Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe最新文献

{"title":"Comparative reactivity of hypohalous acids with proteins: Chemistry, biological effects and consequences","authors":"Els A. Hartsema ,&nbsp;Helen Hemmling ,&nbsp;Clare L. Hawkins","doi":"10.1016/j.arres.2025.100119","DOIUrl":"10.1016/j.arres.2025.100119","url":null,"abstract":"<div><div>Hypohalous acids (HOX) are chemical oxidants that are produced by different mammalian heme peroxidases, which can be released by activated immune cells. These oxidants play an important role in innate immunity, owing to their ability to rapidly kill and detoxify pathogens. However, HOX are also implicated in driving host tissue damage, due to the abundance and over-activation of immune cells in many inflammatory pathologies. Proteins are highly abundant in biological systems and constitute key targets for HOX. These reactions lead to the modification of amino acid side chains, together with protein unfolding, fragmentation and aggregation, which have significant structural and functional effects. This has led to a significant research effort focused on gaining a detailed understanding of the molecular mechanisms involved in HOX-induced protein damage, and how it contributes to the progression of disease and mortality. This review describes the reactivity of HOX with proteins, including the mechanisms involved in the modification of specific amino acid residues, and how this contributes to structural and functional changes. We describe potential pathways by which modification of proteins by HOX contribute to disease and outline some strategies to modulate this type of damage therapeutically.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"14 ","pages":"Article 100119"},"PeriodicalIF":0.0,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox Metabolomics of Menthol in Children's Plasma with Second-Hand Cigarette and Electronic Cigarette Exposures","authors":"Matthew Ryan Smith ,&nbsp;Zachery R. Jarrell ,&nbsp;Ken H Liu ,&nbsp;Choon-Myung Lee ,&nbsp;Edward T Morgan ,&nbsp;Young-Mi Go ,&nbsp;Dean P. Jones","doi":"10.1016/j.arres.2025.100122","DOIUrl":"10.1016/j.arres.2025.100122","url":null,"abstract":"<div><h3>Background</h3><div>Cigarettes and electronic cigarettes generate many redox-active materials which could impact children's health through second-hand exposures. High-resolution metabolomics methods enable use of non-targeted mass spectrometry of plasma to test for redox consequences of second-hand exposures.</div></div><div><h3>Objectives</h3><div>Our objectives were to test for oxidative stress metabolites and altered metabolic pathways associated with second-hand exposure to redox-active flavorants and flavorant metabolites in plasma of infants and children.</div></div><div><h3>Methods</h3><div>Untargeted plasma metabolomics data for infants and children in a population known to include individuals with second-hand exposures to cigarettes and electronic cigarettes were analyzed for cotinine and metabolites of flavorants. A metabolome-wide association study (MWAS) was performed separately for cotinine and menthol glucuronide, derived from the redox-active flavorant, menthol. Pathway enrichment analysis was used to identify metabolic pathways, and xMWAS was used to detect metabolic communities associated with flavorant metabolites.</div></div><div><h3>Results</h3><div>Menthol glucuronide was one of several flavorant metabolites positively correlated with cotinine. MWAS and pathway enrichment analysis revealed that some pathways associated with both menthol glucuronide and cotinine, while others only associated with menthol glucuronide, including sphingolipid, glycerophospholipid, antioxidant, N-glycan and mitochondrial energy metabolism. 4-hydroxynonenal and other oxidized lipids positively correlated with menthol glucuronide.</div></div><div><h3>Discussion</h3><div>The results show that flavorants from second-hand electronic cigarette and cigarette exposures in infants and children are associated with changes in redox metabolism which are known to associate with human lung diseases.