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Quercetin triggers iron-dependent cell death in Saccharomyces cerevisiae. 槲皮素引发酿酒酵母菌铁依赖性细胞死亡。
IF 3
Biochimie Pub Date : 2026-10-01 Epub Date: 2026-08-03 DOI: 10.1016/j.biochi.2026.07.016
Sujeong Kim, Dong Gun Lee
{"title":"Quercetin triggers iron-dependent cell death in Saccharomyces cerevisiae.","authors":"Sujeong Kim, Dong Gun Lee","doi":"10.1016/j.biochi.2026.07.016","DOIUrl":"10.1016/j.biochi.2026.07.016","url":null,"abstract":"<p><p>Quercetin, a ubiquitous polyphenolic flavonoid, exhibits antimicrobial effects associated with apoptosis-like cell death. However, whether quercetin induces ferroptosis-like cell death, a recently recognized form of regulated cell death (RCD), in microbial cells remains unclear. To investigate its antifungal mode of action, Saccharomyces cerevisiae, a model organism with a well-characterized vacuolar iron-storage system, was used. Given the role of oxidative stress in quercetin-induced antimicrobial activity, intracellular reactive oxygen species (ROS) generation was first examined. Quercetin treatment significantly increased superoxide (O<sub>2</sub><sup>-</sup>) levels and intracellular iron accumulation, thereby promoting iron redox cycling and hydroxyl radical (•OH) production. This iron-dependent oxidative stress was accompanied by glutathione (GSH) depletion, enhanced lipid peroxidation, and subsequent loss of membrane integrity. In addition, quercetin-induced oxidative stress caused alterations in mitochondrial mass and membrane potential. Despite extensive oxidative damage, no evidence of apoptosis-like cell death, including DNA fragmentation or caspase activation, was detected. In contrast, lipid ROS accumulation was evident, and several oxidative changes were alleviated by pretreatment with ferrostatin-1, a lipid ROS scavenger and ferroptosis inhibitor, before quercetin exposure. Collectively, these findings demonstrate that quercetin induces ferroptosis-like cell death in S. cerevisiae through iron-dependent oxidative damage and lipid peroxidation.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":"150-160"},"PeriodicalIF":3.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148671571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The NfsB-like nitroreductase RdxA in Helicobacter pylori is a flavin reductase: possible implications for metronidazole resistance. 幽门螺杆菌中nfsb样硝基还原酶RdxA是一种黄素还原酶:可能与甲硝唑耐药有关。
IF 3
Biochimie Pub Date : 2026-09-28 DOI: 10.1016/j.biochi.2026.09.017
Ana Paunkov, Sarjo A Gibba, David Leitsch
{"title":"The NfsB-like nitroreductase RdxA in Helicobacter pylori is a flavin reductase: possible implications for metronidazole resistance.","authors":"Ana Paunkov, Sarjo A Gibba, David Leitsch","doi":"10.1016/j.biochi.2026.09.017","DOIUrl":"10.1016/j.biochi.2026.09.017","url":null,"abstract":"<p><p>The microaerophilic bacterium Helicobacter pylori infects a large proportion of the global human population and is the leading cause for peptic ulcer disease and gastric cancer. The H. pylori eradication therapy rests on four compounds, including the 5-nitroimidazole metronidazole. Unfortunately, metronidazole resistance in H. pylori is an increasingly pressing and severe problem. In most metronidazole-resistant H. pylori isolates mutations in the rdxA gene can be found. RdxA is an NfsB-like nitroreductase and was reported to reduce metronidazole to toxic intermediates. Since nitroreductases can often also act as flavin reductases, we hypothesized that RdxA could reduce flavins. Indeed, we identified RdxA from H. pylori (Hp RdxA) as a potent flavin reductase with a submicromolar K<sub>m</sub> for FMN. RdxA also reduced FAD and riboflavin but was inhibited when these substrates were added in low concentrations. Hp RdxA was also inhibited by most nitroaromatic compounds tested. Surprisingly, the enzyme was most strongly inhibited by metronidazole, and no reduction of metronidazole by RdxA could be observed, neither under aerobic nor anaerobic conditions. In contrast, the RdxA homologue from Campylobacter jejuni, Cj RdxA, proved to be an efficient nitroreductase which reduced all nitroaromatic compounds offered, including metronidazole. Cj RdxA also reduced flavins. Based on our observations, we propose a novel, if tentative model in which Hp RdxA does not render H. pylori susceptible to metronidazole by directly reducing the drug's nitro group, but rather by reducing intracellular iron stocks.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Structural insights and functional implications of ENTPD5 splice variants in low-grade adult type diffuse gliomas and glioblastoma. ENTPD5剪接变异在低级别成人型弥漫性胶质瘤和胶质母细胞瘤中的结构见解和功能意义。
