Antioxidants最新文献

{"title":"Single and Combined Effects of Polystyrene Nanoplastics and Dibutyl Phthalate on Hybrid Snakehead (<i>Channa maculata</i> ♀ × <i>Channa argus</i> ♂).","authors":"Mi Ou, Ziwen Yang, Yuntao Lu, Yang Zhang, Yang Zou, Yueying Deng, Yuandong Sun, Haiyang Liu, Qing Luo, Shuzhan Fei, Kunci Chen, Dandan Gao, Jian Zhao","doi":"10.3390/antiox14091084","DOIUrl":"10.3390/antiox14091084","url":null,"abstract":"<p><p>The ecological impact of microplastic pollution in freshwater ecosystems has received growing scientific attention, although research on freshwater species remains limited compared to marine organisms. This study investigates the individual and combined toxicological impacts of polystyrene nanoparticles (PSNPs) and dibutyl phthalate (DBP) on hybrid snakehead (<i>Channa maculata</i> ♀ × <i>Channa argus</i> ♂), a commercially important freshwater fish. PSNPs inhibited growth, induced hepatic and intestinal lesions, and delayed ovarian development, co-exposure with DBP exacerbated these effects. qPCR analysis revealed significant up-regulation of inflammation-related genes in the liver but inhibitory effects in the intestines, indicating that PSNPs and DBP provoke immune modulation and systemic pro-inflammatory responses. Furthermore, PSNPs and DBP induced oxidative damage in the liver and intestines by affecting antioxidant enzyme activity. 16S rRNA sequencing revealed that PSNPs and DBP altered intestinal microbiota composition, particularly reducing Proteobacteria abundance. Correlation analyses indicated negative associations between the abundances of Proteobacteria and Firmicutes and antioxidant parameters (SOD and MDA), suggesting microbiota-mediated impacts on host metabolism and physiological health. These findings highlight the ecological threat of microplastics and phthalates in freshwater environments and underscore the need for targeted conservation strategies.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review of the Potential Use of Antioxidants in Spinal Cord Injuries.","authors":"Agnieszka Nowacka, Maciej Śniegocki, Ewa Ziółkowska","doi":"10.3390/antiox14091081","DOIUrl":"10.3390/antiox14091081","url":null,"abstract":"<p><p>Spinal cord injury (SCI) is a debilitating neurological condition marked by primary mechanical damage followed by a complex secondary injury cascade, in which oxidative stress plays a central role. Mitochondrial dysfunction, ionic imbalance, and inflammatory responses drive excessive generation of reactive oxygen and nitrogen species, leading to lipid peroxidation, protein and DNA damage, apoptosis, and progressive neurological impairment. Antioxidant-based therapies have emerged as promising neuroprotective strategies, with compounds such as A91 peptide, curcumin, edaravone, ginsenosides, and glutathione demonstrating preclinical efficacy in reducing oxidative damage, restoring redox balance, modulating signaling pathways (e.g., Nrf2, NF-κB, MAPK, PI3K/Akt), and enhancing neuronal survival. While therapeutic outcomes depend on injury severity, timing, and combinatorial approaches, translating these findings into clinical practice and integrating antioxidants with cell-based therapies, biomaterials, and rehabilitation offers a critical avenue for improving functional recovery in SCI.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electrochemical Measures for Determining the Total Antioxidant Capacity of Açaí Pulp (<i>Euterpe oleracea</i>) at a Glassy Carbon Electrode.","authors":"Tabata N Feijoó, Luis D Loor-Urgilés, Danyelle M de Araújo, Elisama V Dos Santos, Marília Oliveira Fonseca Goulart, Carlos A Martínez-Huitle","doi":"10.3390/antiox14091082","DOIUrl":"10.3390/antiox14091082","url":null,"abstract":"<p><p>Antioxidants, such as flavonoids, are influential secondary metabolites that play a significant role in regulating human health. Açaí, known for its potent antioxidant properties, has gained popularity in the nutritional field. However, there is a need for accurate methods to quantify its antioxidant capacity. Therefore, the goal of this investigation was to determine the total antioxidant capacity of frozen açaí pulp by applying the concept of the electrochemical quantitative index (EQI) using the cyclic voltammetry technique. The electrochemical response of ethanolic extracts obtained by a nonconventional ultrasound bath was investigated in the anodic region. The results clearly showed redox behavior at +0.37 V and +0.27 V (vs. Ag/AgCl) for the anodic and cathodic peaks, respectively, when evaluated by cyclic voltammetry at a glassy carbon (GC) electrode. By investigating a constant ethanolic extract concentration (0.2%) and analyzing the scan rate and supporting electrolyte effects, it was determined that the frozen açaí pulp extract presented an EQI of about 2.3 µA/V. Similarly, the concept of the EQI was extended to the use of the differential pulse voltammetry profile of a 0.2% ethanolic açaí extract on different supporting electrolytes, which showed that some experimental conditions needed improvement. Still, maintaining pH with a buffer solution in the anodic region is crucial to ensure reproducibility. The antioxidant capacity was also determined using the 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical assay to compare the electrochemical results. The Folin-Ciocalteu colorimetric test was applied to determine the total phenolic content of the extract.