Journal of Trace Elements in Medicine and Biology最新文献

{"title":"Key role of the CSE/transsulfuration pathway in macrophage phenotypic change under iron overload","authors":"Zhaoji Yuan ,&nbsp;Yuxuan Chen ,&nbsp;Yijun Xin ,&nbsp;Yong Zhang ,&nbsp;Zihao Dong ,&nbsp;Jianxu Wang ,&nbsp;Xiangdong Wang ,&nbsp;Guang Yang ,&nbsp;Siying Li","doi":"10.1016/j.jtemb.2025.127611","DOIUrl":"10.1016/j.jtemb.2025.127611","url":null,"abstract":"<div><h3>Background</h3><div>Iron homeostasis has a significant impact on the phenotypic transformation of macrophages and is implicated in various diseases. In this study, we evaluated the effect of cystathionine-gamma-lyase (CSE)/transsulfuration pathway in iron-overload induced macrophage phenotype change.</div></div><div><h3>Methods</h3><div>The biochemical parameters, such as qRT-PCR, western blot, fluorescence staining, were assessed both <em>in vitro</em> and <em>in vivo</em>.</div></div><div><h3>Results</h3><div>Iron overload disrupts iron metabolism and alters the expression of genes involved in iron transport, resulting in the polarization of macrophages towards the M1 phenotype and an alternating activation state of M2. Meanwhile, excessive iron led to an increase in lipid peroxidation levels and disrupted cysteine metabolism. By utilizing erastin to inhibit SLC7A11 activity and block exogenous cysteine uptake, we were able to observe the exacerbation of the proinflammatory state in macrophages under conditions of cysteine deprivation. The CSE/transsulfuration pathway, serves as the primary route for endogenous cysteine synthesis. In the presence of iron overload, the expression of CSE was upregulated and further enhanced by cysteine deprivation. Deletion of CSE in CSE-knockout mice exacerbated the inflammatory transition of iron-overloaded macrophages by impacting cysteine metabolism and ferritinophagy.</div></div><div><h3>Conclusion</h3><div>The CSE/transsulfuration pathway regulated macrophage phenotype change under iron-overload, which may offer novel insights into potential therapeutic strategies for iron overload-related disorders.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"88 ","pages":"Article 127611"},"PeriodicalIF":3.6,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143172368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sub-lethal toxicity effects of iron oxide nanoparticles (IONPs) on the biochemical, oxidative biomarkers, and metabolic profile in Caridina fossarum","authors":"Hamidreza Shahryari ,&nbsp;Iman Sourinejad ,&nbsp;Amin Gholamhosseini ,&nbsp;Mahdi Banaee","doi":"10.1016/j.jtemb.2025.127613","DOIUrl":"10.1016/j.jtemb.2025.127613","url":null,"abstract":"<div><h3>Backgrounds</h3><div>This study aimed to assess the toxicity effect of iron oxide nanoparticles (IONPs) on the biochemical and oxidative markers in freshwater miniature shrimp (<em>Caridina fossarum</em>).</div></div><div><h3>Materials and methods</h3><div>Based on the pre-test results, 540 shrimp were distributed into six trial groups in triplicate and exposed to sub-lethal concentrations of Fe3O4 nanoparticles at 0.0, 40, 80, 120, 160, and 320 µg L⁻¹ for 14 days. Next, biochemical parameters and oxidative biomarkers were measured.</div></div><div><h3>Results</h3><div>The results showed that exposure to 120 µg L⁻¹ ≤ of IONPs significantly increased aspartate aminotransferase activity in <em>C. fossarum</em>. Alanine aminotransferase activity showed a significant increase at 320 µg L⁻¹ . Similarly, alkaline phosphatase activity was meaningfully elevated at 160 and 320 µg L⁻¹ . Lactate dehydrogenase activity notably increased at 120 and 320 µg L⁻¹ of IONPs. IONPs at ≥ 80 µg L⁻¹ significantly reduced gamma-glutamyl transpeptidase and butyrylcholinesterase activities. Cholesterol and triglyceride levels significantly increased at 320 µg L⁻¹ . Exposure to 80 µg L⁻¹ ≤ of IONPs significantly increased superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase activities in <em>C. fossarum</em>. Moreover, total antioxidant capacity and malondialdehyde content increased considerably in shrimp exposed to different concentrations of IONPs. Exposure to IONPs could induce oxidative stress, disrupt protein structures, oxidize sulfur-containing and essential aromatic and aliphatic amino acids, impair nucleic acid stability, and change lipid metabolism and membrane integrity.