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"14 ","pages":"Article 100122"},"PeriodicalIF":0.0,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reconnoitering the role of Lipid Metabolites in Ferroptosis","authors":"Manikandan Vani Raju ,&nbsp;Meenakshi Kaniyur Chandrasekaran ,&nbsp;Rathi Muthaiyan Ahalliya ,&nbsp;Gopalakrishnan Velliyur Kanniappan","doi":"10.1016/j.arres.2024.100117","DOIUrl":"10.1016/j.arres.2024.100117","url":null,"abstract":"<div><div>Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation. It is different from other cell death forms like apoptosis, necrosis, and autophagy. Unlike apoptosis, ferroptosis is induced by the accumulation of reactive lipid peroxides and lacks the typical features of cell lysis. Ferroptosis is regulated through mechanisms involving iron accumulation and lipid peroxidation, primarily driven by lipoxygenases. Glutathione Peroxidase 4 (GPX4) plays a critical role by mitigating lipid hydroperoxide accumulation. The incorporation of polyunsaturated fatty acids into cellular membranes, facilitated by enzymes such as ACSL4 and LPCAT3, enhances susceptibility to ferroptosis. Ferroptosis is implicated in various pathological conditions, including cancer, neurodegenerative diseases, and ischemic injuries. This review explores the potential of lipid metabolites as ferroptosis inducers for cancer therapy. By synthesizing recent findings on the interplay between ferroptosis and lipid metabolism, this study highlights new research directions and therapeutic strategies across diverse diseases.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"14 ","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143138846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2-Chloro- and 2-Bromopalmitic acids inhibit mitochondrial function in airway epithelial cells","authors":"Karina Ricart ,&nbsp;Kyle S. McCommis ,&nbsp;David A. Ford ,&nbsp;Rakesh P. Patel","doi":"10.1016/j.arres.2024.100118","DOIUrl":"10.1016/j.arres.2024.100118","url":null,"abstract":"<div><div>2-Chloropalmitic acid (2-ClPA) and 2-bromopalmitic acid (2-BrPa) increase in inflammatory lung disease associated with formation of hypochlorous or hypobromous acid, and exposure to halogen gases. Moreover, these lipids may elicit cell responses that contribute to lung injury, but the mechanisms remain unclear. Here, we tested the hypothesis that 2-ClPA and 2-BrPA induce metabolic defects in airway epithelial cells by targeting mitochondria. H441 or primary human airway epithelial cells were treated with 2-ClPA or 2-BrPA and bioenergetics measured using oxygen consumption rates and extracellular acidification rates, as well as respiratory complex activities. Relative to vehicle or palmitic acid, both 2-halofatty acids inhibited ATP-linked oxygen consumption and reserve capacity, suggestive of increased proton leak. However, neither 2-ClPA nor 2-BrPA altered mitochondrial membrane potential, suggesting proton leak does not underlie inhibited ATP-linked oxygen consumption. Interestingly, complex II activity was significantly inhibited which may contribute to diminished reserve capacity, but activity of complexes I, III and IV remain unchanged. Taken together, the presented data highlight the potential of 2-halofatty acids to disrupt bioenergetics and in turn cause cellular dysfunction.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"14 ","pages":"Article 100118"},"PeriodicalIF":0.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143138848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of thiol/disulfide homeostasis and ischemia-modified albumin in metabolic syndrome patients","authors":"Raju Rana ,&nbsp;Shobha U Kamath ,&nbsp;B Ananthakrishna Shastri ,&nbsp;Shashikiran U ,&nbsp;G Arun Maiya ,&nbsp;Ullas Kamath ,&nbsp;Raghavendra Rao S ,&nbsp;Vani Lakshmi R","doi":"10.1016/j.arres.2024.100116","DOIUrl":"10.1016/j.arres.2024.100116","url":null,"abstract":"<div><h3>Introduction</h3><div>Ischemia-modified albumin (IMA) and thiol-disulfide homeostasis (TDH) have emerged as valuable markers of oxidative stress in various disease states, including diabetic nephropathy. However, limited research has been conducted on these markers in individuals with metabolic syndrome (MetS), particularly those with comorbid type 2 diabetes mellitus (T2DM). This study aims to investigate the roles of TDH and IMA in the context of MetS.</div></div><div><h3>Materials and methods</h3><div>We enrolled 162 participants, comprising three groups of 54 subjects each: healthy controls, patients with MetS alone, and patients with both MetS and T2DM. IMA levels and TDH parameters were measured spectrophotometrically. Statistical analyses included one-way analysis of variance (ANOVA) and correlation studies.