Oxidative Medicine and Cellular Longevity最新文献

{"title":"Trapping DNA Radicals With DMPO Reduces Hypochlorous Acid-Induced 8-oxo-7,8-dihydro-2'-deoxyguanosine and Mutagenesis in Lung Epithelial Cells.","authors":"C M Lopez, D C Ramirez, S E Gomez Mejiba","doi":"10.1155/omcl/8868348","DOIUrl":"10.1155/omcl/8868348","url":null,"abstract":"<p><p>Pulmonary neutrophilic inflammation (PNI) is the recruitment and activation of neutrophils in the microvasculature with the release of myeloperoxidase (MPO) in the airways. Bystander epithelial cells can take up MPO, where it can generate HOCl. HOCl can react with DNA, generating DNA radicals, which then decay to produce several mutagenic end-oxidation products, such as 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dGuo). Herein, we aimed to test whether HOCl-induced DNA radicals precede DNA oxidation and mutagenesis in A549 human lung epithelial cells as an in vitro model that resembles PNI. Interestingly, by trapping HOCl-induced DNA radicals, the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) blocks the formation of 8-oxo-dGuo and possibly other end-oxidation products, forming DNA-DMPO nitrone adducts. By preventing DNA oxidation, DMPO reduces the mutation of the hypoxanthine phosphoribosyl transferase (<i>hrpt</i>) gene, one of the genes most sensitive to oxidative damage. The transcription factor p53 is known as the master regulator of the cell response to genomic damage. By trapping DNA radicals, DMPO also blocks the translocation of p53 to the cell nucleus, suggesting that by trapping DNA radicals with DMPO, end-oxidation products are prevented, and the cell response to genomic damage is blunted. Trapping DNA radicals to reduce the accumulation of HOCl-induced mutagenic end-oxidation products will provide new therapeutic avenues to reduce genotoxic damage during PNI.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"8868348"},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233070","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}

{"title":"Caffeine, MitoQ, and GABA Prophylaxis of Mitochondrial Dysfunction Induced in Human Pulmonary Cells by Normobaric-Hyperoxia and Hyperbaric-Hyperoxia.","authors":"Tanvir Hossain, Jackson T Secor, David M Eckmann","doi":"10.1155/omcl/5589475","DOIUrl":"10.1155/omcl/5589475","url":null,"abstract":"<p><p>Exposure to hyperoxia lasting either a few days at normobaria or a few hours at hyperbaria induces pulmonary oxygen toxicity. Cellular functional changes resulting from oxygen toxicity include alterations in both mitochondrial dynamics and bioenergetics. The primary goal of this study was to quantify the prophylactic effects of three compounds, caffeine, MitoQ, and γ-aminobutyric acid (GABA), to protect human pulmonary cells in vitro from mitochondrial alterations induced by normobaric- and hyperbaric-hyperoxic conditions. Using cultured lung microvascular and pulmonary artery endothelial cells as well as A549 cells, we examined mitochondrial dynamic and bioenergetics function following exposure to normobaric-hyperoxic (5% CO₂ and 95% O₂ for 72 h) and hyperbaric-hyperoxic (~5% CO₂ equivalent and remainder O₂ at pressure of 4.8 atmosphere absolute (ATA) for 4 h) conditions in the presence of the drugs. Mitochondrial respiration parameters, inner membrane potential, motility, intracellular distribution, and size were measured, along with quantitation of respiration complex levels. Redistribution of intracellular ATP-linked respiration was determined. Comparisons of results were made to controls under normobaric-normoxic conditions. Effects of the drugs under control conditions were also measured. Presence of the drugs resulted in differential effects on hyperoxia-induced alterations in cellular respiration function, stability of mitochondrial potential, and distribution of ATP-linked respiration within the cell. Inclusion of these drugs also produced unique signatures for respiration complex protein levels. Moreso for caffeine than for MitoQ and GABA, its inclusion in the face of hyperoxic exposure served to preserve mitochondrial bioenergetics function, primarily by promoting intracellular redistribution of mitochondrial volume to the perinuclear space. These results indicate a potential role for pharmacologic prophylaxis via therapeutics targeted to support mitochondrial function as a means of protecting the lung from hyperoxia-induced pulmonary cellular oxygen toxicity.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"5589475"},"PeriodicalIF":0.0,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12479159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200504","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}

