Biological Trace Element Research最新文献

Magnesium is the second most common ion at the intracellular level (IC). Its abundance reflects its important role in the organism. Homeostasis is achieved through a delicate balance between ingestion, excretion, and reservoir, which collectively maintain physiological levels. Western dietary habits are prevalent today, often resulting in insufficient magnesium intake and compromised status. In the intestine, there are several inhibitors and enhancers of magnesium absorption. This includes physicochemical and dietary factors. This narrative review aims to evaluate the nutritional factors affecting magnesium bioavailability. These factors can be considered when planning a healthy diet and determining Dietary Reference Intakes (DRIs) for the population to prevent deficiency and non-communicable diseases. The recommendations are directed to reduce the intake of sodium, enhancing the intake of fruits and vegetables, known to be powerful alkalinizing sources and mineral-rich food.

Selenium (Se), an essential micronutrient with potent antioxidant properties, may modulate cardiometabolic health through multiple physiological pathways, including redox regulation and the modulation of inflammatory responses. This study aimed to investigate the relationships between serum Se levels and pro-inflammatory cytokines, adhesion molecules, and carotid intima-media thickness (CIMT) as early indicators of endothelial dysfunction in patients with metabolic syndrome (MetS). A total of 191 patients aged 20 to 50 years, diagnosed with MetS, were included in the study. In addition to glucolipid metabolic parameters, serum levels of Se, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and monocyte chemoattractant protein-1 (MCP-1) were assessed. Ultrasonography was applied to measure the CIMT among the participants. The mean serum levels of TNF-α (p-trend = 0.037), MCP-1 (p-trend = 0.005), and VCAM-1 (p-trend = 0.002) revealed decreasing trends with increasing quartiles of serum Se. Similarly, a significant decrease in the mean CIMT was observed in the participants with increasing quartiles of serum Se (p-trend < 0.001). Serum Se levels were inversely correlated with TNF-α (r = -0.24, p < 0.001), MCP-1 (r = -0.30, p < 0.001), VCAM-1 (r = -0.34, p < 0.001), and CIMT (r = -0.47, p < 0.001). In conclusion, we observed significant inverse relationships between serum Se levels and pro-atherogenic and pro-inflammatory biomarkers, as well as the mean CIMT, in patients with MetS. Se supplementation may represent a targeted nutritional strategy for reducing cardiovascular risk in patients with MetS who have low serum Se levels.

Sixteen Angus crossbred steers were used to determine the impact of trace mineral (TM) source, diet type, and monensin and tylosin supplementation on rumen fermentation characteristics. Experiment 1: Steers were adapted to a finishing diet before being assigned dietary treatments. A 2 × 2 factorial arrangement of treatments was utilized with factors: (1) TM source (sulfate; STM or hydroxy; HTM) and (2) with or without monensin and tylosin (MT). Following the 28-day feeding period, rumen samples were collected at 0, 2, and 4 h post-feeding. Experiment 2: Steers were adapted to a lactating dairy cow diet and assigned dietary treatments for 28 days. A 2 × 2 factorial arrangement of treatments was utilized. Factors included (1) TM source (STM or HTM) and (2) with or without monensin (M). On day 29, rumen samples were collected at 0, 2, and 4 h post-feeding. Rumen fluid samples from both experiments were analyzed for short chain fatty acids (SCFA), pH, and ammonia concentrations. Experiment 1: Molar proportions of acetate were lesser (P < 0.04) and propionate greater (P < 0.01) in steers receiving HTM compared to steers receiving STM. Experiment 2: Total SCFA production was greater (P < 0.01) in steers supplemented with HTM compared to STM. Supplementation of M reduced the molar proportion (P < 0.01) of acetate and increased (P < 0.05) molar proportions of propionate and butyrate. These data indicate that TM source and M may modulate rumen fermentation characteristics but their impacts on rumen fermentation may be diet dependent.