</div></div><div><h3>Results</h3><div>IMA levels were significantly elevated, and thiol levels were significantly reduced in participants with MetS compared to healthy controls (<em>P</em> &lt; 0.001). IMA levels showed a strong positive association with diastolic blood pressure and fasting blood glucose (FBG) (<em>P</em> &lt; 0.001). High-density lipoprotein cholesterol, native thiol, and total thiol were also strongly associated (<em>P</em> &lt; 0.001). In contrast, triglycerides, waist circumference, and FBG were negatively correlated with thiol levels.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrated elevated oxidative stress in patients with MetS, as evidenced by increased IMA levels and decreased thiol concentrations. These parameters may be valuable markers for monitoring disease progression and potential complications in MetS.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"14 ","pages":"Article 100116"},"PeriodicalIF":0.0,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143138847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRF2 protects lung epithelial cells from wood smoke particle toxicity","authors":"Sarah E. Lacher ,&nbsp;Tessa Schumann ,&nbsp;Ryan Peters ,&nbsp;Christopher Migliaccio ,&nbsp;Andrij Holian ,&nbsp;Matthew Slattery","doi":"10.1016/j.arres.2024.100115","DOIUrl":"10.1016/j.arres.2024.100115","url":null,"abstract":"<div><div>Wildfire smoke is a potential source of oxidative stress in lung epithelial tissue. The response to oxidative stress is controlled by the transcription factor NRF2, which is the central regulator of antioxidant gene expression. If wood smoke particle (WSP) exposure induces reactive oxygen species (ROS) in epithelial cells, then NRF2 may protect against pathological conditions resulting from increased oxidative stress through changes in gene expression. We used two lung epithelial cell lines to test this hypothesis <em>in vitro</em>: A549, which harbor a mutation resulting in constitutive activation of NRF2, and BEAS-2B, which show limited NRF2 activity under basal conditions, but high inducibility during oxidative stress. In BEAS-2B cells, WSP exposure leads to increased cellular ROS, activation of NRF2, and upregulation of the NRF2 target genes <em>NQO1, GCLM,</em> and <em>SRXN1</em>. WSP exposure also increased ROS in A549 cells, although NRF2 activation and antioxidant gene upregulation were less robust as both were basally high in this cell line. Overall, the degree of ROS induction by WSP across cell lines is dependent upon NRF2 activity, and a similar pattern was observed for WSP cytotoxicity. WSP also sensitized both cell lines to the ferroptosis inducer erastin in a manner that is correlated with NRF2 activity. Knockout of <em>NRF2</em> in A549 resulted in higher WSP-induced ROS generation, cytotoxicity, and erastin sensitivity. Taken together, these results suggest that NRF2 serves as a protective factor against wood smoke induced ROS and oxidative stress in lung epithelial cells.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"13 ","pages":"Article 100115"},"PeriodicalIF":0.0,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142427235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Piceatannol reduces radiation-induced DNA double-strand breaks by suppressing superoxide production and enhancing ATM-dependent repair efficiency","authors":"Tomoya Suzuki ,&nbsp;Ryoya Tetsuka ,&nbsp;Atsuya Iwasaki ,&nbsp;Tsutomu Shimura ,&nbsp;Ryoichi Hirayama ,&nbsp;Asako J Nakamura","doi":"10.1016/j.arres.2024.100114","DOIUrl":"10.1016/j.arres.2024.100114","url":null,"abstract":"<div><p>In contemporary society, humans are susceptible to various radiation-borne hazards, including exposure to therapeutic modalities using low-linear energy transfer (low-LET) radiations (X-rays and γ-rays), natural high-LET radiation sourced from cosmic rays, as well as nuclear accidents such as the Fukushima Daiichi Nuclear Power Plant incident. Therefore, this threat incites an imminent necessity to develop novel radioprotective agents against a wide range of LET radiation and elucidate the underlying molecular mechanisms. This study aimed at assessing the radioprotectivity of Piceatannol (PIC), a potent antioxidant polyphenol present in abundance in passion fruit, by investigating its effects on radiation-induced reactive oxygen species (ROS) production and the consequent DNA double-strand break (DSB) capacity and cellular senescence. Specifically, total ROS was evaluated by DCFDA staining, mitochondrial superoxide by MitoSOX staining, DSB by γ-H2AX immunostaining, and cellular senescence by Senescence-associated-β-galactosidase staining.