Biological Trace Element Research最新文献

{"title":"Metal Homeostasis Imbalance as Potentially Contributing Mechanism in Onset of Cardiac Disorders in Individuals with Chronic Obstructive Pulmonary Disease and Chronic Kidney Disease.","authors":"Ana Cirovic, Jovan Jevtic, Nemanja Brankovic, Aleksandar Cirovic","doi":"10.1007/s12011-026-05330-z","DOIUrl":"https://doi.org/10.1007/s12011-026-05330-z","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD) are common non-communicable diseases associated with disturbances in metal and metalloid homeostasis and an increased risk of cardiovascular disorders. However, the mechanisms underlying these associations remain incompletely understood. Therefore, this study investigated whether COPD or CKD is associated with altered accumulation of selected metals and metalloids in the left ventricular myocardium. We analyzed 57 autopsy-derived left ventricular myocardial specimens, including 12 individuals with COPD, 11 with CKD, and 34 controls (mean age 70 ± 14 years). Concentrations of arsenic, lead, calcium, cadmium, mercury, manganese, magnesium, iron, copper, nickel, and zinc were determined using inductively coupled plasma mass spectrometry (ICP-MS). Individuals with COPD had significantly higher myocardial cadmium concentrations, whereas individuals with CKD exhibited lower myocardial iron concentrations in unadjusted analyses. Zn levels and Zn/Cu and Zn/Fe ratios were inversely correlated with Pb, As, and Hg. After adjustment for the presence of cardiomyopathy, myocardial cadmium concentrations remained significantly higher, while magnesium concentrations were significantly lower in individuals with COPD compared with controls. No significant differences remained between individuals with CKD and controls. Higher myocardial cadmium and lower magnesium concentrations in individuals with COPD suggest altered myocardial metal homeostasis that may be relevant to COPD-associated cardiac alterations. Further studies are needed to clarify the mechanisms and clinical significance of these findings.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined sodium selenite-cinnabar suppresses mercury accumulation and modulates nephrotoxic responses in mice.","authors":"Yuzhou Zhuo, Xiaoqin Liu, Zhihui Dai","doi":"10.1007/s12011-026-05332-x","DOIUrl":"https://doi.org/10.1007/s12011-026-05332-x","url":null,"abstract":"<p><p>Cinnabar (ZS) is a commonly used in traditional Chinese medicine (TCM), but its clinical application is limited owing to mercury (Hg) related toxicity. This study aimed to explore the kidney toxic and related mechanisms of ZS combined with sodium selenite (Na₂SeO₃). Eighty specific-pathogen-free (SPF) male Kunming (KM) mice were randomly divided into ten groups: control (0.5% CMC-Na), HgS (50 mg·kg^- 1), ZhuShaAnShenWan (ZSASW) (600 mg·kg^- 1), Hg(NO₃)₂ (1.2 mg·kg^- 1), cinnabar-L(ZS-L) (50 mg·kg^- 1), cinnabar-H (ZS-H) (200 mg·kg^- 1), Na₂SeO₃ (1 mg·kg^- 1), ZS-Na₂SeO₃ (50 mg/kg-1 mg·kg^- 1), HgS-Na₂SeO₃ (50 mg·kg^- 1-1 mg·kg^- 1) and ZSASW-Na₂SeO₃ (600 mg·kg^- 1-1 mg·kg^- 1). All mice received intragastric administration once daily for 30 consecutive days. Kidney contents of Hg, selenium (Se) and other trace elements were measured by inductively coupled plasma-mass spectrometry (ICP-MS) and related detection instruments. Kidney histopathological lesions, cell apoptosis and serum levels of creatinine (Cre), blood urea nitrogen (BUN) and uric acid (UA) were detected to assess renal injury. The results demonstrated that the kidney cell apoptosis rate higher in Na₂SeO₃ (P < 0.05) and ZS-H groups (P < 0.05) than in ZS-L and ZS-Na₂SeO₃ combination groups. Serum kidney function indexes were obviously increased in HgS-Na₂SeO₃, Na₂SeO₃ groups compared with the control group (P < 0.05). The mercury content in the kidneys of the ZS-H group was 10.51 µg·g^- 1, ZS-L group was 7.99 µg·g^- 1, while that of the ZS-Na₂SeO₃ group was 3.43 µg·g^- 1. Inorganic mercury exhibited stronger kidney accumulation capacity than ZS and ZSASW. The toxic effect of ZS is not equivalent to that of inorganic mercury. The content of Hg in kidney was positively correlated with the dose. Co-administration of Na₂SeO₃ and ZS could lower kidney mercury accumulation. This could result from suppressed intestinal Hg absorption or formation of inert in-vivo complexes. Relevant component interactions should be fully considered when evaluating the safety and toxicity of ZS.