Nasal polyps (NP) are benign mucosal outgrowths associated with chronic inflammation that can significantly reduce quality of life. This study aimed to evaluate changes in inflammation, oxidative stress, and trace element homeostasis in NP patients and to identify potential non-invasive diagnostic biomarkers. A total of 22 patients with NP and 19 healthy individuals were included in the study. Serum levels of trace elements, including zinc (Zn), copper (Cu), and selenium (Se), were measured using inductively coupled plasma mass spectrometry (ICP-MS). Biochemical parameters including white blood cell count (WBC), red blood cell count (RBC), platelet count (PLT), eosinophils (EO), hemoglobin (HGB), glucose, creatinine, alanine aminotransferase (ALT), and thyroid-stimulating hormone (TSH) were assessed, along with inflammatory indices such as neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR). Data were analyzed using classical statistical methods, including the Shapiro-Wilk test, independent samples t-test, Mann-Whitney U test, and receiver operating characteristic (ROC) analysis. Multivariate analyses such as principal component analysis (PCA), orthogonal partial least squares discriminant analysis (OPLS-DA), and variable importance in projection (VIP) scoring were performed. In addition, machine learning algorithms including Naive Bayes, support vector machines (SVM), random forest, k-nearest neighbors (KNN), and logistic regression were employed. SHapley Additive exPlanations (SHAP) analysis was used to interpret the most influential features of the best-performing model. Compared to controls, NP patients exhibited significantly higher levels of WBC, Cu, glucose, and NLR along with significantly lower levels of Zn, PLR and the Zn/Cu ratio. Specifically, the mean Zn level was 2130.974 ± 3516.317 µg/mL in the NP group versus 11,331.127 ± 27,697.378 µg/mL in controls (p = 0.018). Cu (AUC = 0.866), glucose (AUC = 0.777), and WBC (AUC = 0.748) showed strong discriminative power. OPLS-DA revealed clear group separation, highlighting Cu, Zn/Cu, glucose, Se, and PLR as high-impact variables. Optimized logistic regression achieved 100% classification accuracy, with SHAP analysis confirming Zn, Zn/Cu, Cu, and glucose as the most influential features. These preliminary findings suggest that inflammation, trace element imbalance, and metabolic alterations can be detected biochemically in NP patients. Parameters such as serum Zn and Cu levels, Zn/Cu ratio, glucose, and inflammatory indices may serve as promising non-invasive diagnostic biomarkers. Further validation in larger and independent cohorts is warranted before clinical implementation.

Zinc deficiency is closely related to oxidative stress, inflammation, and programmed cell death. In this study, mouse models with normal zinc (Con), zinc deficiency (L-Zn), and high zinc (H-Zn) and an in vitro model of AML-12 hepatocytes were established to systematically explore the effects of zinc deficiency on hepatic oxidative stress, inflammation, and programmed cell death. In vivo experiments showed that zinc deficiency significantly increased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in the liver (P < 0.05), inhibited the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), and induced hepatocyte edema, inflammatory infiltration, and an increase in the number of TUNEL-positive apoptotic cells. Using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, it was found that zinc deficiency activated the NF-κB pathway (increased expression of p-IκB α and p-NF κB p65), significantly increased the expression of pro-inflammatory factors (TNF-α, IL-6, IL-1β, IL-18), and decreased the anti-inflammatory factor IL-10. In addition, zinc deficiency upregulated apoptosis-related genes (Cyt-C, Bax, Bcl-2, Caspase-3/9), necroptosis marker indicators (RIPK1, RIPK3, MLKL), and key molecules of pyroptosis (NLRP3, ASC, GSDMD, Caspase-1), indicating the programmed cell death is activated in a number of ways. In vitro experiments further verified the above experimental results. Flow cytometry showed that the apoptosis rate of AML-12 cells in the L-Zn group (17.20%) was significantly higher than that in the Con group (4.75%) and the H-Zn group (2.55%). The experiment concluded that zinc supplementation could effectively alleviate oxidative damage, inhibit the inflammatory pathway, and reduce the expression of programmed cell death-related factors. This study confirms that zinc deficiency activates programmed cell death through a multimodal pattern and provides a theoretical basis for studies related to zinc intake imbalance leading to liver injury.