IF 3
Biochimie Pub Date : 2026-09-25 DOI: 10.1016/j.biochi.2026.09.014
Eloisa Dalsin, Lidielle Oliveira Morais, Eronides Anathan de Heberle Salau, Luana Suéling Lenz, Rodrigo Ligabue Braun, Débora Czarnabay, Guido Lenz, Márcia Rosângela Wink
{"title":"Structural insights and functional implications of ENTPD5 splice variants in low-grade adult type diffuse gliomas and glioblastoma.","authors":"Eloisa Dalsin, Lidielle Oliveira Morais, Eronides Anathan de Heberle Salau, Luana Suéling Lenz, Rodrigo Ligabue Braun, Débora Czarnabay, Guido Lenz, Márcia Rosângela Wink","doi":"10.1016/j.biochi.2026.09.014","DOIUrl":"10.1016/j.biochi.2026.09.014","url":null,"abstract":"<p><p>NTPDase5 is an endoplasmic reticulum nucleotidase that couples anabolism to adaptive bioenergetic responses in tumors with oncogenic alterations. Initially classified as a proto-oncogene due to the induction of a truncated isoform in hamsters, it was later suggested that in humans, this isoform results from alternative splicing. This study models the protein structures encoded by ENTPD5 splice variants in gliomas from TCGA, reclassified as oligodendrogliomas and glioblastomas according to the latest WHO criteria, and investigates the functional implications of ENTPD5 transcript variants using Hallmark and KEGG enrichment analyses. We identified two contrasting transcriptomic profiles, defined by the preference for one of two alternative ENTPD5 terminal exons. Preferential use of exon 17 was associated with hormonal and immunomodulatory programs, while preferential use of exon 19 showed the opposite pattern, correlating positively with proliferation and DNA/RNA regulatory signatures and negatively with gene sets linked to microenvironment-modulatory pathways. Alternative splicing of these exons may produce transcript variants encoding isoforms that differ at the putative catalytic site, one of which lacks a conserved apyrase domain. Our findings highlight the association between ENTPD5 alternative splicing and glioma transcriptional programs and underscore the need to consider ENTPD5 splice variants in future research and therapy development.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149066772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Molecular characterization of the type 2 diabetes-associated interleukin-6 receptor single nucleotide polymorphism p.V385I (rs2228146). 2型糖尿病相关白介素-6受体单核苷酸多态性p.V385I (rs2228146)的分子特征。
IF 3
Biochimie Pub Date : 2026-09-24 DOI: 10.1016/j.biochi.2026.09.015
Eric Brüggemann, Christoph Garbers
{"title":"Molecular characterization of the type 2 diabetes-associated interleukin-6 receptor single nucleotide polymorphism p.V385I (rs2228146).","authors":"Eric Brüggemann, Christoph Garbers","doi":"10.1016/j.biochi.2026.09.015","DOIUrl":"10.1016/j.biochi.2026.09.015","url":null,"abstract":"<p><p>The cytokine Interleukin-6 (IL-6) activates its target cells through the membrane-bound IL-6 receptor (IL-6R). IL-6 crucially controls important metabolic functions of the human body. Low-grade inflammation, including increased IL-6 serum levels, contribute to the development of autoimmune diseases like type 2 diabetes (T2D). In this study, we have analyzed the single nucleotide polymorphism of the IL-6R rs2228146 that is associated with T2D and results in the exchange of a single amino-acid residue within the IL-6R protein (p.V385I). We show that the affected amino-acid residue is located within the transmembrane helix of the IL-6R. The IL-6R-V385I variant matures properly and is transported to the cell surface in comparable amounts as the IL-6R-WT, which is clearly distinct from the established IL-6R SNP rs2228145. We further show that IL-6R-V385I can be cleaved by the metalloproteases ADAM10 and ADAM17, generating a soluble IL-6R, and that the membrane-bound form can perform IL-6 classic signaling.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sphingolipids as central regulators of therapy resistance and immunity in lung cancer. 鞘脂作为肺癌治疗抵抗和免疫的中枢调节因子。
IF 3
Biochimie Pub Date : 2026-09-23 DOI: 10.1016/j.biochi.2026.09.012
Morgane Paque, Anisa Aliju, Arnaud Blomme