</div></div><div><h3>Conclusion</h3><div>In conclusion, significant changes in biochemical parameters, oxidative biomarkers, and metabolic profile disruptions in <em>C. fossarum</em> exposed to sub-lethal concentrations of IONPs indicated cellular damage and oxidative stress.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"88 ","pages":"Article 127613"},"PeriodicalIF":3.6,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143172369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of blood selenium with dyslipidemia in children and adolescents: a cross-sectional analysis","authors":"Feiqi Lin ,&nbsp;Zhiyuan Chen","doi":"10.1016/j.jtemb.2025.127596","DOIUrl":"10.1016/j.jtemb.2025.127596","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to examine the association between blood selenium levels and dyslipidemia in children and adolescents.</div></div><div><h3>Methods</h3><div>Data from the National Health and Nutrition Examination Survey (NHANES) 2011–2020 were analyzed, including 8191 participants aged 6–19 years. Dyslipidemia was defined by elevated total cholesterol (TC ≥ 200 mg/dL), lowered high-density lipoprotein cholesterol (HDL-C &lt; 40 mg/dL), or elevated non-HDL-C (≥ 145 mg/dL). Associations between blood selenium levels and dyslipidemia were examined using multivariate logistic regression, linear regression, and restricted cubic spline (RCS) analysis.</div></div><div><h3>Results</h3><div>The study population had a mean age of 12.33 years, with 51.21 % boys. After adjusting for multiple confounding factors, including dietary selenium intakes and supplementation, higher blood selenium levels were associated with increased odds of dyslipidemia and its components. In the highest quartile of blood selenium (&gt;193.99 μg/L), adjusted odds ratios (ORs) were 1.60 (95 % confidence interval [CI]: 1.23–2.08) for dyslipidemia, 1.70 (95 % CI: 1.19–2.43) for elevated TC, 1.38 (95 % CI: 0.97–1.96) for lowered HDL-C, and 1.73 (95 % CI: 1.20–2.48) for elevated non-HDL-C. A significant nonlinear association was observed, with dyslipidemia prevalence increasing notably above a threshold of 184.28 μg/L (<em>P</em>-nonlinearity=0.02), following a J-shaped curve. Subgroup analysis revealed significant interaction by race (<em>P</em>-interaction=0.02), with non-Hispanic White individuals showing a stronger association (OR=1.83, 95 % CI: 1.19–2.80) compared to other racial groups (OR=1.40, 95 % CI: 1.05–1.88).</div></div><div><h3>Conclusion</h3><div>Elevated blood selenium levels are associated with higher prevalence of dyslipidemia in children and adolescents, particularly among non-Hispanic White individuals. The association is nonlinear, with a notable increase in the prevalence of dyslipidemia observed above a blood selenium level of 184.28 μg/L. These findings suggest a need for further research to understand selenium's role in lipid profiles and its implications for public health.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127596"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Water-soluble organic selenometabolites of alfalfa (Medicago sativa L.) green biomass-derived fractions” [J. Trace Elem. Med. Biol. 86 (2024) 127545]","authors":"Éva Domokos‑Szabolcsy ,&nbsp;Áron Soós ,&nbsp;Béla Kovács ,&nbsp;Zoltán Kovács ,&nbsp;Mihály Dernovics","doi":"10.1016/j.jtemb.2024.127579","DOIUrl":"10.1016/j.jtemb.2024.127579","url":null,"abstract":"","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127579"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of mercury exposure on male reproduction: Mechanistic insights","authors":"Bhawna Kushawaha ,&nbsp;Rajkumar Yadav ,&nbsp;Satish Kumar Garg ,&nbsp;Emanuele Pelosi","doi":"10.1016/j.jtemb.2025.127598","DOIUrl":"10.1016/j.jtemb.2025.127598","url":null,"abstract":"<div><div>Mercury is a pervasive environmental toxin with significant negative effects on human health. In occupational settings, incidents such as the Minamata and Niigata disease in Japan and the large-scale methylmercury poisoning in Iraq have highlighted the severe health impacts of mercury exposure. It is widely accepted that all forms of mercury