Antioxidants最新文献

{"title":"Valproic Acid Enhances the Anticancer Effect of L-Ascorbic Acid by Upregulating Sodium-Dependent Vitamin C Transporter 2 in Colorectal Cancer.","authors":"Kawalin Kantawong, Hakim Meutia Diva, Phuong T Ho, Ahlim Lee, Misae Kiba, Mi-Gi Lee, Hee Kang, Taek-Kyun Lee, Sukchan Lee","doi":"10.3390/antiox14070864","DOIUrl":"10.3390/antiox14070864","url":null,"abstract":"<p><p>Vitamin C, also known as L-ascorbic acid (AA), functions as a pro-oxidant in cancer at high doses and exerts anticancer effects by generating reactive oxygen species (ROS) and selectively inducing damage to cancer cells. However, AA at low doses promotes cancer cell proliferation. The efficacy of high-dose AA therapy is frequently restricted by inadequate intracellular AA uptake, resulting from low expression of sodium-dependent vitamin C transporter 2 (SVCT2). In this study, we investigated whether valproic acid (VPA), a histone deacetylase inhibitor, could circumvent this constraint by increasing the expression of SVCT2 in colorectal cancer cells, including HCT-116 and DLD-1 with low SVCT2 levels. We found that VPA increased SVCT2 expression in both cell lines. Co-treatment with AA and VPA increased the number of apoptotic cells and enhanced intracellular AA uptake via VPA-upregulated SVCT2, followed by increased ROS production in both cell lines. Furthermore, the combination increased the synergistic anticancer effects and suppressed the hormetic dose response of AA in both cell lines. In a xenograft mouse model, co-treatment decreased tumor size and increased the tumor growth inhibition ratio compared to treatment with AA or VPA alone. Accordingly, VPA treatment enhanced SVCT2 expression in colorectal cancer cells, suppressed the hormetic dose-response effect of AA, and improved the potential of high-dose AA therapy as an anticancer agent.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selenomethionine Counteracts T-2 Toxin-Induced Liver Injury by Mitigating Oxidative Stress Damage Through the Enhancement of Antioxidant Enzymes.","authors":"Yan Wang, Mingxia Zhou, Suisui Gao, Pishun Li, Xiaofeng Zheng, Di Tu, Lingchen Yang","doi":"10.3390/antiox14070866","DOIUrl":"10.3390/antiox14070866","url":null,"abstract":"<p><p>T-2 toxin, a highly toxic feed contaminant, poses a significant health risk to both humans and animals, particularly targeting the liver. This study aimed to investigate the protective effects and underlying mechanisms of selenomethionine (SeMet) against T-2-induced liver injury in mice. We pretreated mice with SeMet before exposing them to an acute liver injury model induced by T-2. By assessing indicators related to liver injury, oxidative stress, inflammatory response, and mitochondrial disorder, we found that SeMet mitigated T-2-induced liver damage. Specifically, SeMet upregulated the gene expression and activity of antioxidant enzymes like glutathione peroxidase 1 (GPX1), which consequently reduced reactive oxygen species (ROS), inflammatory cytokines levels, and normalized mitochondrial biogenesis. Conclusively, SeMet effectively alleviated T-2-induced mitochondrial overproduction, inflammatory responses, and oxidative stress damage in hepatocyte primarily by enhancing GPX1 and other antioxidant enzymes, thereby exerting a protective effect on the liver. This study provides theoretical and experimental support for further research and application of SeMet in the livestock industry.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Variation in Arterial Stiffness and Markers of Oxidative Stress in Patients with Type 2 Diabetes Mellitus from Different Ethnic Groups.","authors":"Karima Zitouni, Mia Steyn, Joanna Lewis, Frank J Kelly, Paul Cook, Kenneth A Earle","doi":"10.3390/antiox14070858","DOIUrl":"10.3390/antiox14070858","url":null,"abstract":"<p><p>Diabetes is the world's leading cause of renal and premature cardiovascular disease. There are marked differences between groups of patients with different ethnicities in their susceptibility to diabetes and its renal and cardiovascular complications. Novel markers of developing diabetes complications are related to disturbances in oxidative metabolism. In this cross-sectional study, we measured the arterial stiffness in patients of differing ethnicities with type 2 diabetes mellitus and assessed the relationship of their ethnicity with systemic markers of oxidative stress. Patients from black, African and Caribbean, and Asian minor ethnic groups were studied, with white patients with T2DM (<i>n</i> = 170) without evidence of cardiovascular disease (CVD). The vascular stiffness was measured by infrared finger-photoplethysmography. The oxidative stress burden was assessed by measuring the urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), activities of plasma glutathione peroxidase (GPx-3), superoxide