Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)最新文献

Background: Selenium is an element with diverse biological effects that, at higher concentrations, can cause oxidative stress and cell damage. Therefore, it is essential to understand its impact on yeast cells, which can serve as a model for studying selenium toxicity.

Objective: This study aimed to evaluate the effect of selenium on the physiology, cellular structure, and oxidative response of the yeasts Saccharomyces cerevisiae ATCC 7090 and Rhodotorula glutinis CCY 20-2-26. Changes in cellular structure, reactive oxygen species (ROS) levels, and ultrastructural alterations were examined under the influence of varying selenium concentrations.

Methods: Yeast cells were cultured in various selenium concentrations. The analysis included spectroscopic methods, flow cytometry, electron microscopy (TEM, SEM), and analysis of the surface chemical composition of yeast biomass (XPS). ROS and peroxide levels, as well as changes in cell structure, were also assessed.

Results: The yeast Saccharomyces cerevisiae demonstrated the ability to adapt its cellular structure to the presence of selenium, resulting in an increase in the proportion of C-C and C-H bonds to 53.5 % (at a concentration of 10 mg Se⁴⁺/L). Superoxide production increased by 26.14 % at a concentration of 10 mg Se⁴⁺/L, while ROS levels remained low (0.21 %). In Rhodotorula glutinis, however, over 50.71 % of cells were in a state of early apoptosis at a concentration of 20 mg Se⁴⁺/L, and the integrity of cellular structures was severely compromised. XPS analysis revealed the presence of Se-S bonds, suggesting the involvement of detoxification mechanisms involving selenium binding to the thiol groups of proteins and peptides, forming less toxic selenium-sulfur complexes.

Conclusion: This study demonstrated that the yeast S. cerevisiae exhibits a greater ability to adapt to selenium stress than R. glutinis. Selenium detoxification mechanisms, exemplified by the formation of selenium-sulfur complexes, play a crucial role in the response to oxidative stress. These results could serve as a starting point for further research on the effects of selenium on yeast cells.

Purpose: To comprehensively review the role of selenium (Se) in male reproductive health, placing this review above the previous reviews synthesizing selenium forms, mechanistic pathways, and actionable supplementation/monitoring strategies in clinical settings,focusing on its biochemical forms, antioxidant functions, and effects on sperm parameters, fertility outcomes, and interactions with other micronutrients.

Methods: A literature review was conducted using PubMed, Scopus, and Web of Science (2000-2025) to identify studies examining Se metabolism, selenoprotein activity (GPx1/4 and SELENOP), dose-response relationships, and co-supplementation with vitamin E and zinc. Data pertaining to selenium (Se) forms, modulation of antioxidant enzymes (such as superoxide dismutase and catalase), markers of oxidative stress (including malondialdehyde and reactive oxygen species), sperm function, hormone synthesis, and toxicity thresholds were collected and synthesized.

Results: Organic selenium (Se) demonstrated superior bioavailability and enhanced GPx4 and SELENOP activity, thereby reducing lipid peroxidation in germ cells. Animal research has found that dietary Se in the best concentrations (0.25-0.35 mg Se/kg in breeder roosters; 0.5-1.0 mg/kg in other models) maximizes the process of spermatogenesis, and elemental nano-selenium has the best effects relative to sodium selenite and seleno-yeast, whereas Se deficiency induces cell apoptosis via the PI3K/AKT pathway. Human trials revealed that a daily intake of 100 µg Se improved sperm motility (p = 0.023) and resulted in an 11 % increase in paternity. Se supplementation at concentrations of 2-5 μg/ml enhanced sperm viability; however, excessive intake of > 300 µg/day impaired motility. Co-supplementation with vitamin E or zinc further enhanced the antioxidant defense.

Conclusion: Selenium plays a crucial role in male reproductive health through its dose-dependent antioxidant and endocrine function. Structured clinical trials are essential to determine the optimal form, dosage, and combination of selenium with other micronutrients to enhance fertility while mitigating the risk of U-shaped toxicity.