Artemisia species are known for their rich phytochemical diversity; however, their ability to accumulate a wide range of minerals and metals from the soil raises significant safety concerns, particularly in therapeutic and dietary contexts. This review provides data on elemental composition across 64 Artemisia species, evaluating their nutritional, medicinal and environmental implications. Data collection was carried out using various databases, including SciELO, Google Scholar, Medline, ScienceDirect, PubMed, Web of Science and Scopus. Around 220 records were searched and data on elemental content in Artemisia species was finalized from around 170 papers. Data showed various reported essential macro elements with varied levels in Artemisia species such as carbon (C), calcium (Ca), potassium (K), magnesium (Mg), nitrogen (N), silicon (Si), sodium (Na), phosphorus (P), sulfur (S) and which are critical for maintaining physiological functions. Additionally, the presence of micro elemnts in Artemisia including boron (B), barium (Ba), beryllium (Be), bismuth (Bi), bromine (Br), chlorine (Cl), cobalt (Co), cesium (Cs), copper (Cu), europium (Eu), iron (Fe), germanium (Ge), hafnium (Hf), iodine (I), lithium (Li), lutetium (Lu), manganese (Mn), molybdenum (Mo), rubidium (Rb), antimony (Sb), selenium (Se), samarium (Sm), thorium (Th), titanium (Ti), thallium (Tl), ytterbium (Yb), zinc (Zn) and zirconium (Zr) was reported. Despite the plants' considerable nutritional and medicinal potential, the review also focused the concerning levels of metalloids like arsenic (As) and metals like aluminum (Al), silver (Ag), gold (Au), cadmium (Cd), cerium (Ce), chromium (Cr), gallium (Ga), mercury (Hg), lanthanum (La), niobium (Nb), nickel (Ni), lead (Pb), scandium (Sc), tin (Sn), strontium (Sr), yttrium (Y) and vanadium (V). Artemisia species serve as both valuable nutritional and medicinal resources and potential accumulators of toxic elements. This review further explores how various elements affect plant health including Artemisia, highlighting the mechanisms of metals detoxification as well as the importance of careful management practices.

Erectile dysfunction (ED) is a common complication of diabetes. Diabetes leads to the decrease of zinc (Zn) content, and zinc deficiency can cause sexual dysfunction, hypoplasia of sexual organs, and secondary sexual characteristics. The purpose of this study was to explore the protective effect of metformin combined with zinc on erectile function in diabetic mice induced by streptozotocin (STZ). Ten of 50 male mice were randomly selected as the control group (group C), and the remaining 40 mice were randomly divided into the diabetes treatment group (group D), diabetes + zinc group (group Z), diabetes + metformin group (group M), and diabetes + metformin + zinc group (group ZM), with 10 mice in each group. The diabetic mouse model was induced by high-fat diet (HFD) and STZ. Diabetic mice in group Z were given oral zinc (10 mg/kg) once a day for 4 weeks, group M diabetic mice were given metformin (200 mg/kg) once a day for 4 weeks, diabetic mice in group ZM were given metformin and zinc once a day for 4 weeks, and group C and group D were given the same amount of sterile water. The mice that fasted overnight were killed, and blood samples and penises were collected for further experiments. The combined treatment of zinc and metformin can reduce penis weight and improve the structural damage of the cavernous body caused by diabetes. The combined treatment of zinc and metformin can improve the serum zinc content and the fluorescence intensity of free zinc ions in penis and correct the unbalanced zinc homeostasis by changing the expressions of zinc transporter (ZnT3, ZnT8, ZIP10, and ZIP14) in penis tissue. The results showed that combined treatment with zinc and metformin can increase the expression of Bcl-2, decrease the expression of Bax and caspase-3, and decrease the apoptosis index of cavernous cells caused by diabetes. In addition, the combined treatment of zinc and metformin can increase the levels of SOD, NO, and cGMP in penis tissue; decrease MDA level; inhibit TGF-β1/Smad3 pathway-related proteins; increase the expression levels of eNOS, α-SMA, and CD31 proteins; and reduce collagen deposition in the penis. In a word, we found that zinc combined with metformin can inhibit the TGF-β1/Smad3 pathway; correct the imbalance of zinc homeostasis in the cavernous body; reduce the levels of oxidative stress, fibrosis, and apoptosis; and improve the structural damage of the cavernous body in male type 2 diabetic mice.

