrocurcumin exhibits neuroprotective effects by inhibiting neuron ferroptosis via activity of iPLA2β/p38 MAPK phosphorylation in rat TBI model.","authors":"Yonghong Bi, Lan Luo, Pengyu Duan, Zhehao Jin, Xiaoqian Zhang, Guanghui He, Xiaoyan Li, Weiyu Feng, Bing Zhang","doi":"10.1080/10715762.2025.2465282","DOIUrl":"10.1080/10715762.2025.2465282","url":null,"abstract":"Ferroptosis characterized by iron-dependent lipid peroxidation induced by traumatic brain injury (TBI) is an important factor that aggravates diseases. Studies have shown that tetrahydrocurcumin (THC) has neuroprotective effects in brain injury. However, whether THC inhibits neurocyte ferroptosis after TBI and its mechanism remains unclear. To investigate this, a weight-drop model in rats and H2O2 induced oxidative stress model in SH-SY5Y cells were established, and THC was used for treatment. Immunohistochemical staining showed that iron deposition reached its peak at 8th day after TBI. We found that THC remarkably inhibited iron accumulation in the cortical cortex and corpus callosum, improved neurological damage, reduced acute cerebral edema, weight loss, oxidative stress, and inflammation. Furthermore, the activity of iPLA2β was significantly reduced, and phosphorylation of p38 was increased after TBI, while THC alleviated the decrease in iPLA2β activity and increase in the level of P-p38. It confirmed that THC effectively mitigated ferroptosis, while iPLA2β inhibitor s-BEL could reverse the effects of THC on ferroptosis in vivo and in vitro experiments. In addition, SB202190 which is an inhibitor of p38 could enhance THC protection and lessen formation of ferroptosis-related proteins in cells. In conclusion, these findings suggested that THC may promote neurological function recovery after TBI by inhibiting neuron ferroptosis via activity of iPLA2β/P-p38.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"152-168"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Carboxymethylnaringenin: a promising antioxidant in the aqueous physiological environment. 羧甲基柚皮素：一种在水生理环境中很有前途的抗氧化剂。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-02-01 Epub Date: 2025-02-14 DOI: 10.1080/10715762.2025.2466685

Quan V Vo, Nguyen Thi Hoa, Adam Mechler

{"title":"Carboxymethylnaringenin: a promising antioxidant in the aqueous physiological environment.","authors":"Quan V Vo, Nguyen Thi Hoa, Adam Mechler","doi":"10.1080/10715762.2025.2466685","DOIUrl":"10.1080/10715762.2025.2466685","url":null,"abstract":"The synthetic naringenin derivative (2S)-8-carboxymethylnaringenin (CMN) was developed for the treatment of bacterial and viral respiratory infections. There are indications that CMN may act as an antioxidant, however, no studies have been conducted in this regard. This work is aimed at assessing the antiradical capacity of CMN against various physiologically relevant species in physiological environments by using thermodynamic and kinetic calculations. According to the results, CMN only exhibits modest HOO• antiradical activity in lipid medium, modeled here as pentyl ethanoate solvent, with an overall rate constant (koverall) of 2.01 × 102 M-1 s-1. However, significant antiradical activity is predicted for the aqueous medium (koverall = 2.60 × 105 M-1s-1) that is equivalent to the activity of the reference antioxidant Trolox. In a screen performed on a range of radicals, HO•, NO2, SO4•-, N3•, CH3O•, CCl3O•, CH3OO•, and CCl3OO• were also successfully scavenged by CMN in water at physiological pH. Therefore, other than a potent drug, CMN is also a good antioxidant in polar environments.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"183-189"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of repeated sprint training in hypoxia on acute and chronic redox balance modulation. 缺氧条件下重复短跑训练对急慢性氧化还原平衡调节的影响。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-22 DOI: 10.1080/10715762.2024.2443609

M Chambion-Diaz, R Faiss, V Pialoux, G P Millet

{"title":"Effect of repeated sprint training in hypoxia on acute and chronic redox balance modulation.","authors":"M Chambion-Diaz, R Faiss, V Pialoux, G P Millet","doi":"10.1080/10715762.2024.2443609","DOIUrl":"10.1080/10715762.2024.2443609","url":null,"abstract":"Little is known regarding the effects high-intensity training performed in hypoxia on the oxidative stress and antioxidant systems. The aim of this study was to assess the potential effect of 4 weeks of repeated sprint training in hypoxia (RSH) on the redox balance. Forty male well-trained cyclists were matched into two different interventions (RSH, n = 20) or in normoxia, RSN, n = 20) and tested twice (before (Pre-) and after (Post-) a 4-week of training) for performance (repeated sprint ability (RSA) test), oxidative stress, and antioxidant status. Antioxidant enzyme activity (Superoxide Dismutase, Glutathione Peroxidase, and catalase), NO metabolites (NOx: nitrites and nitrates), ferric reducing antioxidant power, Malondialdehyde (MDA), nitrotyrosine, and carbonyls were measured in plasma. At Post-, MDA, and carbonyls increased (p < 0.05) in the RSN group both at rest (+90.6%) and also acutely in response to RSA (+22.9%); but not in RSH. At Post-, in the RSH group, catalase increased (p < 0.05) both at rest (+44.7%) and in response to the RSA test (+66.3%). At Post-, SOD, and nitrotyrosine decreased after RSA and at rest, regardless of the group (p = 0.0012 and p = 0.0413, respectively). At Post-, NOx decreased after the RSA test, regardless of the group (p < 0.05). In conclusion, several weeks of RSH training limits the increase in oxidative stress markers both at rest and in response to RSA test. Moreover, such training downregulated SOD activity, possibly due to an overproduction of reactive oxygen species. These findings could constitute a paradigm shift with a better enzymatic adaptation after RSH concomitant with a distinct reactive oxygen species (ROS) production between RSH and RSN.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"1-8"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0