{"title":"Sphingolipids as central regulators of therapy resistance and immunity in lung cancer.","authors":"Morgane Paque, Anisa Aliju, Arnaud Blomme","doi":"10.1016/j.biochi.2026.09.012","DOIUrl":"10.1016/j.biochi.2026.09.012","url":null,"abstract":"<p><p>Lung cancer remains the deadliest cancer worldwide, with most patients exhibiting poor responses to current therapies and rapidly developing treatment resistance. Cancer cells can acquire resistance by rewiring their metabolism. In particular, dysregulated lipid metabolism promotes therapy resistance in multiple cancer types, including lung cancer. In addition to their role in shaping cell membrane, sphingolipids have recently emerged as key mediators of intra- and extracellular communication, triggering oncogenic signaling pathways and affecting immune cell functions. Through the accumulation of specific intermediates, such as ceramide derivatives, dysregulated sphingolipid metabolism can directly influence cell fate, ultimately promoting therapy resistance and immune escape. Consequently, sphingolipids are now considered as major regulators of resistance to chemo-, radio-, and immune checkpoint inhibition therapy. In this review, we will give an overview of the mechanisms by which sphingolipids orchestrate drug resistance and tumor immunity in lung cancer. We will also discuss the potential of targeting sphingolipid metabolism as a promising therapeutic strategy in lung cancer.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149032149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Proteomic characterisation of the neurotoxic venoms of South Asian kraits and an assessment of drivers of venom variation. 南亚Kraits神经毒性毒液的蛋白质组学特征和毒液变异驱动因素的评估。
IF 3
Biochimie Pub Date : 2026-09-23 DOI: 10.1016/j.biochi.2026.09.006
Alka Sahu, Anita Malhotra, Avinash C Visvanathan, John Benjamin Owens, Sourish Kuttalam, Vishal Santra, Karthikeyan Vasudevan
{"title":"Proteomic characterisation of the neurotoxic venoms of South Asian kraits and an assessment of drivers of venom variation.","authors":"Alka Sahu, Anita Malhotra, Avinash C Visvanathan, John Benjamin Owens, Sourish Kuttalam, Vishal Santra, Karthikeyan Vasudevan","doi":"10.1016/j.biochi.2026.09.006","DOIUrl":"10.1016/j.biochi.2026.09.006","url":null,"abstract":"<p><p>Snake venoms are complex biochemical arsenals shaped by evolutionary processes such as ecological interactions, geographic variation, phylogenetic constraints, and ontogenetic changes. In South Asia, kraits of the genus Bungarus are medically important snakes, yet studies on venom composition and the drivers of venom variation remain limited. We analyzed the inter-specific and intra-specific venom composition of nineteen snakes belonging to five Bungarus species. Using a bottom-up proteomics approach involving RP-HPLC and tandem mass spectrometry we characterized the venom components into toxin families (TxFA) and functional classes (TxFU) and identified between 22 and 105 different toxin proteins in these venoms. The proteomes were dominated by phospholipase A<sub>2</sub> and three-finger toxins, together constituting over 85 % of the total venom and were associated with pre- and post-synaptic neurotoxicity respectively. TxFU resolved the venom toxin composition better than TxFA for the five species. Intra-specific variation in venom composition in Bungarus caeruleus was not influenced by geographic distance. Inter-specific variation in venom composition in five Bungarus species was shaped by phylogeny rather than geography. This highlights the need for a regionally representative antivenoms that includes venoms of non-target krait species.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149031850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Apolipoprotein D modulates obesity-linked inflammation and metabolic syndrome development in a sex dependent manner. 载脂蛋白D以性别依赖的方式调节肥胖相关炎症和代谢综合征的发展。
IF 3
Biochimie Pub Date : 2026-09-23 DOI: 10.1016/j.biochi.2026.09.008
Guillaume Fyfe-Desmarais, Océane Robert, Nayel Milan Ammouche, Nathan Ghafari, Tania Guillemette, Éric Rassart, Lekha Sleno, Catherine Mounier