</p><p>The results demonstrated that PIC administration prior to exposure to both X-ray and high-LET radiation impeded radiation-induced DSB by suppressing ROS production. Interestingly, post-irradiation PIC treatment did not alter ROS levels but enhanced the efficiency of Ataxia Telangiectasia Mutated (ATM)-mediated DSB repair. Additionally, post-irradiation PIC treatment diminished senescence-associated beta-galactosidase levels, indicating that it hinders cellular senescence.</p><p>Conclusively, PIC exerts radioprotective effects against a wide range of LET radiation. The study findings validate the potential application of PIC not only as a radical scavenger but also as a novel DSB repair-activating radioprotective agent.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"13 ","pages":"Article 100114"},"PeriodicalIF":0.0,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000213/pdfft?md5=b11373d91805a1cf814a18ae661dec23&pid=1-s2.0-S2667137924000213-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142149241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phytochemical-mediated modulation of signaling pathways: A promising avenue for drug discovery","authors":"Jibon Kumar Paul ,&nbsp;Mahir Azmal ,&nbsp;ANM Shah Newaz Been Haque ,&nbsp;Omar Faruk Talukder ,&nbsp;Meghla Meem ,&nbsp;Ajit Ghosh","doi":"10.1016/j.arres.2024.100113","DOIUrl":"10.1016/j.arres.2024.100113","url":null,"abstract":"<div><p>Phytochemicals are bioactive compounds derived from plants, renowned for their therapeutic potential. This study explores their pivotal roles in therapy and drug development, focusing on their interactions with crucial Signaling pathways and biological processes. Phytochemicals such as curcumin from turmeric, resveratrol from grapes, and epigallocatechin gallate (EGCG) from green tea, exert their effects primarily by modulating key pathways like PI3K/AKT, MAPK-ERK, Wnt, and Hedgehog, which are integral to cellular functions and disease progression. Phytochemicals like curcumin demonstrate potent anticancer activities by inhibiting proteins involved in cell proliferation, inducing apoptosis, and suppressing angiogenesis. Phytochemicals such as resveratrol also exhibit anti-inflammatory properties by targeting cytokine production and oxidative stress pathways, thereby alleviating chronic inflammatory conditions implicated in various diseases. Their (eg. EGCG's) antioxidant capabilities help neutralize free radicals and reduce oxidative damage, contributing to cellular health and longevity. Moreover, phytochemicals play a pivotal role in metabolic disorders such as diabetes and obesity by regulating glucose metabolism, lipid profiles, and insulin sensitivity. They also show promise in neurodegenerative diseases by protecting neuronal cells, enhancing cognitive functions, and potentially mitigating neuroinflammation and oxidative stress. For instance, berberine, an alkaloid found in several plants, shows promise in regulating glucose levels and improving insulin sensitivity. Additionally, ginsenosides from ginseng are known to protect neuronal cells, enhance cognitive functions, and potentially mitigate neuroinflammation and oxidative stress in neurodegenerative diseases. Despite their promising therapeutic benefits, challenges remain, particularly in ensuring bioavailability and standardization of phytochemical extracts for clinical use. Advances in screening techniques and formulation strategies aim to enhance their efficacy and integration into modern therapeutic approaches. Their multifaceted roles in modulating cellular processes underscore their importance as potential alternatives or complements to traditional pharmacotherapies, driving innovation in drug development and personalized medicine.