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Importance of Multifaceted Approach for Accurate and Comprehensive Evaluation of Oxidative Stress Status in Biological Systems.","authors":"Borut Poljšak, Polona Jamnik, Irina Milisav","doi":"10.3390/antiox14091083","DOIUrl":"10.3390/antiox14091083","url":null,"abstract":"<p><p>Oxidative stress is caused by an imbalance between the formation of reactive oxygen species (ROS) and the activity of antioxidant defense system, which disrupts redox signaling and causes molecular damage. While there are numerous methods to measure oxidative stress, the complex and dynamic nature of ROS production and antioxidant reactions requires a multi-faceted approach. Direct methods such as electron spin resonance (ESR) and fluorescent probes measure ROS directly but are limited by the short lifespan of certain species. Indirect methods such as lipid peroxidation markers (e.g., malondialdehyde, MDA), protein oxidation (e.g., carbonyl content), and DNA damage (e.g., 8-oxo-dG) provide information on oxidative damage, but they do not capture the real-time dynamics of ROS. The antioxidant defense system, which includes enzymatic components such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), further complicates assessment, as it responds dynamically to oxidative challenges. Furthermore, the compartmentalized nature of ROS production in organelles and tissues coupled with the temporal variability of oxidative damage and repair underscores the need to integrate multiple assessment methods. This commentary highlights the limitations of using single assays and emphasizes the importance of combining complementary techniques to achieve a comprehensive assessment of oxidative stress. A multi-method approach ensures accurate identification of ROS dynamics, antioxidant responses, and the extent of oxidative damage, providing crucial insights into redox biology and its impact on health and disease.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing Mitochondrial Function for Post-Stroke Rehabilitation: Unlocking Antioxidant Power.","authors":"Gabriela Olaru, Ana-Maria Buga, Raluca Elena Sandu, Vlad Padureanu, Dragos George Popa, Daniela Calina","doi":"10.3390/antiox14091080","DOIUrl":"10.3390/antiox14091080","url":null,"abstract":"<p><p>Post-stroke rehabilitation has evolved to encompass advanced approaches that aim to optimize recovery for ischemic stroke survivors. Despite this progress, recovery remains limited, partly due to persistent oxidative stress and mitochondrial dysfunction that contribute to neuronal and muscular impairment. One such promising avenue is the stimulation of antioxidant capacity and the enhancement of mitochondrial function. Mitochondria are crucial for energy production and neuroprotection, which are essential for neurorecovery. This review explores the mechanisms involved in the role of mitochondrial function and antioxidant therapies, focusing on motor recovery after ischemic stroke and \"brain-muscle axis\" interplay in post-stroke rehabilitation. A comprehensive synthesis of clinical trial data is provided, highlighting interventions targeting mitochondrial bioenergetics, redox regulation, and mitochondrial dynamics. Furthermore, the review delves into the potential of recent mitochondrial-targeted therapies as adjuncts to traditional rehabilitation techniques, providing a more holistic approach to recovery. Emerging evidence suggests these therapies can reduce oxidative injury and support neuroplasticity; however, translation into consistent clinical benefit remains uncertain due to heterogeneity in study designs, endpoints, and patient populations. By understanding and leveraging the dynamics of mitochondrial function, healthcare providers can significantly enhance the rehabilitation outcomes for people with a range of conditions, from musculoskeletal disorders to neurological impairments.