Background: Consistent evidence from randomized controlled trials has shown that overexposure to selenium induces type 2 diabetes. However, uncertainties remain about the specific species and doses of selenium that trigger such diabetogenic effect.

Methods: We investigated the long-term effects of selenium exposure on diabetes risk using data from a natural experiment in Northern Italy. During 1974-1985, a small cohort of residents had been consuming drinking water with an unusually high content of inorganic hexavalent selenium, selenate (8-10 μg/L), close to the standard of the European Union and other countries of 10 μg/L. Using data from a population-based registry, we compared the prevalence of type 2 diabetes in 2013 in selenate-exposed (n = 1310) and unexposed residents (n = 56,251).

Results: In December 2013, the prevalence of diabetes in exposed and unexposed cohorts was 9.85 % and 10.29 %, respectively, with a multivariable-adjusted prevalence ratio of 0.95 (95 % confidence interval 0.81-1.12). Results were similar after stratifying by sex, age, and country of birth.

Conclusions: Overall, these results do not support the hypothesis that consumption of water with inorganic hexavalent selenium levels close to the European limit increases the risk of type 2 diabetes. Null results could be due to non-differential outcome misclassification, other sources of bias, or the fact that selenate is a non-diabetogenic selenium species or that the dose of exposure was too low to elicit an adverse effect.

Objective: Non-alcoholic fatty liver disease (NAFLD) represents a significant public health concern, ranking among the most critical liver diseases worldwide. The potential role of metals in the body in the development of NAFLD remains unclear. This study aims to explore potential associations between plasma metals and NAFLD odds among Chinese rural women.

Methods: In this cross-sectional study, 1988 rural women residing in southern China were measured for plasma concentrations of 22 metals and Fibrosis-4 scores representing the severity of liver fibrosis in patients with NAFLD. To address potential multicollinearity and identify the most relevant metals, the least absolute shrinkage and selection operator (LASSO) regression was first applied to select candidate metals for subsequent analyses. Logistic regression was then used to evaluate the associations between plasma metals and the odds of NAFLD and hepatic fibrosis. Nonlinear associations between plasma metals and NAFLD odds were explored using a restricted cubic splines (RCS) model.

Results: Elevated plasma levels of nickel(Ni), selenium(Se), and antimony(Sb) were found to be associated with an increased odds of NAFLD after adjustment for covariates in logistic regression. In the RCS model, a nonlinear relationship with NAFLDwas shown for Ni and Co. Furthermore, plasma Ni was positively associated with the OR of hepatic fibrosis.

Conclusion: Our findings indicate that four trace metals in the plasma (Ni, Se, Co, and Sb) were associated with non-alcoholic fatty liver disease among rural women in Southern China. Future studies are recommended to see whether the findings are applicable to other populations and to examine biological mechanisms underlying the associations.

Aluminum (Al) is the most widely distributed neurotoxic metallic element in the environment, and prolonged exposure can lead to cognitive impairment and increase the risk of developing Alzheimer's disease (AD). This article systematically reviews the critical mechanisms underlying aluminum-induced neurotoxicity: mediating neuronal apoptosis through activation of oxidative stress pathways and induction of mitochondrial dysfunction; engaging programmed cell death modalities such as necroptosis via activation of the RIP1/RIP3/MLKL signaling pathway; disrupting the homeostasis of neurotransmitter systems including glutamatergic and cholinergic pathways; and impairing synaptic plasticity. Neuroimaging studies demonstrate that magnetic resonance imaging (MRI) has revealed significant gray matter volume reduction in the hippocampus and frontal lobes of aluminum-exposed individuals, accompanied by disrupted functional connectivity in the default mode network (DMN) and diminished white matter integrity. Magnetic resonance spectroscopy (MRS) analyses indicate neuronal metabolic disturbances, while quantitative susceptibility mapping (QSM) further demonstrates abnormal cerebral iron deposition. These pathological manifestations may synergistically interact with β-amyloid (Aβ) protein aberrant aggregation and neurofibrillary tangles (NFTs) formation mediated by tau protein hyperphosphorylation. Although multimodal MRI techniques provide a crucial approach for dynamic monitoring of aluminum neurotoxicity, the research on its specific biomarker system requires further refinement. By conducting an in-depth exploration of the neural mechanisms underlying cognitive impairment induced by aluminum exposure and evaluating the feasibility of MRI-based imaging techniques as biomarkers for assessing aluminum neurotoxicity, this study aims to establish a theoretical foundation for early warning of cognitive dysfunction and development of targeted intervention strategies.