{"title":"Purple Corn Extract Prevents Doxo-Induced Cardiotoxicity by Counteracting AMPK Activation and p53 Acetylation in HL-1 and Primary Cardiomyocytes.","authors":"Francesca Cappellini, Debora Zorzan, Federica Tomay, Marta Toccaceli, Alessandra Marinelli, Marina Mancini, Annalisa Bucchi, Chiara Tonelli, Katia Petroni","doi":"10.1155/omcl/7786043","DOIUrl":"10.1155/omcl/7786043","url":null,"abstract":"<p><p>Doxorubicin (Doxo) is an anthracycline widely used as a chemotherapeutic agent for many solid and hematological cancers. Its clinical use is limited due to a cumulative dose-dependent and irreversible cardiotoxicity that can cause progressive cardiomyopathy and congestive heart failure. A cardioprotective therapy that can decrease heart damage without reducing the anticancer efficacy during Doxo therapy is of utmost importance. Anthocyanins (ACNs) are renowned cardioprotective agents thanks to their antioxidant and anti-inflammatory properties. An ACN-rich diet from purple corn, which mainly contains cyanidin 3-glucoside (C3G) and its acetylated derivatives, has been previously shown to be effective in reducing Doxo-induced cardiotoxicity in mice. Aiming at unveiling the molecular mechanisms involved in ACN protection, we considered the fibroblast growth factor 21/AMP-activated protein kinase/SIRTUIN1 (FGF21/AMPK/SIRT1)/p53 pathway in murine HL-1 cardiomyocytes treated with Doxo in the presence or absence of purple corn extract (RED). Our work shows that Doxo-induced AMPK activation is restored to control levels by the RED extract. p53 acetylation was increased by the RED extract and upon Sirt1 silencing, indicating that p53 acetylation is SIRT1-dependent and suggesting that the RED extract may affect SIRT1 activity through AMPK. Notably, increased p53 acetylation led to decreased levels of cleaved-caspase 3 and Puma and p21 transcript levels, indicating a reduced level of apoptosis. The RED-induced cardioprotection and p53 acetylation were confirmed in mouse primary cardiomyocytes. In conclusion, the RED extract may prevent cardiomyocytes apoptosis through the modulation of AMPK and acetylation of p53.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"7786043"},"PeriodicalIF":0.0,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12463520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186439","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}

{"title":"RETRACTION: TLR4 Modulates Senescence and Paracrine Action in Placental Mesenchymal Stem Cells via Inhibiting Hedgehog Signaling Pathway in Preeclampsia.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9805286","DOIUrl":"https://doi.org/10.1155/omcl/9805286","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2022/7202837.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9805286"},"PeriodicalIF":0.0,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12446583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113949","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}

{"title":"RETRACTION: Overexpression of hsa_circ_0061817 Can Inhibit the Proliferation and Invasion of Lung Cancer Cells Based on Active Compounds.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9832815","DOIUrl":"https://doi.org/10.1155/omcl/9832815","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2022/4509019.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9832815"},"PeriodicalIF":0.0,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080299","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}

{"title":"Corrigendum to \"circAMOTL1L Suppresses Renal Cell Carcinoma Growth by Modulating the miR-92a-2-5p/KLLN Pathway\".","authors":"","doi":"10.1155/omcl/9898405","DOIUrl":"https://doi.org/10.1155/omcl/9898405","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2021/9970272.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9898405"},"PeriodicalIF":0.0,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207274","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}