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling Wound Healing Properties of Biostimulated Walnut Kernel Extracts via Epithelial Mesenchymal Transition: Switching a Nutritional Matrix into a Therapeutic Remedy.","authors":"Riccardo Fedeli, Elia Ranzato, Simona Martinotti, Manuela Giovanna Basilicata, Ludovica Marotta, Marianna Fava, Ilaria Cursaro, Giulio Tremori, Gregorio Bonsignore, Gabriele Carullo, Sandra Gemma, Giovanna Aquino, Pietro Campiglia, Giacomo Pepe, Stefania Butini, Stefano Loppi, Giuseppe Campiani","doi":"10.3390/antiox14091079","DOIUrl":"10.3390/antiox14091079","url":null,"abstract":"<p><p>Walnuts (<i>Juglans regia</i> L.) are recognized for their rich nutritional profile and health-promoting properties. This study investigates the impact of biostimulation, via wood distillate application, on the chemical composition and therapeutic potential of walnut kernels, focusing on their wound healing activity. Biostimulated walnuts showed enhanced levels of phenolic compounds including antioxidants, sugars, and amino acids compared to untreated or agrochemically treated controls. Phytocomplexes extracted from walnut kernels using green methodologies were tested on human keratinocytes (HaCaT), revealing pro-migratory effect, boosted by biostimulation. Molecular analyses demonstrated the activation of epithelial-mesenchymal transition (EMT) pathways, marked by downregulation of epithelial markers and upregulation of mesenchymal genes such as MMP3, MMP9, vimentin, and SMAD3. Furthermore, a synergistic effect was observed between extracts derived from biostimulated kernels and manuka honey in promoting wound closure. These findings suggest that kernels from biostimulated walnuts may serve as functional foods, paving the way for their use in regenerative medicine.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heat Tolerance in <i>Magallana hongkongensis</i>: Integrative Analysis of DNA Damage, Antioxidant Defense, and Stress Gene Regulation.","authors":"Tuo Yao, Xiaodi Wang, Jie Lu, Shengli Fu, Changhong Cheng, Lingtong Ye","doi":"10.3390/antiox14091075","DOIUrl":"10.3390/antiox14091075","url":null,"abstract":"<p><p>Water temperature stands as a crucial environmental element, exerting an impact on the survival and growth of organisms in aquaculture. Heat stress poses a significant threat to the survival and aquaculture of the Hong Kong oyster <i>Magallana hongkongensis</i> (also known as <i>Crassostrea hongkongensis</i>), yet the underlying physiological and molecular mechanisms remain poorly understood. This study investigated the effects of elevated temperatures (35 °C and 37 °C) on survival, DNA damage, antioxidant enzyme activities, and gene expression related to apoptosis, inflammation, and heat shock proteins (HSPs) in <i>M. hongkongensis</i>. The median lethal temperature (LT50) of <i>M. hongkongensis</i> was determined to be 37.09 °C, with significant mortality observed at 35 °C compared with the control (29 °C). Antioxidant enzyme activities (SOD, CAT, and GPx) and T-AOC were up-regulated initially but exhibited divergent patterns under prolonged stress, indicating a temperature-dependent threshold for oxidative defense. Comet assay results also showed that heat stress induced severe DNA damage in hemocytes. Moreover, heat stress significantly up-regulated mRNA expression of apoptosis-related genes (<i>Caspase-2</i>, <i>Caspase-8</i>, <i>Bax</i>, and <i>P53</i>), inflammatory genes (<i>TNF</i>, <i>p38-MAPK</i>, and <i>AP-1</i>), and HSP family members (<i>Hsp70</i>, <i>Hsp90</i>, <i>Hsp27</i>, and <i>Hsp68</i>). The expression peaks of these genes were generally earlier and more pronounced at 37 °C, reflecting intensified cellular damage and protective responses. Collectively, this study demonstrates that <i>M. hongkongensis</i> employs integrated antioxidant, apoptotic, inflammatory, and HSP-mediated mechanisms to counteract heat stress, but temperatures exceeding 35 °C disrupt these defenses, leading to survival impairment. These findings provide critical insights into the heat adaptation strategies of <i>M. hongkongensis</i> and serve as a scientific foundation for developing sustainable aquaculture practices to mitigate summer heat stress.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management and Prevention of Neurodegenerative Disorders: Can Antioxidant-Rich Dietary Interventions Help?","authors":"Diksha Nagpal, Shivangi Nema, Shakti Nagpal, Murali Monohar Pandey, Deepak Kaushik, Himanshu Kathuria","doi":"10.3390/antiox14091078","DOIUrl":"10.3390/antiox14091078","url":null,"abstract":"<p><p>Neurodegenerative diseases are associated with the senescence of functional neurons, which hampers brain functions. These diseases are caused by the accumulation of reactive oxygen species, reactive nitrogen species, cholinesterase malfunction, neuronal inflammation, and mitochondrial dysfunction. The incidence of neurodegenerative disease has been on the rise. Current therapeutic interventions are expensive, exhibit poor efficacy, and have numerous side effects. Several studies have explored the potential of crucial dietary substances rich in antioxidants and micronutrients in alleviating the clinical