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association of Copper Intake with Hearing Loss: a Cross-Sectional Study.","authors":"Qilei Zhang, Feng Wang, Siqi Yang, Yafeng Yu","doi":"10.1007/s12011-026-05326-9","DOIUrl":"https://doi.org/10.1007/s12011-026-05326-9","url":null,"abstract":"<p><p>Currently, evidence for the relationship between copper intake and hearing loss (HL) is insufficient; therefore, further research is needed. This study aimed to investigate the potential association between copper intake and HL in adults in the United States. We conducted a retrospective cross-sectional study using data from 2777 participants of the 2015-2016 National Health and Nutrition Examination Survey (NHANES). Measurements of copper intake and HL were collected for all participants. Multivariate logistic regression, restricted cubic spline, and subgroup analyses were used to assess the research objectives. In fully adjusted Model 3, continuous dietary copper intake was inversely associated with speech-frequency hearing loss (SFHL, OR = 0.71, 95%CI:0.55-0.91, p = 0.008) and high-frequency hearing loss (HFHL, OR = 0.74, 95%CI:0.60-0.91, p = 0.004). Relative to Q1, Q3 and Q4 showed significant inverse associations with SFHL; significant inverse associations with HFHL were found in Q2 and Q4 rather than Q3. Significant linear trends across quartiles existed for both outcomes (Table 2). Subgroup analyses indicated significant sex interaction for SFHL (p = 0.023). Significant inverse associations between copper intake and two types of hearing loss were only observed in females. Heterogeneous associations were found across subgroups stratified by age, chronic disease and noise exposure, with most interaction terms non-significant (Table 3, Fig. 3). Restricted cubic spline models demonstrated no statistically significant nonlinear association between dietary copper intake and either SFHL (p for non-linearity = 0.328) or HFHL (p for non-linearity = 0.616) (Fig. 2). Our findings suggested an inverse linear association between dietary copper intake and hearing loss among US adults, and this association was modified by sex, being statistically significant only in females. Further research is needed to explore the underlying mechanisms.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carvacrol Modulates Cadmium-Induced Behavioral, Biochemical, Histopathological, and Metabolomic Alterations in rats.","authors":"Nigar Abbak, Emirhan Nemutlu, Tuba Reçber, Asli San Dagli Gul, Fatma Bahar Sunay, Okan Arihan","doi":"10.1007/s12011-026-05280-6","DOIUrl":"10.1007/s12011-026-05280-6","url":null,"abstract":"<p><p>Cadmium (Cd) is a toxic heavy metal that causes multi-organ damage, including neurotoxicity. Carvacrol (CAR), a natural phenolic compound obtained from aromatic plants, is known for its protective properties. This study investigated the effects of CAR against Cd-induced toxicity through comprehensive behavioral assessments including the Open Field Test (OFT), Elevated Plus Maze (EPM), Barnes Maze, and Rotarod test, while plasma biochemical parameters, liver and kidney histopathology, and untargeted metabolomic profiles (plasma and brain) were also evaluated. Male Wistar albino rats were randomly divided into six groups and orally administered Cd (50 mg/kg) and/or CAR (20 or 40 mg/kg body weight) for 12 days. CAR alone increased locomotor activity, altered neuroprotective related metabolic