Chronic kidney disease of unknown etiology (CKDu) is highly prevalent in agricultural communities of rural areas. Environmental risks such as potentially toxic elements (PTEs) are hypothesized to be the primary contributors; however, existing research is inconsistent. This study aimed to explore the association between various PTEs (Al, Ni, As, Cd, Hg, and Pb) and their interactions in CKDu in eastern Uttar Pradesh. This was a tertiary hospital-based case-control study recruiting 211 CKDu patients along with 214 age and gender-matched controls from the same region. Urea and creatinine levels were measured using the Cobas 6000. Estimated Glomerular Filtration Rate (eGFR) was calculated based on the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine equation. PTEs were measured in the serum and urine using Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). Single and multi-element exposures were explored using regression model analysis. PTE levels in both serum and urine were higher in the CKDu group than in the control group and were correlated with eGFR. Multivariate regression identified that serum Cd (β =  - 0.382, p < 0.001), As (β =  - 0.332, p < 0.001), Hg (β =  - 0.250, p < 0.001), and Al (β =  - 0.222, p < 0.001) were independently associated with CKDu. From Weighted Quartile Square (WQS) regression analysis, the maximum weight in disease prevalence was Cd (41%, β = 0.78) followed by As (32%, β = 0.42) and Al (17%, β = 0.32). A Gaussian process classifier and Bayesian kernel machine regression were used to measure the overall effect of PTEs as mixtures on CKDu. Al, As, Cd, and Hg levels were independently associated with eGFR and CKDu prevalence. However, all PTEs correlated with eGFR, signifying their bioaccumulation with or without causation.

The imbalance of trace elements plays an important role in childhood malnutrition, but previous studies are usually specific to certain elements. We aimed to examine the individual and joint associations between multiple elements and the risk of protein-energy malnutrition (PEM) in young school children. This study measured the serum levels of zinc (Zn), copper (Cu), chromium (Cr), cobalt (Co), vanadium (V), manganese (Mn), and nickel (Ni) in 1832 out of 5152 children aged 6 to 9 years by using inductively coupled plasma mass spectrometry (ICP-MS). The individual and joint associations between elements and the risk of PEM were assessed using logistic regression, Restricted Cubic Spline (RCS), Bayesian Kernel Machine Regression (BKMR), and Weighted Quantile Sum Regression (WQS) models, respectively. Serum concentrations of Zn, Cu, Co, V, Mn, and Ni were significantly lower in the PEM group than in controls (all P < 0.005). Higher quartile concentrations of Zn (OR = 0.52), Cu (OR = 0.59), V (OR = 0.52), Mn (OR = 0.51), and Ni (OR = 0.68) were associated with lower PEM risk (all P_trend < 0.05). RCS model indicated non-linear relationships between Zn, Cu, Cr, Co, V, Mn, and PEM risk. Interactions were found between Zn, Mn, and Co on the risk of PEM. Both BKMR and WQS models revealed a negative joint association between the seven elements and PEM risk (OR =  - 0.102), with Mn (40.4%) and Zn (19.1%) identified as the strongest contributors. Serum concentrations of Zn, Cu, Co, V, and Mn were relatively lower in children with PEM and exhibited non-linear associations with the risk of PEM. The joint association of seven trace elements was negative with the risk of PEM, in which Mn and Zn contribute the most. Additionally, Mn, Zn, and Co exhibited pairwise interactions. These findings highlight the importance of maintaining balanced trace element levels to mitigate PEM in children.

Manganese (Mn) and iron (Fe) are essential trace metals. Both are essential for multiple physiological processes, including brain function, metabolism, and cellular respiration. However, excessive exposure to these metals can have detrimental health effects, particularly in occupational exposures, such as mining, welding, battery production, and iron and steel manufacturing. Mn and Fe accumulate in astrocytes, especially in brain regions involved in motor control and cognition, such as the substantia nigra and globus pallidus in the basal ganglia. Excessive exposure to Mn and Fe induces oxidative stress, neuronal damage and neurodegeneration, and has been implicated in various neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). Here, we investigated the effects of combined Mn and Fe exposure on C8-D1A astrocytic cells and explored the associated oxidative stress pathways. Our results demonstrated that Mn exposure decreased Superoxide dismutase 2 (Sod2) mRNA expression and one of its upstream regulators, Signal Transducer and Activator of Transcription 3 (STAT3) protein and gene levels, associated with an increase in oxidative stress, whereas Fe exposure had no effect on this pathway. Interestingly, combined Mn and Fe exposure decreased reactive oxygen species (ROS) levels and upregulated the expression of the antioxidant gene NAD(P)H quinone dehydrogenase 1 (NQO1) compared to Mn and Fe exposure alone. Our findings suggest that combined Mn and Fe exposure activate the Nuclear factor erythroid 2-related factor 2 (NRF2)/NQO1 antioxidant signaling pathway in C8-D1A astrocytic cells, mitigating oxidative stress and protecting cells from damage. By understanding these mechanisms, novel therapeutic targets for neurodegenerative diseases associated with occupational metal exposures may be identified.