dismutase (SOD) activities, and concentration of selenium. The vascular stiffness and 8-OHdG were higher in the white than in the Black patients (9.68 m/s vs. 9.26 m/s, <i>p</i> = 0.021 and 292.8 ng/mL vs. 200.9 ng/mL, <i>p</i> = 0.0027, respectively). Meanwhile, the GPx-3 and SOD activities and selenium were lower in the white than in the Black patients (283.3 U/L vs. 440.4 U/L, <i>p</i> < 0.0001; 37.5 U/L vs. 75.6 U/L, <i>p</i> = 0.0007; and 1.14 vs. 1.28 µmol/L, <i>p</i> = 0.0001, respectively). In regression modelling, the 8-OHdG/creatinine ratio was an independent predictor of vascular stiffness in the white patient group (β = 0.23 m/s per unit increase in ln(8-OHdG/creatinine) [95% CI, 0.03 to 0.42]; <i>p</i> = 0.021) but not in the Black patient group (<i>p</i> = 0.29). Increased vascular stiffness, lower endogenous antioxidant defense, and greater levels of oxidative damage were found in patients of white ethnicity, which could contribute to the higher incidence of CVD compared with patients from Black minor ethnic groups with diabetic renal disease.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gallic Acid Alleviates Acetaminophen-Induced Acute Liver Injury by Regulating Inflammatory and Oxidative Stress Signaling Proteins.","authors":"Jing Zhao, Yuan Zhao, Shuzhe Song, Sai Zhang, Guodong Yang, Yan Qiu, Weishun Tian","doi":"10.3390/antiox14070860","DOIUrl":"10.3390/antiox14070860","url":null,"abstract":"<p><p>Acetaminophen (APAP) overdose is a major cause of drug-induced liver injury (DILI) globally, which necessitates effective therapies. Gallic acid (GA), a naturally abundant polyphenol, possesses potent antioxidant and anti-inflammatory properties that may overcome the limitations of N-acetylcysteine (NAC), such as its narrow therapeutic window. This study systematically investigated the hepatoprotective effects and underlying molecular mechanisms of GA against APAP-induced acute liver injury (ALI). Mice received an intraperitoneal injection of APAP (300 mg/kg), followed by an oral administration of GA (50 or 100 mg/kg) or NAC (150 mg/kg) 1 h post-intoxication. Both GA and NAC significantly ameliorated hypertrophy and histopathological damage, as evidenced by reduced serum ALT/AST levels and inflammatory cytokines. TUNEL staining revealed a marked suppression of apoptotic and necrotic cell death, further supported by the downregulation of pro-apoptotic Bax and the upregulation of anti-apoptotic Bcl-2 mRNA expression. GA and NAC treatment restored hepatic glutathione (GSH) content, enhanced antioxidant enzyme gene expression, and reduced malondialdehyde (MDA) accumulation. Mechanistically, GA and NAC inhibited MAPK phosphorylation while activating AMPK signaling. Taken together, these findings demonstrate that GA mitigates APAP-induced ALI by modulating oxidative stress and inflammation through the regulation of MAPK/AMPK signaling proteins.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal Bisphenol A Exposure Impairs Fetal Heart Development: Molecular and Structural Alterations with Sex-Specific Differences.","authors":"Alessandro Marrone, Anna De Bartolo, Vittoria Rago, Francesco Conforti, Lidia Urlandini, Tommaso Angelone, Rosa Mazza, Maurizio Mandalà, Carmine Rocca","doi":"10.3390/antiox14070863","DOIUrl":"10.3390/antiox14070863","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, with increasing evidence suggesting that their origins may lie in prenatal life. Endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA), have been implicated in the alteration of fetal programming mechanisms that cause a predisposition to long-term cardiovascular vulnerability. However, the impact of prenatal endocrine disruption on fetal heart development and its sex-specific nature remains incompletely understood. This study investigates the molecular and structural effects of low-dose prenatal BPA exposure on fetal rat hearts. Our results reveal that BPA disrupts estrogen receptor (ER) signaling in a sex-dependent manner, with distinct alterations in ERα, ERβ, and GPER expression. BPA exposure also triggers significant inflammation, oxidative stress, and ferroptosis; this is evidenced by elevated NF-κB, IL-1β, TNF-α, and NLRP3 inflammasome activation, as well as impaired antioxidant defenses (SOD1, SOD2, CAT, and SELENOT), increased lipid peroxidation (MDA) and protein oxidation, decreased GPX4, and increased ACSL4 levels. These alterations are accompanied by increased markers of cardiac distension (ANP, BNP), extracellular matrix remodeling mediators, and pro-fibrotic regulators (Col1A1, Col3A1, TGF-β, and CTGF), with a more pronounced response in males. Histological analyses corroborated these molecular findings, revealing structural alterations as well as glycogen depletion in male fetal hearts, consistent with altered cardiac morphogenesis and metabolic stress. These effects were milder in females, reinforcing the notion of sex-specific vulnerability. Moreover, prenatal BPA exposure affected myocardial fiber architecture and vascular remodeling in a sex-dependent manner, as evidenced by reduced expression of desmin alongside increased levels of CD34 and Ki67. Overall, our findings provide novel insights into the crucial role of prenatal endocrine disruption during fetal heart development and its contribution to the early origins of CVD, underscoring the urgent need for targeted preventive strategies and further research into the functional impact of BPA-induced alterations on postnatal cardiac function and long-term disease susceptibility.