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"13 ","pages":"Article 100113"},"PeriodicalIF":0.0,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000201/pdfft?md5=73e609cfc573df68e79c3b632927c8d7&pid=1-s2.0-S2667137924000201-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142149240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Absence of mitochondrial CX9C-CX10C protein Cox12 generates oxidative and nitrosative stress in Saccharomyces cerevisiae: Implication on cellular redox homeostasis","authors":"Soumyajit Mukherjee ,&nbsp;Shubhojit Das ,&nbsp;Sourav Kumar Patra ,&nbsp;Mayukh Das ,&nbsp;Sanjay Ghosh ,&nbsp;Alok Ghosh","doi":"10.1016/j.arres.2024.100112","DOIUrl":"10.1016/j.arres.2024.100112","url":null,"abstract":"<div><p>Mitochondrial intermembrane space (IMS) harbors a series of small, evolutionarily conserved redox-active cysteine-rich proteins. These proteins are essential for the functioning of cytochrome c oxidase, but their role in maintaining cellular redox processes is unknown. Here, we find out that in the absence of two such cysteine-rich Cx₉C-Cx₁₀C proteins, cytochrome c oxidase subunit 12 (Cox12) or cytochrome c oxidase assembly factor 6 (Coa6), <em>Saccharomyces cerevisiae</em> cells become sensitive under the oxidative and nitrosative stress. Interestingly, knockout of <em>COX12</em> generates a significant amount of endogenous reactive oxygen species (ROS) and reactive nitrogen species (RNS) as evidenced by FACS analysis. Moreover, cellular redox status, redox-active enzymes glutathione reductase, catalase, S-nitroso glutathione reductase, and protein nitration were significantly affected in Cox12 null cells. Further, we found that an overexpression of <em>COX12</em> partially protects mitochondrial respiratory subunit Sdh2 under oxidative and nitrosative stress. Taken together, we provide proof of evidence that cysteine-rich proteins in the IMS dynamically control the cellular redox milieu and actively prevent reactive nitrogen and oxygen species generation.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"13 ","pages":"Article 100112"},"PeriodicalIF":0.0,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000195/pdfft?md5=f795c7f807f8d09ef7d402872b728a55&pid=1-s2.0-S2667137924000195-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142098073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring oxysterols and protein carbonylation in cervicovaginal secretions as biomarkers for cervical cancer development","authors":"Busra Kose ,&nbsp;Serkan Erkanlı ,&nbsp;Alper Koçak ,&nbsp;Coskun Guzel ,&nbsp;Theo Luider ,&nbsp;Irundika H.K. Dias ,&nbsp;Ahmet Tarik Baykal","doi":"10.1016/j.arres.2024.100111","DOIUrl":"10.1016/j.arres.2024.100111","url":null,"abstract":"<div><p>Cervical cancer, a major global health issue and the fourth most common cancer among women, is strongly linked to Human Papillomavirus (HPV) infection. Emerging evidence indicates that oxidative stress plays a critical role in the carcinogenesis of cervical tissue. This study investigates the relationship between oxidative stress markers—specifically oxysterols, lipid oxidation, and protein carbonylation—and the progression of cervical neoplasia.</p><p>Oxysterols, which are elevated in various inflammatory diseases and cancers, were measured in cervicovaginal fluid samples using LC-MS/MS. The targeted oxysterols included 27-hydroxycholesterol (27-OHC), 7β-hydroxycholesterol (7β-OHC), 7-ketocholesterol (7-KC), and 7α,27-dihydroxycholesterol (7α,27-diOHC). Among these, 7α,27-dihydroxycholesterol was significantly increased in correlation with the severity of neoplastic stages. In parallel, protein carbonylation, an indicator of cellular oxidative stress, was assessed. Results revealed higher levels of protein carbonylation in neoplastic samples compared to non-neoplastic controls. These modifications were further analysed through redox proteomics to identify the specific proteins affected.</p><p>The study demonstrates that elevated lipid oxidation and protein carbonylation in cervicovaginal secretions are linked to the development and progression of cervical cancer. Identifying these biomarkers may improve screening strategies, enabling the identification of individuals at increased risk for cervical neoplasia and guiding timely interventions.</p></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"13 ","pages":"Article 100111"},"PeriodicalIF":0.0,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667137924000183/pdfft?md5=9aa608a17eb8ee499fd581b8b30174ce&pid=1-s2.0-S2667137924000183-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142089021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}