Biological Trace Element Research最新文献

Tibetan Plateau, which was once a severe endemic area of Kashin-Beck disease (KBD), was low with selenium in the soil geochemical background and with harsh environment, thus resulting in selenium deficiency in local foods while high environmental-derived oxidative stress and inflammatory responses in human body. Diet was the major selenium source for humans, while external environment conditions could influence selenium consumption and disturb the selenium metabolism. This study explored the influence on urinary selenium of Tibetan population from the pespevtive of selenium intake, represented by food patterns and selenium concentration, and from the perspective of selenium metabolism caused by environmental stress. From 2019 to 2022, 572 food consumption questionnaires of Tibetan residents, matched urine samples, staple food samples, and local agricultural soil and water samples were collected. Environmental stressors, including absolute oxygen concentration, temperature-humidity index and ultraviolet radiation intensity were considered. Statistical analysis and Random Forest (RF) were used to explore the association, contribution importance and interactive effect of the factors above on urinary selenium concentrations. Urinary selenium concentrations of Tibetan residents were still generally low, declined with age whereas no difference was found between genders. In terms of food consumption patterns, dietary diversity score (DDS) and non-local food intake, poultry consumption frequency in particular were positively associated with urinary selenium, exerted a pro-linear relationship. Highland barley and wheat flour selenium concentrations showed positive impact on the urinary selenium concentrations, and the magnitude of impact was more obvious when the highland barley selenium concentration exceeded 0.04 µg/g, and the wheat flour selenium concentration was lower than 0.051 µg/g. The soil and water selenium concentrations also positively influenced the urinary selenium concentrations. Environmental stressors exerted distinct influencing curves on urinary selenium concentrations, with higher ultraviolet radiation intensity (UVRI) and lower environmental comfort induced by cold and dry conditions positively regulating urinary selenium concentrations, while oxygen concentration exhibited a marginal effect only when it reached a certain threshold. Food diversity, non-local food intake, staple food selenium concentrations and local agricultural selenium concentrations were all important factors for elevating the selenium status among Tibetan residents. Environmental stressors regulated the urinary selenium concentrations differently due to the divergent action pathways on the selenium depletion and metabolism. Correspondingly, increasing the food diversity through introducing non-local food, increasing the selenium level of local food and elevating the human selenium reference standards were suggested.

Lead (Pb) is a neurotoxic heavy metal that crosses the placental barrier and may affect fetal development. However, the effects of chronic developmental Pb exposure on oxidative stress, stress-related endocrine responses, and depression-like behavior, particularly regarding sex differences, remain unclear. This study evaluated the effects of chronic Pb exposure from gestation to adulthood on redox balance, corticosterone responses, and depression-like behavior in male and female mice. Pregnant C57BL/6J mice received 250 ppm lead acetate in drinking water from gestational day 0 until offspring reached adulthood. Depression-like behavior was assessed using the forced swimming and tail suspension tests. Reactive oxygen species and lipid peroxidation were measured in the prefrontal cortex and hippocampus, and plasma corticosterone was quantified following behavioral stress. Chronic Pb exposure increased immobility in both behavioral tests and increased oxidative stress markers in the prefrontal cortex and hippocampus, with sex- and region-dependent differences. Pb exposure also altered corticosterone dynamics in both sexes: males showed a delayed corticosterone peak, whereas females exhibited a prolonged response that remained elevated 24 h after stress. Overall, chronic developmental Pb exposure was associated with depression-like behavior, oxidative imbalance, and altered corticosterone responses in a sex-dependent manner. These findings highlight biological sex as an important factor influencing the neurobehavioral, redox, and stress-related endocrine consequences of chronic developmental Pb exposure.

Background: Type 2 diabetes mellitus (T2DM) is associated with increased oxidative stress and a high burden of cardiovascular disease. Coronary angiography introduces several potential physiological influences, including contrast exposure, vascular manipulation, fasting, and peri-procedural fluid administration. However, short-term changes in circulating trace elements and antioxidant biomarkers after the procedure remain insufficiently characterized. Because these factors were not examined separately in the present study, any observed pre-post differences were interpreted as associations rather than proof of contrast-induced vascular injury.

Objective: The present study aimed to evaluate acute pre- and post-procedural changes in circulating trace elements and oxidative stress biomarkers in patients with T2DM undergoing coronary angiography for suspected or known CAD.