including methylmercury and mercuric chloride have the potential to induce toxic effects in mammals, and there is increasing concern about the impact of environmentally relevant levels of mercury on reproductive functions. This review summarizes current knowledge on the mechanisms of mercury toxicity, focusing specifically on its impact on male reproductive health across species. We searched the literature and found that mercury exposure is associated with testicular degeneration, altered spermatogenesis, and Leydig cell deformation. In addition, mercury can disrupt sperm motility, steroidogenesis and interfere with the hypothalamic-pituitary-gonadal axis by generation of reactive oxygen species, inducing mitochondrial dysfunction, epigenetic changes, and DNA damage. At the molecular level, mercury has been found to dysregulate the expression of key steroidogenic and spermatogenic genes, significantly reducing overall fertility potential. However, specific mechanisms of action remain to be fully elucidated. Similarly, comprehensive data on the potential transgenerational effects of paternal mercury exposure are lacking. In this review, we discuss both animal and human studies, and highlight the need for further research due to lack of standardization and control for variables such as lifestyle, immune system function, and exposure concentrations.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127598"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FESTEM","authors":"","doi":"10.1016/S0946-672X(25)00022-7","DOIUrl":"10.1016/S0946-672X(25)00022-7","url":null,"abstract":"","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127609"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143103524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of neuroprotective potential of Cuscuta reflexa in aluminium chloride-induced experimental model of Alzheimer’s disease: In vitro and in vivo studies","authors":"Pallavi Gangarde,&nbsp;Shvetank Bhatt,&nbsp;Rohini Pujari","doi":"10.1016/j.jtemb.2025.127612","DOIUrl":"10.1016/j.jtemb.2025.127612","url":null,"abstract":"<div><h3>Background &amp; aims</h3><div><em>Cuscuta reflexa</em> (family Convolvulaceae), commonly known as giant dodder or Amarbel, is a parasitic plant that has garnered attention in pharmacological research due to its diverse bioactive compounds and potential therapeutic applications. Scientific studies have validated its traditional uses in folk medicine, highlighting its pharmacological activities. Alzheimer's Disease (AD) is a neurodegenerative disorder marked by the buildup of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT) in the brain, leading to synaptic impairment and the gradual loss of neurons. Currently, no effective medication is available to treat the development and progression of the disease. Hence, there is a rising concern about using alternative therapy such as herbal medicine to limit the progression of AD and improve the quality of a patient’s life with minimum side effects. The plant <em>Cuscuta reflexa</em> has traditionally been claimed to possess neuroprotective effects but has not yet been validated scientifically. The present study aimed to investigate the potential of the hydroalcoholic extract of <em>Cuscuta reflexa</em> (CRE) to ameliorate the neurodegenerative effect of aluminium chloride (AlCl₃) using <em>in vitro</em> and in <em>vivo</em> studies.</div></div><div><h3>Methods</h3><div>The neuroprotective activity of CRE was evaluated using <em>in vitro</em> and <em>in vivo</em> experimental models of AlCl₃-induced AD.</div></div><div><h3>Results</h3><div>The <em>in vitro</em> study showed that CRE markedly reduced AlCl₃-induced cytotoxicity in PC12 cells. The <em>in vivo</em> study using the AlCl₃-induced AD rat model showed that CRE treatment improved learning and memory, as evaluated using the open field test (OFT) and Morris water maze (MWM) test. CRE also showed the reduction in oxidative stress induced by AlCl₃ in the brains of the rats by virtue of the significant decrease in oxidative stress biomarker malondialdehyde (MDA) and increase in the antioxidant parameters such as reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD). Further, CRE exhibited its cholinergic activity by lowering the AlCl₃-induced enhanced levels of acetylcholinesterase (AChE) in the brains of rats. Histopathological analysis of the brains of rats showed that CRE treatment prevented the reactive changes and the damage in the neuronal tissue caused due to the AlCl₃.