{"title":"Apolipoprotein D modulates obesity-linked inflammation and metabolic syndrome development in a sex dependent manner.","authors":"Guillaume Fyfe-Desmarais, Océane Robert, Nayel Milan Ammouche, Nathan Ghafari, Tania Guillemette, Éric Rassart, Lekha Sleno, Catherine Mounier","doi":"10.1016/j.biochi.2026.09.008","DOIUrl":"10.1016/j.biochi.2026.09.008","url":null,"abstract":"<p><p>Obesity, or the excessive and often deleterious accumulation of body fat, is a disease that has gained in prevalence over time. This fat accumulation is often the starting point of other obesity-related pathology, such as low-grade systemic inflammation, insulin resistance, glucose intolerance, hepatic steatosis, behavioral changes including increased anxiety and depression, renal dysfunction, and cardiovascular problems, all of which are costly on a personal and societal level. Apolipoprotein D (ApoD), a circulating lipocalin that accumulates in largely in the liver, has been implicated in a number of processes such as altered lipid metabolism in the liver, inflammation modulation and decreased oxidative stress through direct neutralization of lipid peroxides. Knowing that ApoD has metabolism modulating, anti-inflammatory, and antioxidant proprieties, we set out to find if overexpression of ApoD could mitigate obesity linked pathologies. For this, male and female transgenic mice overexpressing the human ApoD were put on a high fat, high sugar diet for 12 weeks. Metabolic, inflammatory, oxidative stress and behavior parameters were assessed. Male mice overexpressing HApoD were significantly more protected from inflammation, liver steatosis and metabolic deterioration caused by the diet, while overexpression of ApoD in females was detrimental for liver inflammation and steatosis, and was detrimental for glucose homeostasis. Circulating hormone levels analysis revealed an altered profile in transgenic mice, and progesterone receptor activation was higher in transgenic mice fed the high fat, high sugar diet. This study demonstrates for the first time sex differences related to ApoD's function, which is most likely related to progesterone metabolism.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149031522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of low magnitude vibration on mesenchymal stem cell osteogenic potential and phenotype. 低强度振动对间充质干细胞成骨潜能和表型的影响。
IF 3
Biochimie Pub Date : 2026-09-23 DOI: 10.1016/j.biochi.2026.09.013
Vitali V Maldonado, Neel H Patel, C Lowry Barnes, Rebekah M Samsonraj
{"title":"Effects of low magnitude vibration on mesenchymal stem cell osteogenic potential and phenotype.","authors":"Vitali V Maldonado, Neel H Patel, C Lowry Barnes, Rebekah M Samsonraj","doi":"10.1016/j.biochi.2026.09.013","DOIUrl":"10.1016/j.biochi.2026.09.013","url":null,"abstract":"<p><p>Mechanical stimulation, particularly low magnitude vibration (LMV), has been shown to increase bone mineral density (BMD) in vivo and the osteogenic potential of bone marrow-derived mesenchymal stem cells (BM-MSCs). However, much remains unknown about its mechanisms of action and effects on cell phenotype. To better understand this phenomenon, we subjected BM-MSCs cultures to in vitro LMV at 32-37 Hz, 0.3-0.4 g for 20 min every day. Gene and protein expression, calcium deposition, actin structure, and cytokine/growth factor secretion were assessed. Additionally, we investigated the role of PIEZO1, a mechanosensitive ion channel, alongside its chemical activation using YODA1 and PIEZO1 silencing. Based on the results from this study, we divided six BM-MSC groups derived from different donors into two categories: LMV-responsive and LMV-nonresponsive. The LMV-nonresponsive groups did not show an overall increase in osteogenic potential with LMV while the LMV-responsive groups experienced a consistent increase in calcium deposits, upregulation of COL1A1, OCN, and CYR61 genes, and a significant increase in PIEZO1 protein. Additionally, LMV-responsive BM-MSCs had a reduction in cell spreading area after 3 days of daily LMV, a significant reduction in some key pro-inflammatory cytokines including IL-1α, IL-1β, and TNFα, and no significant changes in the expression of senescence-associated proteins. By implementing PIEZO1 silencing, we found that this channel is essential to increase calcification in BM-MSC cultures following LMV treatment. Altogether, these findings show the effects of mechanical stimulation on BM-MSC phenotype and the role of PIEZO1 in this process.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149031692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Optimized high-resolution respirometry defines the bioenergetic signature of Drosophila melanogaster thoracic muscle. 优化的高分辨率呼吸测量定义了黑腹果蝇胸肌的生物能量特征。
IF 3