Methods: Thirty patients with T2DM undergoing coronary angiography were prospectively enrolled. Serum Cu, Zn, Fe, Mn, Cd, and Pb were measured by flame atomic absorption spectrometry, and serum GSH and MDA were assessed spectrophotometrically. Analyte-specific paired comparisons included 25 participants for trace elements, 22 for GSH, and 21 for MDA. Serum trace elements (Cu, Zn, Fe, Mn, Cd, Pb) are reported in mg/L, GSH in µmol/g protein, and MDA in µmol/L. Blood samples were collected immediately before and immediately after the angiographic procedure; a fixed, standardized post-procedural time interval in minutes was not recorded in the study database.

Results: Post-procedural measurements showed reductions in circulating Cu (- 15.4%, unadjusted p = 0.009) and Zn (- 32.5%, p < 0.001) and an increase in serum GSH (+ 98.6%, p < 0.001). No statistically significant pre-post differences were observed for Fe, Mn, Cd, Pb, or MDA. After correction for eight biomarker comparisons, the Zn and GSH findings remained statistically significant, whereas the Cu finding did not meet the Bonferroni-adjusted threshold of p < 0.00625. These observations describe short-term circulating biomarker changes but do not establish a specific mechanism or isolate the effects of contrast exposure from other procedural factors.

Conclusions: In this exploratory paired study, coronary angiography was associated with short-term changes in circulating Zn and GSH in patients with T2DM; the Cu finding did not remain significant after conservative correction for multiple comparisons. The absence of a comparator group and the potential effects of sampling time, hemolysis, hydration, hemodilution, and other procedural factors preclude causal or mechanistic conclusions. Larger controlled studies are required.

Hormonal disturbances that women in postmenopause face favor increased redistribution of fat into visceral compartments, leading to central obesity and related disorders. The mechanisms underlying dysregulated zinc (Zn) metabolism in individuals with obesity and related disorders remain unresolved. This study aimed to investigate the association between serum Zn levels and conventional and novel anthropometric parameters in the cohort of postmenopausal women in Montenegro. A cohort of 94 postmenopausal women (mean age 64.55 ± 8.71 years) was consecutively included. Zn determination was performed using inductively coupled plasma optical emission spectrometry. Multivariable ordinal logistic regression analysis was used to estimate associations of demographic data, obesity-related scores, and laboratory markers with Zn tertile levels. Serum Zn levels were negatively correlated with conventional [body mass index (BMI) and waist-to-height ratio (WHtR)] and novel [body adiposity index (BAI), body roundness index (BRI), and cardiometabolic index (CMI)] anthropometric parameters in postmenopausal women. Although no difference in hip circumference and height across Zn tertiles was found, the BAI, as a composite index of both parameters, showed an association with serum Zn levels. Similarly, despite no difference in waist circumference across Zn tertiles, the BRI as a composite index of waist circumference and height was correlated with Zn levels. Serum Zn concentrations were positively associated with HDL-C levels, but not with other lipid parameters. The measurement of new anthropometric parameters, in addition to traditional ones, may add a contribution to the relationship between adiposity indices and serum Zn levels in postmenopausal women.

Cadmium (Cd), as a common environmental pollutant, spreads in the ecosystem through nutrient transfer, posing potential hazards to livestock health and indirectly harming humans through the food chain. Cd can impair the immune function. Interestingly, Cd can also cause lung damage through apoptosis, but the mechanism of its lung toxicity remains unclear. MicroRNAs (miRNAs) are key post-transcriptional regulators implicated in various pathological processes, including inflammation and apoptosis. In this experiment, a pig model of Cd poisoning was established by administering 20 mg/kg CdCl₂ to the diet over a 40-day period. The actual Cd accumulation in pig lung tissue was confirmed by ICP-MS. Results showed that Cd exposure downregulated miR-130a and upregulated miR-532 in pig lung tissue. Bioinformatics prediction and experimental verification confirmed that miR-130a directly targets the Th1 marker tumor necrosis factor-α (TNF-α), while miR-532 targets the Th2 marker chemokine receptor 4 (CCR4). Downregulation of miR-130a relieved its inhibitory effect on TNF-α, and upregulation of miR-532 inhibited on CCR4, leading to a shift in the Th1/Th2 balance toward Th1. Furthermore, the Th1/Th2 imbalance induced by Cd activated the endoplasmic reticulum stress (ERS) pathway. The activated ERS pathway subsequently induced apoptosis. Collectively, our findings demonstrate that Cd exposure regulates the miR-130a/TNF-α and miR-532/CCR4 axes to induce Th1/Th2 imbalance, which further triggers ERS-mediated apoptosis in pig lung tissue. These observational results provide a reference solution for the pathogenesis of Cd-induced lung diseases in pigs, and lay a research foundation for the prevention and treatment intervention of Cd-related diseases in the livestock industry.