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Proteomics and Metabolomics Reveal Spermine Enhances Sperm Freezability via Antioxidant Pathways.","authors":"Lewei Guo, Zhuoxuan Gu, Bing Wang, Yunuo Wang, Jiaorong Chen, Yitong Li, Qiuju Zheng, Jing Zhao, He Ding, Hongyu Liu, Yi Fang, Jun Wang, Wenfa Lyu","doi":"10.3390/antiox14070861","DOIUrl":"10.3390/antiox14070861","url":null,"abstract":"<p><p>Sperm freezability exhibits marked individual variability, yet the mechanisms remain unclear. Using bulls as the experimental model, we integrated proteomic (sperm) and metabolomic (seminal plasma) analyses of high-freezability (HF) and control (CF) bulls to identify key biomarkers associated with sperm freezability. Post-thaw motility and membrane integrity were significantly higher in HF bulls (<i>p</i> < 0.05). Sperm proteome analysis revealed upregulated antioxidant proteins (PRDX2, GSTM4), heat shock proteins (HSP70, HSP90), and key enzymes in arginine and proline metabolism (PRODH, LAP3). Seminal plasma metabolomics revealed elevated spermine in HF bulls. Meanwhile, we found that spermine abundance was positively correlated with post-thaw motility, as well as with the expression levels of both PRODH and LAP3 (r > 0.6, <i>p</i> < 0.05). Functional validation demonstrated that 200 μM spermine supplementation in cryopreservation extenders enhanced post-thaw motility, kinematic parameters (VAP, VSL, VCL), membrane integrity, and acrosome integrity (<i>p</i> < 0.05). Concurrently, spermine enhanced antioxidant enzyme (SOD, CAT, GSH-Px) activity and reduced ROS and MDA levels (<i>p</i> < 0.05). Our study reveals a spermine-driven antioxidant network coordinating sperm-seminal plasma synergy during cryopreservation, offering novel strategies for semen freezing optimization.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research on the Hormonomics of Three <i>Lilium</i> Species and Their Flavonoid Diversification and Specificity.","authors":"Xuanyu He, Jie Fang, Biwei Hong, Xueying Zhang, Linying Li, Yuqing He, Chaomin Chen, Shuang Liang, Zelong Xu, Chunlan Peng, Jirong Huang, Gaojie Hong, Qundan Lv","doi":"10.3390/antiox14070862","DOIUrl":"10.3390/antiox14070862","url":null,"abstract":"<p><p>Hormonomics represents an innovative approach to plant physiology and biochemistry. We utilized hormonomics to analyze the hormone profiles of three lily bulbs. The hormones specifically enriched in BiFeng7 lily show a strong response to secondary metabolism pathways, while the Diwanghuang lily profile was predominantly focused on growth. Physiological experiments demonstrated that Diwanghuang exhibited higher levels of primary nutrients, whereas BiFeng7 displayed a greater concentration of secondary metabolites and enhanced antioxidant capacity. Through untargeted metabolomic analysis, it was revealed that BiFeng7 highly enriched four flavonoid glycosides, two flavones, one flavan, one pyranoflavonoid, two isoflavonoid O-glycosides and one rotenoid. These findings provide valuable information for developing breeding strategies and cultivation practices aimed at achieving ornamental quality, nutritional value, or stress resilience outcomes. This research demonstrates the practical application of hormone profiling in plant evaluation and offers insights into the mechanisms underlying flavonoid synthesis in lilies, serving as a reference for breeding stress-resistant lily varieties.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Negative Air Ions Attenuate Nicotine-Induced Vascular Endothelial Dysfunction by Suppressing AP1-Mediated FN1 and SPP1.","authors":"Sha Xiao, Tianjing Wei, Mingyang Xiao, Mingming Shan, Ziqi An, Na Li, Jing Zhou, Shuang Zhao, Xiaobo Lu","doi":"10.3390/antiox14070859","DOIUrl":"10.3390/antiox14070859","url":null,"abstract":"<p><p>Nicotine-induced oxidative stress contributes significantly to vascular endothelial dysfunction. While negative air ions (NAIs) demonstrate potential blood-pressure-regulating and antioxidant properties, their mechanistic role remains unclear. This study examined the effects of NAIs against nicotine-induced oxidative damage and vascular endothelial injury in