manifestations of such deadly diseases. Consumption of sufficient antioxidants, fatty acids, and polyphenols in regular diets delays the onset of neurodegenerative diseases. Several medicinal plants, such as Withania somnifera, <i>Curcuma longa</i>, Panax ginseng, Ginkgo biloba, aloe vera, Punica granatum, and various phytoextracts, contain such micronutrients in reasonable amounts. Specific dietary interventions, supplements, and patterns such as the Mediterranean-DASH intervention for neurodegenerative delay, ketogenic, paleolithic, and Wahls elimination diets have been beneficial in neurodegenerative conditions. These diet interventions and other functional foods can be an attractive, non-invasive, and inexpensive approach in the management and prevention of neurodegenerative conditions. This review discusses potential pharmacological bases involved in neurodegeneration, covering mitochondrial damage, impaired mitophagy, neuroinflammation, ferroptosis, glymphatic clearance dysfunction, brain-body interactions, and disruption of vagus nerve stimulation. The review further highlights clinical diet interventions and assorted functional foods, including fruits, vegetables, vitamins, specific supplements, and special diets, for neurodegenerative conditions. The discussion extends insights into clinical research and trials of these functional foods under neurodegenerative conditions. Overall, dietary interventions show promise in the prevention and management of neurodegenerative conditions.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Intersection of Glycosylation and Ferroptosis in Cancer.","authors":"Jihan Kim, Junghyun Kim, Man S Kim","doi":"10.3390/antiox14091077","DOIUrl":"10.3390/antiox14091077","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation, has emerged as a critical mechanism in cancer biology and therapy. Aberrant glycosylation is a hallmark of cancer, influencing cellular processes from proliferation to immune evasion. Recent evidence has revealed previously underappreciated crosstalk between glycosylation and ferroptosis in cancer cells, where specific glycosylation modifications can determine cellular susceptibility to ferroptotic cell death. This review summarizes the current understanding of how N-linked glycosylation, O-linked glycosylation, and glycosaminoglycan biosynthesis modulate sensitivity to ferroptosis in various cancers. We examine the molecular mechanisms underlying glycosylation-dependent ferroptosis regulation, including the roles of key glycosyltransferases and glycan structures in the oxidative stress response. Furthermore, we discuss the therapeutic potential of targeting the glycosylation-ferroptosis axis for cancer treatment in this emerging field.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1-Mediated Redox and Senescence Regulation in Cancer: Mechanisms and Therapeutic Implications.","authors":"Yejin Son, Minyeong Han, Xuefeng Wu, Yoon-Seok Roh","doi":"10.3390/antiox14091076","DOIUrl":"10.3390/antiox14091076","url":null,"abstract":"<p><p>Silent information regulator type 1 (SIRT1), a NAD⁺-dependent deacetylase, is a central regulator of cancer cell adaptation to oxidative stress and senescence. By deacetylating redox-sensitive transcription factors, such as p53, FOXOs, PGC-1α, and NF-κB, SIRT1 suppresses apoptosis, delays senescence, enhances mitochondrial function, and attenuates pro-inflammatory senescence-associated secretory phenotypes. These mechanisms collectively promote tumor progression and contribute to resistance to therapy. Reactive oxygen species (ROS), long regarded as damaging byproducts, are now recognized as critical modulators of cancer biology. Although moderate ROS levels drive oncogenic signaling, excessive ROS accumulation triggers DNA damage, oxidative stress, and senescence. To survive these hostile conditions, cancer cells reinforce antioxidant defenses and exploit the NAD⁺-SIRT1 axis to maintain redox balance and evade senescence. The objective of this review was to provide an integrated framework linking SIRT1-mediated deacetylation to redox regulation and senescence control in cancer. We synthesized mechanistic insights into SIRT1 interactions with its substrates, highlighted cancer type-specific functions in ovarian, breast, liver, lung, and gastrointestinal malignancies, and critically evaluated the dual role of SIRT1 as both a longevity factor and an oncogenic driver. Finally, we explored the therapeutic implications of the pharmacological inhibition of SIRT1 as a strategy to restore senescence, increase ROS vulnerability, and overcome therapy resistance. This synthesis underscores the potential of the SIRT1-redox-senescence axis as a promising target in precision oncology.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 9","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}