</div></div><div><h3>Conclusion</h3><div>Conclusively, CRE ameliorated AlCl₃-induced neurobehavioural toxicity in the rat model of AD by virtue of its anti-inflammatory, antioxidant, cholinergic and neuroprotective effects which suggests its use in the treatment of progressive neural damage and cognitive deficits in AD patients.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"88 ","pages":"Article 127612"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143194487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How does zinc chelation affect liver sphingolipid metabolism in an Alzheimer's-like model?","authors":"Ebru Afşar ,&nbsp;Deniz Kantar","doi":"10.1016/j.jtemb.2025.127589","DOIUrl":"10.1016/j.jtemb.2025.127589","url":null,"abstract":"<div><h3>Background</h3><div>The present study aimed to evaluate the impact of Cyclo-Z, a combination of Cyclo (His-Pro) plus zinc, on hepatic sphingolipid (SL) metabolism and antioxidant properties in a rat model of Alzheimer's disease (AD).</div></div><div><h3>Methods</h3><div>Alzheimer's disease rat model created via intracerebroventricular (i.c.v.) amyloid beta-42 oligomer (AβO) injection into the lateral ventricles. Cyclo-Z administration was performed with daily gavage for 3 weeks after the AβO injection. Ceramide, ceramide kinase (CERK), sphingosine 1 phosphate (S1P), glutathione (GSH), total oxidant capacity (TOS), 4-hydroxynonenal (HNE) and caspase-3 levels were measured with Elisa kit in liver tissue.</div></div><div><h3>Results</h3><div>S1P, CERK and GSH levels increased and ceramide, TOS, 4 HNE, and caspase-3 levels decreased in the liver tissues of AD group. Cyclo-Z treatment decreased S1P, CERK, ceramide and caspase-3 levels but increased TOS and 4-HNE levels in the liver tissues of AD group.</div></div><div><h3>Conclusion</h3><div>These results showed that SL metabolism was modulated to generate an anti-apoptotic defense system in liver tissue of AD rats</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127589"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between co-exposure to multiple heavy metals and age-related macular degeneration: A cross-sectional study","authors":"Mu-hong Wei ,&nbsp;Ju-xiao Li ,&nbsp;Jing Mi ,&nbsp;Qing Wang ,&nbsp;Feng Xu ,&nbsp;Che Xu","doi":"10.1016/j.jtemb.2024.127573","DOIUrl":"10.1016/j.jtemb.2024.127573","url":null,"abstract":"<div><h3>Background &amp; aims</h3><div>Accumulating evidence suggests that exposure to single heavy metal can facilitate the progression of age-related macular degeneration (AMD). However, the effects of exposure to mixtures of heavy metals on AMD remain largely unexplored. This study aims to investigate both the joint and individual impacts of arsenic (As), mercury (Hg), cadmium (Cd), and lead (Pb) on AMD within a co-exposure framework.</div></div><div><h3>Methods</h3><div>Data from subjects participating the US National Health and Nutrition Examination Survey (NHANES, 2005–2008) were analyzed. Concentrations of As, Hg, Cd, and Pb were determined in urine by inductively coupled plasma dynamic reaction cell mass spectrometry (ICP-DRC-MS) for As and Hg, and inductively coupled plasma mass spectrometry (ICP-MS) for Cd and Pb. The weighted quantile sum (WQS) and Bayesian kernel machine regression (BKMR) models were employed to assess the effects of heavy metal mixtures on AMD risk.</div></div><div><h3>Results</h3><div>Both WQS and BKMR analyses consistently revealed a significant overall association between heavy metal mixtures and the risk of all types of AMD. The combined effect was more evident among patients with early AMD compared to those with late AMD. Cd and Hg were the main contributors driving these combined effects within the context of metal mixtures. Elevated urinary levels of Cd were positively correlated with an increased risk for all types as well as early AMD. Higher exposure to Hg corresponded with an elevated risk for early AMD. Furthermore, BKMR analysis indicated that the influence of Cd on early AMD exhibited a non-linear pattern.