spontaneously hypertensive rats (SHRs). Western blotting was used to detect the expression levels of the α7nAChR/MAPK/AP1 pathway. Transcriptomic sequencing was performed to identify the differentially expressed genes after treatment with nicotine or NAIs. Furthermore, reactive oxygen species (ROS), endothelin-1 (ET-1), and [Ca²⁺]_i levels were detected in human aortic endothelial cells (HAECs) treated with nicotine, and the relationship between transcription factor activator protein 1 (AP1) and the target genes was further elucidated through ChIP-qPCR. Nicotine exposure in SHRs elevated blood pressure and induced oxidative damage through α7nAChR/MAPK/AP1 pathway activation, causing endothelial structural disruption. These effects manifested as decreased NO/eNOS and increased ET-1/ET_ab expression, while these changes were reversed by NAIs. In HAECs, nicotine impaired proliferation while increasing oxidative stress and [Ca²⁺]_i levels. This endothelial damage was markedly attenuated by either NAIs or <i>fibronectin 1</i> (<i>Fn1</i>)/<i>secreted phosphoprotein 1</i> (<i>Spp1</i>) knockdown. Mechanistically, we identified AP1 as the transcriptional regulator of <i>FN1</i> and <i>SPP1</i>. NAIs attenuate nicotine-induced endothelial dysfunction in hypertension by inhibiting AP1-mediated FN1 and SPP1 activation, providing novel insights for smoking-associated cardiovascular risk.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-Term Intake of <i>Euphorbia tirucalli</i> Latex Modifies Kidney Function in Rats: Possible Role of Oxidative Stress and Inflammatory Response.","authors":"Edgar Hell Kampke, Maria Eduarda Souza Barroso, Leonardo da Silva Escouto, Luciana Polaco Covre, Ágata Lages Gava, Bianca Prandi Campagnaro, Ricardo Machado Kuster, Silvana Santos Meyrelles","doi":"10.3390/antiox14070856","DOIUrl":"10.3390/antiox14070856","url":null,"abstract":"<p><p>Medicinal plants have been traditionally used for generations, often without scientific validation. <i>Euphorbia tirucalli</i> (<i>E. tirucalli</i>), a plant native to Africa, is commonly employed in folk medicine for treating various ailments, including cancer. However, most studies involving this species are limited to in vitro models, and its systemic effects remain poorly understood. This study aimed to evaluate the impact of <i>E. tirucalli</i> latex on renal function in healthy Wistar rats. Animals were divided into two groups: a control group receiving water and a treated group receiving <i>E. tirucalli</i> latex (13.47 mg/kg) by gavage for 15 days. Renal function was assessed by measuring glomerular filtration rate (GFR), renal plasma flow (RPF), renal blood flow (RBF), renal vascular resistance (RVR), and mean arterial pressure (MAP). Additionally, oxidative stress markers, reactive oxygen/nitrogen species, and inflammatory activity were analyzed in renal tissue. <i>E. tirucalli</i> significantly reduced GFR, RPF, and RBF, while increasing RVR and MAP. Renal tissue exhibited elevated levels of advanced oxidation protein products, myeloperoxidase, nitric oxide, and peroxynitrite/hydroxyl radicals. These findings indicate that <i>E. tirucalli</i> latex adversely affects renal hemodynamics and promotes oxidative and inflammatory damage, suggesting potential nephrotoxic effects, even in healthy subjects.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress Defense Module in Lung Cancers: Molecular Pathways and Therapeutic Approaches.","authors":"Eunsun Lee, Jeong Hee Hong","doi":"10.3390/antiox14070857","DOIUrl":"10.3390/antiox14070857","url":null,"abstract":"<p><p>The regulation of oxidative stress is an effective strategy for treating cancers. Therapeutic strategies for modulating an undesirable redox balance against cancers have included the enhancement of oxidative components, reducing the action of antioxidant systems, and the combined application of radiation and redox-modulating drugs. A precise understanding of redox regulation is required to treat different kinds of cancer. This review focuses on the redox regulation and oxidative stress defense systems of lung cancers. Thus, we highlighted several enzymatic antioxidant components, such as superoxide dismutase, catalase, heme oxygenase-1, peroxiredoxin, glutaredoxin, thioredoxin, thioredoxin reductase, glutathione peroxidase, and antioxidant components, including glutathione, nuclear factor erythroid 2-related factor 2, 8-oxo-7,8-dihydro-2'-deoxyguanosine, and mitochondrial citrate carrier SLC25A1, based on PubMed and Scopus-indexed literature. Understanding the oxidative stress defense system in lung cancer would be beneficial for developing and expanding therapeutic strategies, such as drug development, drug design, and advanced delivery platforms.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 7","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}