pathways and did not cause weight loss. Cd exposure significantly increased body weight loss and anxiety-like behaviors while elevating cortisol, urea, AST, ALT levels and inducing significant histopathological damage in liver and kidney tissues (p < 0.05). Integrated plasma-brain metabolomic analyses revealed that Cd exposure disrupts multiple interconnected biological systems, including the antioxidant defence system, mitochondrial energy pathways, and cell membrane integrity. Although Cd-CAR co-administration partially reversed worsening of the anxiolytic-like behavior, locomotor activity, and renal tissue integrity, it failed to fully prevent Cd-induced toxicity and further aggravated weight loss, biochemical alterations (creatinine, AST, ALT), and metabolic disturbances (p < 0.05). In conclusion, co-administration of CAR with Cd provided only limited and heterogeneous protection that was insufficient to counteract Cd-induced multisystem toxicity. This current study presents a wide assessment to the systemic use of CAR against Cd according to results of behavioral, histopathological, biochemical, and metabolomic parameters.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selenium, Selenoprotein P, and Gut Dysbiosis are Associated with Cartilage Damage in Osteoarthritis Patients.","authors":"Tatiana V Korobeinikova, Anatoly V Skalny, Ali F Aliyev, Nelli I Remizova, Galina D Morozova, Konstantin S Ternovoy, Alexey A Kovalenko, Michael Aschner, Feng Zhang, Andrey O Plotnikov, Yuriy A Khlopko, Guo Xiong, Viktor A Gritsenko, Alexey A Tinkov","doi":"10.1007/s12011-026-05331-y","DOIUrl":"https://doi.org/10.1007/s12011-026-05331-y","url":null,"abstract":"<p><p>The objective of the present study was to evaluate markers of selenium (Se) metabolism and taxonomic characteristics of gut microbiota, as well as their relationship to markers of inflammation and cartilage damage in patients with osteoarthritis (OA). The study enrolled 50 healthy controls, 45 patients with knee OA (kOA), and 41 patients with knee and one-sided hip OA (khOA). Serum selenoprotein P (SELENOP), cartilage oligomeric matrix protein (COMP), lipopolysaccharide (LPS), C-reactive protein (CRP), as well as C3 and C5a complement components were assessed. Serum, hair, and urinary Se levels were evaluated using inductively coupled plasma-mass spectrometry (ICP-MS). Fecal microbiota taxonomy was evaluated by high-throughput sequencing. Patients with kOA and especially khOA were characterized by higher COMP and CRP levels. LPS concentration also tended to be higher in khOA patients. The lowest serum Se and SELENOP levels were observed in khOA patients. The richness of Bacteroidota phylum, classes Bacteroidia and Negativicutes was increased, whereas the abundance of Coriobacteriia was lower in OA patients compared to controls. The relative abundance of families Actinomycetaceae, Anaerovoracaceae, Clostridiaceae, Eggerthellaceae, Lactobacillaceae, Peptostreptococcaceae, Streptococcaceae, and unclassified_Clostridia UCG-014 was reduced in OA patients, while Oscillospiraceae and Prevotellaceae were enriched. Significant group differences were also observed in the richness of certain bacterial genera. Multiple linear regression analysis revealed inverse association between SELENOP and LPS concentrations, while COMP concentration was associated with C5a and SELENOP levels in a positive and negative manner, respectively. Certain bacterial taxa were also considered significant predictors of SELENOP and COMP levels. Therefore, these novel data establish that gut dysbiosis is associated with both cartilage damage and altered Se metabolism in OA.