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that co-exposure to As, Hg, Cd, and Pb is associated with an elevated risk for developing AMD, particularly in its early stages. Furthermore, excessive exposure to Cd and Hg has been identified as key contributing factors in this process.</div></div>","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127573"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotective potential of tectochrysin against vanadium induced heart damage via regulating NLRP3, JAK1/STAT3 and NF-κB pathway","authors":"Yahui Wang ,&nbsp;Hesham M. Hassan ,&nbsp;Abdullah Nisar ,&nbsp;Syeda Sania Zahara ,&nbsp;Ali Akbar ,&nbsp;Ahmed Al-Emam","doi":"10.1016/j.jtemb.2025.127588","DOIUrl":"10.1016/j.jtemb.2025.127588","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Vanadium (VAN) is a significant trace element, but its higher exposure is reported to cause severe organ toxicity. Tectochrysin (TEC) is a naturally derived flavonoid which demonstrates a wide range of pharmacological properties.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Aim&lt;/h3&gt;&lt;div&gt;The current study was planned to assess the cardioprotective potential of TEC against VAN induced cardiotoxicity in rats via regulating biochemical, and histological profile.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Research plan&lt;/h3&gt;&lt;div&gt;Thirty-six male Sprague Dawley rats were apportioned into four groups including the control, VAN (1.5 mg/kg) treated, VAN (1.5 mg/kg) + TEC (2.5 mg/kg) administrated as well as TEC (2.5 mg/kg) alone supplemented group. The doses were administrated for 28 days through oral gavage. The biochemical and histological parameters were evaluated by using qRT-PCR, ELISA, biochemical assays, histological as well as molecular simulation techniques.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Findings&lt;/h3&gt;&lt;div&gt;VAN intoxication reduced the activities of catalase (CAT) (84.25 %), glutathione peroxidase (GPx) (65.28 %), glutathione reductase (GSR) (78.52 %), heme oxygenase-1 (HO-1) (81.81 %), superoxide dismutase (SOD) (83.71 %) and glutathione (GSH) (76.86 %) contents while upregulating the levels of reactive oxygen species (ROS) (87.26 %) and malondialdehyde (MDA) (91.32 %). Moreover, VAN administration increased the gene expressions of &lt;em&gt;nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3)&lt;/em&gt; (91.47 %)&lt;em&gt;, monocyte chemoattractant protein-1 (MCP-1)&lt;/em&gt; (92.51 %)&lt;em&gt;, interleukin-6 (IL-6)&lt;/em&gt; (83.63 %)&lt;em&gt;, tumor necrosis factor-alpha (TNF-α)&lt;/em&gt; (89.43 %)&lt;em&gt;, janus kinase 1 (JAK1)&lt;/em&gt; (95.55 %)&lt;em&gt;, signal transducer&lt;/em&gt; and &lt;em&gt;activator of transcription 3 (STAT3)&lt;/em&gt; (91.25 %)&lt;em&gt;, nuclear factor-kappa B (NF-κB)&lt;/em&gt; (81.31 %)&lt;em&gt;, interleukin-18 (IL-18)&lt;/em&gt; (93.27 %)&lt;em&gt;, interleukin-1 beta (IL-1β)&lt;/em&gt; (85.79 %) and &lt;em&gt;cyclooxygenase-2 (COX-2)&lt;/em&gt; (82.12 %). The levels of CK-MB (89.43 %), BNP (91.73 %), NT-proBNP (93.64 %), CPK (87.56 %), LDH (92.62 %), troponin I (94.25 %), troponin T (97.53 %) and CRP (88.45 %) were increased following the VAN intoxication. Besides, VAN exposure upregulated the levels of Caspase-9 (89.52 %), Bax (95.52 %) and Caspase-3 (92.52 %) while reducing the levels of Bcl-2 (75.66 %). The structural integrity of cardiac tissues was extensively disrupted following VAN-induced intoxication. However, TEC treatment remarkably ameliorated cardiotoxicity via regulating abovementioned dysregulations induced by VAN exposure. At the end, molecular docking (MD) analysis was accomplished to confirm the potential protective effect of TEC against VAN prompted cardiac dysfunction. It was detected that TEC can strongly bind with the active site of &lt;em&gt;JAK1, NF-kB and STAT3&lt;/em&gt; which also confirm its cardioprotective effect against VAN provoked cardiac dysfunction.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;VAN intox","PeriodicalId":49970,"journal":{"name":"Journal of Trace Elements in Medicine and Biology","volume":"87 ","pages":"Article 127588"},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}