Background and objective: Rapid industrialization and urbanization have caused a significant increase in environmental pollution of bio-elements in India. Changes in bio-element concentrations, particularly an imbalance in the normal homeostasis in the blood leads to severe neurodegenerative effect. There has been very limited data on the association of bio-elements and cognitive decline. Present study performed the quantitative profiling of circulatory bio-element in cognitively impaired (CI) patients.

Methods: Elemental quantification of 19 elements were performed inductively coupled plasma mass spectrometry (Agilent Technologies, USA). A total of 65 participants were recruited for the study. All the participants underwent comprehensive clinical and functional assessments for cognitive abilities.

Results: Quantitative profiling revealed a significant increase in eight elements (Li, Al, V, Mn, Co, Ni, Zn, and Ag) in CI patients compared to control. MMSE score analysis was found to be 13.77 ± 0.9921 in CI compared to control 27.78 ± 0.3575. The concentrations of Li (Control; 25.84 ± 3.051 µg /L; CI; 41.52 ± 5.312 µg /L), Al (Control; 2.582 ± 0.739 µg /L; CI; 21.17 ± 6.092 µg /L), V (Control; 2.583 ± 0.739 µg /L; CI; 13.59 ± 2.757 µg /L), Mn (Control; 20.56 ± 1.919 µg /L; CI; 36.06 ± 3.086 µg /L), Co (Control; 2.52 ± 0.220 µg /L; CI; 4.143 ± 0.287 µg /L), Ni (Control; 2.723 ± 0.752 µg /L; CI; 22.83 ± 4.456 µg /L) Zn (Control; 8040 ± 1199 µg /L; CI; 11121 ± 838.6 µg /L) and Ag (Control; 0.7454 ± 0.127 µg /L; CI; 3.302 ± 0.699 µg /L).

Conclusion: Present study suggest that bio-elements (Li, Al, V, Mn, Co, Ni, Zn, and Ag) may contribute to generate a distinctive signature in CI patients, and its detection in elderly might help in early management of element induced neurotoxicity.

Selenium is an essential trace element with a dual role in plant physiology; it acts either as a pro-oxidant or as an antioxidant depending on its concentration and chemical form. A plant assimilates Se present in the soil, which constitutes the main determining factor for its availability due to the presence of different forms (e.g. selenite, selenate, organic Se). Efficient uptake facilitates the assimilation of Se mostly through sulfate transporter genes. Once inside the plant, selenium undergoes complex speciation, transforming into organic compounds like selenomethionine and selenocysteine, which are then distributed throughout the plant tissues. As an antioxidant, selenium plays a crucial role in enhancing plant stress tolerance. Being part of selenoenzymes, e.g. glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), selenium can neutralize reactive oxygen species (ROS) produced inside the cells, protecting them from oxidative deterioration. Selenium treatment enhances the enzyme activities of antioxidation and the accumulation of non-enzymatic antioxidants in plants, thus improving resistance to abiotic stress such as drought, salinity, and heavy metal toxicity. Reaching a higher level, selenium opposes its antioxidant activity and turns into pro-oxidants. Selenium toxicity in plants is characterized by a redox imbalance, causing excessive production of certain types of ROS and their related oxidative stress. This pro-oxidant activity further compounds cellular damage since it may disrupt the metabolism of essential metals. To apply selenium safely, it is important to know precisely at what concentrations it ceases to have beneficial effects on health. Despite these challenges, selenium biofortification may be a good method to improve the nutritional quality of crops and to uplift human health. Selenium-enriched crops are one of the key food sources of this vital trace element necessary for antioxidant defense and immune function in humans. Future research should focus on optimizing selenium biofortification protocols to maximize the antioxidant properties of selenium while minimizing the risk of pro-oxidant effects so as to promote sustainable agriculture and human nutrition.