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148910589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Toxicogenomic Analysis Reveals Potential Molecular Signatures Associated with Cadmium-Related Osteoarthritis.","authors":"Lichun Qiao, Husna Wali, Xiangyu Fan, Jing Tang, Yiming Shen, Qingsong Li, Qian Dong, Jing Han, Yijie Guo","doi":"10.1007/s12011-026-05327-8","DOIUrl":"https://doi.org/10.1007/s12011-026-05327-8","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a common chronic joint disease, and cadmium (Cd) exposure may contribute to its progression. This study integrated network toxicology, transcriptomic datasets from the Gene Expression Omnibus (GEO), weighted gene co-expression network analysis (WGCNA), and machine-learning methods to identify molecular signatures potentially associated with Cd exposure-related OA. A total of 740 overlapping targets between Cd-associated genes and OA-related genes were identified. These targets were primarily enriched in oxidative stress, inflammation, apoptosis, extracellular matrix degradation, and the phosphoinositide 3-kinase/protein kinase B (PI3K-Akt), mitogen-activated protein kinase (MAPK), tumor necrosis factor (TNF), nuclear factor kappa B (NF-κB), interleukin 17 (IL-17), and hypoxia-inducible factor 1 (HIF-1) signaling pathways. Integrated transcriptomic analysis identified 174 differentially expressed genes (DEGs), and WGCNA identified the yellow module as the module most strongly associated with OA. Least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and random forest analyses identified BCL6 and FOSL2 as robust diagnostic feature genes. Both genes were consistently down-regulated in OA samples and demonstrated strong diagnostic performance across the analyzed cohorts. These findings suggest that BCL6 and FOSL2 may be potential diagnostic biomarkers of Cd-associated OA.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BTN2A2 Alleviates Arsenic-Induced Liver Fibrosis by Suppressing Pyroptosis and Inflammation.","authors":"Yu Luo, Yusha Liu, Zhenting Zhang, Xiaobo Peng, Xianbin Wang, Min Su, Jiayi Zeng, Ting Hu, Peng Luo","doi":"10.1007/s12011-026-05329-6","DOIUrl":"https://doi.org/10.1007/s12011-026-05329-6","url":null,"abstract":"<p><p>Arsenic is a ubiquitous environmental pollutant that accumulates in the liver upon chronic exposure, driving hepatic injury and carcinogenesis. Hepatic fibrosis is a critical juncture in the progression from chronic damage to cirrhosis and cancer, yet therapeutic strategies targeting the fibrotic stage of arsenic-induced liver disease remain limited. Here, we investigated whether butyrophilin subfamily 2 member A2 (BTN2A2) serves as a protective regulator in arsenic‑induced liver fibrosis and explored its underlying mechanisms. Mice were randomly divided into four groups (n = 6 per group): untreated control, 40 ppm sodium arsenite (NaAsO₂), 80 ppm NaAsO₂, and an intervention group receiving continuous 80 ppm NaAsO₂ in drinking water for 36 weeks with BTN2A2 administration during weeks 32‑36. After 36 weeks, arsenic burdens in urine and hepatic tissue confirmed substantial accumulation, accompanied by a dose‑dependent decline in hepatic BTN2A2 protein expression. Remarkably, BTN2A2 administration alleviated liver fibrosis but did not reduce arsenic accumulation. At the molecular level, BTN2A2 suppressed the hepatic expression of pro‑inflammatory mediators, including interleukin-17 (IL-17), and pyroptotic effectors, concomitantly decreasing NLR family pyrin domain containing 3‌ (NLRP3), Caspase‑1, and Gasdermin D N-terminal domain (GSDMD‑N) protein levels. Flow cytometry further revealed that BTN2A2 restored the intrahepatic immune landscape by reducing T helper 17 cells and increasing regulatory T cells (Tregs). Mechanistically, BTN2A2 suppressed arsenite-triggered NLRP3/Caspase-1/GSDMD-N pyroptotic signaling in hepatocytes and reduced IL-17 secretion, thereby limiting hepatic stellate cell-mediated extracellular matrix deposition. Conversely, siRNA‑mediated knockdown of BTN2A2 in hepatocytes significantly unleashed the pyroptotic cascade, reinforcing BTN2A2 as a genuine negative regulator of hepatocyte pyroptosis. Collectively, these findings demonstrate that BTN2A2 attenuates arsenic‑induced hepatic fibrosis by suppressing IL‑17‑driven inflammation and pyroptosis, supporting its potential as a therapeutic target for environmental arsenic‑associated fibrotic liver disease.