The zinc-to-copper ratio (ZCR) reflects essential metal balance and may be relevant to cardiovascular regulation, yet its association with hypertension in populations exposed to environmental heavy metals remains unclear. We conducted a cross-sectional study of 966 adults (≥ 30 years, recruited in 2008) comprising an exposed group (n = 564) residing within 4 km of the Janghang copper smelter and a non-exposed control group (n = 402) from a rural area approximately 15 km away. Serum zinc, copper, and nickel, along with blood lead, mercury, and urinary cadmium and arsenic were measured. Associations between ZCR and blood pressure were examined using multivariable linear regression, logistic regression, Bayesian kernel machine regression (BKMR), and restricted cubic spline (RCS) analyses, with sensitivity analyses. Higher ZCR was associated with increased systolic and diastolic blood pressure in fully adjusted linear models (SBP: β = 1.75, p = 0.002; DBP: β = 1.47, p < 0.001), with consistent associations in both exposed and control groups. In logistic regression, participants in the highest ZCR tertile had higher odds of hypertension than those in the lowest tertile (adjusted OR = 1.91; 95% CI: 1.25-2.93; p = 0.003). When stratified, the association was more pronounced in the non-exposed group (OR = 2.29; 95% CI: 1.18-4.45; p = 0.014) and somewhat attenuated but still suggestive in the exposed group (OR = 1.71; 95% CI: 0.96-3.06; p = 0.069); the formal interaction test was not statistically significant (p = 0.561). Sensitivity analyses, including exclusion of antihypertensive medication users, yielded consistent findings (OR = 1.83; 95% CI: 1.19-2.80), and the E-value (1.97) indicated limited-to-moderate robustness to unmeasured confounding. Higher ZCR is consistently associated with hypertension across analytical approaches and subgroups, with a suggestive but not statistically significant pattern of effect modification by environmental metal exposure. These findings support ZCR as a potentially informative indicator of essential metal imbalance relevant to blood pressure, warranting further investigation in prospective settings.

Arsenic (As) is an environmental neurotoxicant that induces oxidative stress and cognitive impairment. There are limited therapeutic options to treat As-induced neurotoxicity. This study investigated the potential for repurposing metformin (Met) and memantine (Mem) use alone, and in combination to mitigate As-induced neurotoxicity in male Wistar rats. Fifty rats were randomly divided into five groups of ten each: Group I (control) received normal feed and water, group II- Sodium arsenite (20 mg/kg), group III- Sodium arsenite (20 mg/kg) + Met (75 mg/kg), group IV- Sodium arsenite (20 mg/kg) + Mem (10 mg/kg), and group V- Sodium arsenite (20 mg/kg) + Met (75 mg/kg) + Mem 10 mg/kg), all administered p.o. for 28 days. At the end of drugs treatment, several behavioral, biochemical, and histological evaluations were performed. Results showed that all drug-treated groups demonstrated enhanced spatial and recognition memory as evidenced by increased spontaneous alternation in the Y-maze task and decreased escape latencies in the Morris Water Maze test. In both behaviors, the combination group showed the best results, followed closely by the Mem alone group. All treatment groups, especially the combination, showed the best results by restoring the activity of glutathione peroxidase, catalase, and superoxide dismutase in the cortex and hippocampus. Histological examination to study cellular preservation demonstrated that Mem alone treated group showed better results. Network pharmacology identified 66 intersecting targets; molecular docking indicated that Mem and Met had the strongest affinity for MMP9 and BDNF, respectively. All hub genes showed better binding affinities with Mem as compared to Met. In conclusion, our study demonstrated that Met and Mem improved learning and memory, reduced oxidative stress, and restored cellular density. Further validation to repurpose Met and Mem for their use against As-induced neurotoxicity can be done so that they can be used in human beings in the future.