Biochimie Pub Date : 2026-09-23 DOI: 10.1016/j.biochi.2026.09.007
Felipe Berti Valer, Giulia Covolo Spegiorim, Jonatas Rodrigo Dos Santos, Ana Elisa Caleiro Seixas Azzolini, Marcus Fernandes Oliveira, Luciane Carla Alberici
{"title":"Optimized high-resolution respirometry defines the bioenergetic signature of Drosophila melanogaster thoracic muscle.","authors":"Felipe Berti Valer, Giulia Covolo Spegiorim, Jonatas Rodrigo Dos Santos, Ana Elisa Caleiro Seixas Azzolini, Marcus Fernandes Oliveira, Luciane Carla Alberici","doi":"10.1016/j.biochi.2026.09.007","DOIUrl":"10.1016/j.biochi.2026.09.007","url":null,"abstract":"<p><p>Drosophila melanogaster provides a robust model system for investigating mitochondrial metabolism in muscle tissue, particularly due to availability of fly strains that recapitulate genetic mitochondrial disorders, muscle atrophy, and related pathological conditions. However, most experimental approaches are adaptations of protocols originally developed for mammalian muscles, primarily rodents. Here, we systematically applied and refined variations of these mammalian-based protocols to female adult thoracic muscles of D. melanogaster, with particular emphasis on tissue permeabilization, respiratory substrates, respiratory chain inhibitors, and oxidative phosphorylation uncouplers. Our findings appointed pyruvate as the principal respiratory substrate and suggested succinate as a major anaplerotic contributor to the tricarboxylic acid cycle during NADH dehydrogenase-supported respiration. In addition, Drosophila thoracic muscle exhibits a maximal respiratory flux strongly dependent on ADP levels, with oxidative phosphorylation operating near the maximal capacity of the electron transfer system. We compared thoracic muscle with larvae fillet muscle, as well as murine and human skeletal muscle, revealing species- and tissue-specific differences in mitochondrial metabolism. Finally, we validated our refined protocol in a PINK1 RNAi Drosophila model, extending previous evidence of mitochondrial dysfunction associated with PINK1 deficiency in flies.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149027024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of fine particulate matter on neuroblastoma cell line: metabolic and lipid deregulations and their consequences on the onset of neurological diseases. 细颗粒物对神经母细胞瘤细胞系的影响:代谢和脂质失调及其对神经系统疾病发病的影响
IF 3
Biochimie Pub Date : 2026-09-18 DOI: 10.1016/j.biochi.2026.09.011
Candice Dulong, Ana-Maria Trunfio-Sfarghiu, Adina-Nicoleta Lazar, Nathalie Bernoud-Hubac
{"title":"Effects of fine particulate matter on neuroblastoma cell line: metabolic and lipid deregulations and their consequences on the onset of neurological diseases.","authors":"Candice Dulong, Ana-Maria Trunfio-Sfarghiu, Adina-Nicoleta Lazar, Nathalie Bernoud-Hubac","doi":"10.1016/j.biochi.2026.09.011","DOIUrl":"10.1016/j.biochi.2026.09.011","url":null,"abstract":"<p><p>Particulate Matter (PM) contained in atmospheric pollution can interact with pulmonary, cardiac and nervous systems. Recent studies focus on the impact of PM2.5 on the brain and on their potential role in the onset of neurodegenerative diseases such as Alzheimer's disease. Using human neuroblastoma SH-SY5Y cell line as an in vitro neurodegenerative model, multiple interconnected cellular dysfunctions induced by PM2.5 exposure have been highlighted. This includes mitochondrial damages, endoplasmic reticulum stress, oxidative stress, calcium dyshomeostasis and lipid dysregulation. These alterations activate multiple cell death pathway though apoptosis and autophagy-dependent ferroptosis. This review aims to provide an integrated overview of these mechanisms, to better understand the association between PM2.5 exposure and cell degeneration. A particular attention is given to lipid peroxidation and oxidative damage as emerging drivers of neuronal degeneration. Despite significant advances, important gaps remain regarding the translation of in vitro findings to in vivo models and particularly to human pathology. A better understanding of key molecular events is essential to identify therapeutic targets to mitigate or prevent pollution-related neurodegenerative processes.</p>","PeriodicalId":93898,"journal":{"name":"Biochimie","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149003215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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