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"Radiation-Synthesized Gallotannin Hydrogel Attenuates Trisenox-Induced Nephrotoxicity in Rats: miR-223/TXNIP Axis Modulation of Oxidative Stress and Inflammation\".","authors":"Omayma A R Abo-Zaid, Mostafa A Farrag, Aya S R Shaaban, Hiam Rushdy A Salem, Marwa A Esmat","doi":"10.1007/s12011-026-05301-4","DOIUrl":"https://doi.org/10.1007/s12011-026-05301-4","url":null,"abstract":"<p><p>Arsenic trioxide (ATO) is a potent therapeutic agent against acute promyelocytic leukemia; nevertheless, its clinical utility is severely restricted by dose-limiting nephrotoxicity. This study investigated the protective potential of a radiation-synthesized gallotannin hydrogel (GTH) against ATO-induced kidney injury in rats. Forty male Wistar rats were randomized into four experimental groups: Control, ATO (4 mg/kg, i.p., for 4 weeks), GTH (2 mg/kg, i.p.), and ATO + GTH. GTH treatment was initiated during the third week of ATO administration, with GTH being administrated one hour prior to ATO injection. Following the experimental period, animals were sacrificed, tissue histology was examined, and renal function was assessed by serum urea and creatinine levels. Oxidative stress was evaluated via MDA, SOD, GSH, and GPx markers. Additionally, miR-223 and TXNIP expression levels were quantified using qRT-PCR. Inflammatory mediators (NF-κB, NLRP3, Caspase-1, IL-1β, and IL-18), endoplasmic reticulum (ER) stress markers (PERK, eIF2α, and CHOP), and the apoptotic marker caspase-3 were analyzed by ELISA. Our results revealed that GTH noticeably ameliorated kidney dysfunction, as evidenced by reduced serum urea and creatinine levels. Furthermore, GTH attenuated oxidative stress by decreasing MDA levels and restoring antioxidant enzyme activities (SOD, GSH, and GPx). Histological analysis confirmed that GTH mitigated structural renal damage. Molecularly, GTH administration suppressed the ATO-induced upregulation of miR-223 and TXNIP. This downregulation correlated with a reduction in inflammatory mediators, attenuation of ER stress markers, and decreased apoptosis. These findings demonstrate that radiation-synthesized gallotannin hydrogel (GTH) exerts nephroprotective effects against ATO-induced nephrotoxicity. These benefits are driven by antioxidant, anti-inflammatory, and anti-apoptotic mechanisms mediated via modulation of the miR-223/TXNIP axis.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Manifestations of Lithium Deficiency in the Human Body: What is Known to Date (A Narrative Review).","authors":"Cherpakov R A, Grebenchikov O A, Makarova A M, Antonova V V, Boeva E A","doi":"10.1007/s12011-026-05325-w","DOIUrl":"https://doi.org/10.1007/s12011-026-05325-w","url":null,"abstract":"<p><p>Lithium is a pharmacological agent with a well-established role in psychopharmacology. Interest in its \"trace\" doses as a potential nutrient has increased in the context of geochemical variability of lithium concentrations in drinking water and reports suggesting its possible influence on cognitive status. Within the current regulatory framework, lithium is not recognized as an essential element for humans; no diagnosable \"deficiency syndrome\" exists, nor are there validated biomarkers of lithium status under background exposure. A key methodological premise of this review is to distinguish between two \"dose domains\": therapeutic concentrations (mmol/L) and background intake (µg/day, µg/L). This targeted narrative review critically summarizes evidence on human lithium exposure, candidate status markers, and reported deficiency-related hypotheses in the context of the current absence of a clinically defined lithium-deficiency syndrome, validated