Lead (Pb) exposure remains a global health concern, particularly because of its adverse effects on neurodevelopment during fetal development and childhood. Early-life exposure to Pb during neuronal differentiation can impair neurodevelopment, although the underlying molecular mechanisms remain unclear. In this study, we investigated the cellular and molecular mechanisms underlying Pb-induced neurotoxicity during neural differentiation using SH-SY5Y cells. Our results demonstrated that Pb exposure caused severe injury to differentiating neural cells, leading to cell death with membrane disruption. This form of cell death was resistant to inhibitors of major regulated cell death pathways but was markedly suppressed by selenium supplementation with selenite or by the addition of selenoprotein P, a selenium transport protein. Transcriptome and protein expression analyses revealed that Pb induced endoplasmic reticulum (ER) stress responses. However, individual knockdown of selected ER-resident selenoproteins, including SELENOK, SELENOS, and SELENOT, did not abolish the protective effect of selenium, indicating that none of these proteins is individually indispensable for protection under the present experimental conditions. Peroxiredoxin 6 (PRDX6) knockout SH-SY5Y cells, which exhibit reduced selenium metabolic activity, remained responsive to the protective effect of selenium against Pb-induced cytotoxicity. Moreover, the glutathione peroxidase (GPx) mimetic ebselen also alleviated Pb toxicity under these conditions. These findings indicate that selenium protects differentiating neural cells against Pb-induced injury through mechanisms involving peroxide-reducing activity as well as additional selenium-dependent pathways. Collectively, our findings provide new insights into the molecular basis of Pb-induced neurotoxicity and support a protective role for selenium-dependent stress resistance against Pb-induced cellular injury.

Selenium (Se) is an essential trace element for human health and longevity. However, the spatial association between soil Se content and longevity remains poorly understood at different spatial scales. Therefore, this study investigated the relationship between soil Se and longevity at both the national scale in China and at six representative smaller regions (Heilongjiang Province, Liaohe River Basin, Enshi Prefecture in Hubei, Ankang City in Shaanxi, Lianzhou City and Yingde City in Guangdong). Both traditional statistical methods (e.g., Pearson correlation, OLS regression) and spatial statistical methods (e.g., Moran's I, SLM, SEM) were employed. The results revealed that: (1) At the national scale, soil Se and longevity exhibited a highly significant positive correlation and strong spatial clustering. High-Se/high-longevity clusters were mainly located in southern China, while northern provinces were characterized by low-Se/low-longevity clusters. SEM (R² = 0.31) outperformed OLS (R² = 0.22) and SLM (R² = 0.28), and the SEM model parameters indicated that the positive association persists after controlling for spatial error dependence. (2) At the small-scale level, a highly significant positive correlation was only identified in Lianzhou and Yingde. In Lianzhou, clusters of high Se and high longevity were concentrated in the southern region. SLM (R² = 0.87) outperformed OLS (R² = 0.72); the SLM model parameters indicated that the positive effect of soil Se remains after controlling for spatial lag dependence. (3) Spatial error dependence dominated at the broader scale, whereas spatial lag dependence was more prominent in small regions. Linearity and model performance improved substantially at the small scale. Regions with suitable Se levels showed the strongest Se-longevity associations.

Oxidative stress is widely recognized as a key contributor to the pathogenesis of Parkinson's disease (PD), yet the contribution of genetic variation in selenium-related pathways remains incompletely understood. In this study, we investigated whether selenium-related genetic variations contribute to PD susceptibility in a Han Chinese population comprising 527 sporadic PD patients and 499 controls. Nine polymorphisms in SNCA, EEFSEC, GPX1, GPX4, TXNRD2, SELENOP, SELENOW, SOD2, and CAT were genotyped using improved multiplex ligation detection reaction. Logistic regression analyses adjusted for age and sex were performed to evaluate individual associations. Combined genotype and interaction analyses were conducted to investigate combination effects among the variants and their interactions with SNCA. Among the investigated variants, only SNCA rs356203 was significantly associated with PD after Bonferroni correction. Although no significant association was observed individually for the remaining variants, a genotype combination involving EEFSEC, GPX1, GPX4, and TXNRD2 was significantly associated with reduced PD susceptibility. Interaction analyses using the recessive model revealed no significant interactions between the selenium-related gene variants and SNCA rs356203 in the total population. However, significant sex-specific interactions were observed: EEFSEC with SNCA in males, and TXNRD2 with SNCA in females. These findings confirm the association between SNCA rs356203 and PD risk and suggest that selenium-related genes may modulate PD susceptibility primarily through combined rather than independent effects. Our study also offers novel genetic insights linking SNCA to selenium-related antioxidant pathways in sporadic PD.