Background: The skin's natural functions rely on essential metals such as zinc and copper, which contribute to cell growth, differentiation, and apoptosis. With ageing, low-grade inflammation (inflammaging) develops, and zinc deficiency in skin becomes more common. Data on the distribution of these metals in human skin are limited and there is no information on how the distribution changes with age.

Objectives: Establishing the spatial distribution of zinc and copper in human skin is a first step towards addressing their functions in specific cell layers and skin structures.

Methods: Laser ablation inductively coupled plasma mass spectrometry was employed to map zinc (⁶⁶Zn) and copper (⁶³Cu) in human female Caucasian abdominal and facial skin from young, middle-aged, and older donors at 5-8 µm spatial resolution. A novel bespoke integration method with gelatine micro-droplet standards enabled semi-quantitative comparisons.

Results: In facial skin, zinc concentrations are approximately three- to five-fold higher in the epidermis than in the dermis, whereas qualitative data from abdominal skin show a similar epidermis-enriched zinc signal and were used primarily for method development. In facial skin, copper levels remain relatively uniform between these layers. Facial skin samples from older donors demonstrate increased zinc accumulation in deeper layers, elevated copper levels, and altered copper-to-zinc ratios. Within skin structures, a significant age-related copper enrichment in hair follicles and eccrine sweat glands is observed.

Conclusions: The innovative approach not only pushes the technical limits of mass spectrometric metal imaging but also uncovers novel insights into age-dependent metal redistribution in human skin. Our investigation opens exciting avenues for developing metal-based biomarkers to improve skin health and combat skin ageing.

Background: Metallothioneins (MTs) are crucial metal-binding proteins involved in cellular zinc homeostasis and oxidative stress response. However, the role of metallothionein-related genes (MRGs) in breast cancer (BC) pathogenesis and their potential as therapeutic targets remains poorly understood.

Methods: We integrated two BC datasets, GSE42568 and GSE29044, to identify differentially expressed MRGs. Consensus clustering was applied to classify BC subtypes based on MRGs expression patterns. GSVA evaluated pathway activities between subtypes. LASSO regression, Random Forest, and Logistic Regression were employed to identify core MRGs. A predictive nomogram was constructed and validated using ROC curves, calibration curves, and decision curve analysis. Single-cell RNA sequencing and spatial transcriptomic analyses were performed to characterize core MRGs expression patterns. Finally, in vitro experiments, including PCR, western blot, CCK-8, migration, and invasion assays, were conducted for validation.

Results: Among 62 MRGs analyzed, 30 showed differential expression in BC. Consensus clustering revealed two MTs subtypes with distinct molecular signatures. Functional enrichment analysis indicated significant pathways, including Wnt signaling and zinc ion homeostasis. GSVA highlighted variations in metal ion homeostasis and immune responses between subtypes. Two core MRGs, MT1M and MT1X, were identified through machine learning approaches, both significantly downregulated in BC tissues. The constructed nomogram demonstrated excellent predictive performance. Single-cell analysis revealed cell-type-specific expression patterns, while pathway analysis showed differential activation of oncogenic signaling cascades. Experimental validation confirmed the downregulation of MT1M and MT1X in BC tissues at mRNA and protein levels. Functional assays demonstrated that overexpression of MT1M or MT1X suppressed BC cell viability, migration, and invasion.

Conclusion: Our study establishes MRGs, particularly the core genes MT1M and MT1X, as crucial players in BC heterogeneity and pathogenesis. They serve as promising diagnostic biomarkers and potential therapeutic targets, with their tumor-suppressive roles likely mediated through the modulation of key oncogenic signaling pathways.