biomarkers, and binding nutritional reference standards. A targeted narrative search was conducted in PubMed/MEDLINE, Scopus, Web of Science Core Collection, and eLIBRARY.RU. Regulatory and programmatic documents were retrieved from WHO IRIS, EFSA Publications, the U.S. Environmental Protection Agency (EPA; including the Fifth Unregulated Contaminant Monitoring Rule [UCMR-5] and related materials), the U.S. Geological Survey (USGS), and national regulatory agencies. Selected grey literature was used only to contextualize monitoring practices, exposure assessment, and water-treatment technologies. Because the evidence base is heterogeneous, sources were internally stratified into green, yellow, and red evidence zones. This stratification was used as a transparency tool in a narrative review and was not intended to represent a formal systematic-review risk-of-bias assessment or meta-analytic grading scheme. The combination of \"green\" evidence (lack of recognized essentiality and reference norms, regulatory monitoring without standards, and engineering challenges of lithium removal) and \"yellow\" signals (ecological and cohort associations, preclinical data) does not form a clinically reproducible syndrome of \"lithium deficiency\" in humans. Overall, lithium may be regarded as a candidate \"beneficial trace element,\" for which validated biomarkers and prospective studies are required.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of miRNA-31 & miRNA 192 with Nrf2/NF-κB Biomarkers in Occupational Lead Toxicity: A Cross-Sectional Observational Study.","authors":"Kanishka Kumar, Sudha Anjali, Shailja Sharma, Shweta Rana, Purvi Purohit, Mithu Banerjee, Dharmveer Yadav, Praveen Sharma","doi":"10.1007/s12011-026-05318-9","DOIUrl":"https://doi.org/10.1007/s12011-026-05318-9","url":null,"abstract":"<p><p>Lead (Pb) exposure is a global health threat characterized by oxidative stress. While Nrf2 and NF-κB pathways are known mediators of systemic toxicity, the epigenetic modulation of these defences via microRNAs (miRNAs) in human cohorts remains to be fully elucidated. This study investigates the association between blood lead levels (BLL) and a potential molecular signalling involving miRNA-31, miRNA-192, Nrf2, and NF-κB. In this cross-sectional study, 80 occupationally lead-exposed healthy workers and 80 age-gender matched healthy controls were enrolled. BLL was estimated using Graphite Furnace Atomic Absorption Spectrometry (GFAAS). Relative expressions of miRNA-31, Nrf2, and NF-κB were quantified via RT-PCR, while serum protein levels were measured using commercially available sandwich ELISA kits. The exposed group exhibited significantly higher median BLL compared to controls (p < 0.001). A significant downregulation was observed in Nrf2 mRNA expression (fold change 0.53) and serum protein levels (p < 0.001) in occupationally exposed group. Additionally, the inflammatory transcription factor, NF-κB also showed an increasing trend and a slight positive correlation with BLL. Among miRNAs, miRNA-31 was significantly upregulated (fold change 3.95). In multivariable linear regression, miRNA-31 showed a significant inverse association with Nrf2 expression in the unadjusted model ([Formula: see text], [Formula: see text]). However, after adjusting for blood lead levels, the effect of [Formula: see text] was substantially reduced, while BLL remained significantly and inversely associated with Nrf2 expression ([Formula: see text], [Formula: see text]) Occupational lead exposure is accompanied by systemic miRNA-31 induction and reduced Nrf2 expression. These observational results suggest that blood lead levels exert a primary influence on Nrf2 suppression, offering hypothesis-generating insights into early epigenetic and redox responses during lead toxicity.</p>","PeriodicalId":8917,"journal":{"name":"Biological Trace Element Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}