{"title":"Suppression of Paclitaxel-Induced Neuropathy and Ovarian Tumor Growth by Mn Porphyrin, MnTnBuOE-2-PyP⁵⁺ (BMX-001).","authors":"Ivan Spasojevic, Zhiqing Huang, Welida Tamires Alves da Silva, Weina Duan, Li Du, Cathleen Chen, Jie Cao, Shasha Zhang, Hannah Lee, Gaomong Lo, Artak Tovmasyan, Huaxin Sheng, Ines Batinic-Haberle, Angeles Alvarez Secord","doi":"10.1155/omcl/6333148","DOIUrl":"10.1155/omcl/6333148","url":null,"abstract":"<p><p>Numerous cellular and animal studies demonstrated the ability of redox-active Mn(III) <i>N</i>-alkyl- and <i>N</i>-alkoxyalkylpyridyporphyrins (MnPs) to protect normal tissue while suppressing tumor growth. The mechanism primarily involves the modulation of NF-кB and Nrf2 signaling pathways via catalysis of MnP/H₂O₂-driven protein thiol oxidation. Such differential protection/suppression effects have paved the way of Mn porphyrins (commonly known as mimics of superoxide dismutase) into clinical trials, therefore introducing new line of therapeutics that are affecting cellular redox status/oxidative stress, rather than specific proteins. The most clinically advanced Mn porphyrin, Mn(III) <i>meso</i>-tetrakis(<i>N</i>-n-butoxyethyl-2-pyridyl) porphyrin (MnTnBuOE-2-PyP⁵⁺, BMX-001) has progressed into five Phase II clinical trials, two of those related to the injuries of central nervous system. Currently, no efficient treatment for chemotherapy-induced neuropathy is available in clinics. We therefore employed BMX-001 to assess its effect on paclitaxel (PTX)-induced neuropathy. Mechanical (Von-Frey filaments) and thermal (hot plate) stimulation, toxicity (body weight), muscular coordination and general physical condition (rotarod) of female CD-1 mice were evaluated over 3 weeks with 2 mg/kg daily dosing and also at clinically relevant dosing of 0.8 mg/kg given subcutaneously (SC) twice weekly after 1.6 mg/kg loading dose. Data revealed a significant ability of BMX-001 to suppress peripheral neuropathy and neuroinflammation. Importantly, while protecting peripheral tissue, BMX-001 suppressed the tumor growth of CAOV2 high-grade serous ovarian cancer in a mouse subcutaneous xenograft model. Previously, the strong anticancer effect was only seen when Mn porphyrins were combined with radiation, chemotherapy, and ascorbate (Asc). Our data further demonstrate that high-grade serous ovarian cancer is the first in vivo cancer thus far studied where redox-active Mn porphyrin, as a single agent, exhibits strong anticancer effect, comparable to that of PTX. The effect is presumably due to high tumor levels of BMX-001 and high oxidative stress specific to the aggressive chemoresistant CAOV2 cell line. Such a strong anticancer effect of BMX-001 would allow for lowering the dosing of PTX and reducing the neuropathy. The combined neuropathy protection and anticancer efficacy demonstrate, therefore, strong therapeutic potential of BMX-001 for gynecological cancers. Moreover, the ability of BMX-001 to suppress neuropathy may be relevant for all types of cancer where chemotherapeutics that induce neuropathy are used as a standard-of-care.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"6333148"},"PeriodicalIF":0.0,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12399357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963764","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}

{"title":"Corrigendum to \"Inhibition of Mitofusin-2 Promotes Cardiac Fibroblast Activation via the PERK/ATF4 Pathway and Reactive Oxygen Species\".","authors":"","doi":"10.1155/omcl/9801041","DOIUrl":"https://doi.org/10.1155/omcl/9801041","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2019/3649808.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9801041"},"PeriodicalIF":0.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12377929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963846","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}

{"title":"RETRACTION: lncRNA PDCD4-AS1 Promotes the Progression of Glioma by Regulating miR-30b-3p/METTL7B Signaling.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9827896","DOIUrl":"https://doi.org/10.1155/omcl/9827896","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2023/3492480.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9827896"},"PeriodicalIF":0.0,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963759","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}

{"title":"RETRACTION: Hydrogen Sulfide Is a Regulator of Hemoglobin Oxygen-Carrying Capacity via Controlling 2,3-BPG Production in Erythrocytes.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9892050","DOIUrl":"https://doi.org/10.1155/omcl/9892050","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2021/8877691.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9892050"},"PeriodicalIF":0.0,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12367383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963783","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}