Biological Trace Element Research最新文献

Traumatic brain injury (TBI)-related polytrauma is associated with accelerated fracture healing, yet the systemic redistribution of trace elements during this process remains poorly understood. Materials and methods. 90 female rats were divided into two groups: TBI-accompanied femur fracture and isolated femur fracture (IF). Trace element concentrations (Cu, Zn, Cd, Mg, Ca) were measured in whole blood and bone at 7, 14, and 21 days using atomic absorption spectroscopy. Femur fracture was modeled by blunt guillotine injury, while for TBI modified control cortical impact model was used. Results. On day 14, a metabolic peak was observed in the polytrauma group, with bone calcium level increasing 1.4 times (p < 0.001) and bone zinc increasing by 55% (p < 0.001). By day 21, blood cadmium levels in the polytrauma group rose significantly (p < 0.001), while bone concentrations of other trace minerals decreased. The 14-day mark represents a critical metabolic window for accelerated mineralization in TBI-related polytrauma. While these results are experimental, they suggest that the first two weeks post-trauma are vital for optimizing the mineral environment. Future research should integrate micro-CT and histological analysis to understand if metabolic peaks correlate with callus structure quality and investigate the potential diagnostic or therapeutic role of trace elements.

To investigate the protective effects of three antioxidants-lycopene (LP), proanthocyanidins (PC), and resveratrol (RES)-against Nano-TiO₂-induced reproductive toxicity in male mice. A total of 110 healthy male ICR mice were randomly assigned to 11 experimental groups: the control group, the Nano-TiO₂ group, and combined treatment groups consisting of Nano-TiO₂ with low, medium, and high doses of LP, PC, and RES, respectively. Following 28 days of continuous intragastric administration, epididymal tissues were collected for assessment of semen quality, while testicular tissues were utilized to evaluate histopathological alterations, testicular functional enzyme activities, and markers of oxidative stress. Compared with the control group, after intragastric administration of Nano-TiO₂, the testicular and epididymal coefficients of mice decreased, the sperm count, sperm progressive motility, and sperm motility rate significantly decreased (P < 0.05), the sperm malformation rate significantly increased (P < 0.05), the number of spermatogenic cells in the testicular spermatogenic tubules decreased, and the Johnsen score significantly decreased (P < 0.05). The activities of acid phosphatase (ACP), alkaline phosphatase (AKP), lactate dehydrogenase (LDH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) decreased significantly (P < 0.05). The level of malondialdehyde (MDA) was significantly increased (P < 0.05). After the intervention with the three antioxidants, compared with the Nano-TiO₂ group, the testicular and epididymal coefficients increased. Compared with other doses, medium-dose LP, medium-high-dose PC, and all doses of RES significantly increased the forward motility and sperm motility of mice and significantly reduced the sperm deformity rate(P < 0.05). In addition, various doses of LP, medium - high- doses of PC, and low- doses RES significantly improved pathological damage caused by Nano-TiO₂, such as testicular tissue structural disorder and decreased levels of spermatogenic cells and sperm. The activities of ACP, LDH, SOD, CAT, GSH, and GPx increased significantly (P < 0.05), and the level of MDA in the testicular tissue decreased significantly. LP, PC, and RES had antagonistic effects on male reproductive toxicity induced by Nano-TiO₂, the prominent effects of PC on the testicular organ coefficient and LP, especially 20 mg/kg LP, in improving semen quality and the expression of testicular functional enzymes in male mice need to be given due attention.

The validity of applying universal diagnostic standards across diverse populations is a critical public health concern. This study challenges the suitability of China's national thyroid volume (TTV) criteria by establishing region-specific reference curves for 404 children aged 7-13 years in Xinjiang. Our new sex-specific curves, constructed using GAMLSS models, revealed a goiter prevalence of only 1.5%, a stark contrast to the 9.5% in males and 11.7% in females diagnosed using the national standard (McNemar's test, P < 0.001). This discrepancy underscores a significant overestimation by the current national criteria. Furthermore, our analysis elucidated a nuanced role for iodine: while individual iodine indicators (urinary, salivary, and serum) exhibited significant nonlinear associations with TTV, a composite iodine index showed a protective linear negative correlation (P = 0.012). These findings demonstrate that region-specific standards are imperative for accurate goiter diagnosis. They also suggest that in iodine-sufficient populations, the relationship between iodine and thyroid health is a complex physiological modulation rather than a simple risk paradigm.

Aflatoxin B₁ (AFB₁) exposure is one of the important factors causing cirrhosis and hepatocellular carcinoma. Selenoproteins, key selenium (Se)-containing biomolecules, may mitigate early AFB₁ hepatotoxicity. To identify hepatic selenoproteins as sensitive biomarkers or functional players in AFB₁ exposure, we allotted 44 11-week-old male C57BL/6J mice into six groups (n = 6-8). Following a five-week pre-feeding period on a 0.03 mg Se/kg diet, mice were fed one of three dietary Se levels (0.03, 0.2, or 2.0 mg/kg) for six weeks, with daily gavage of 0 or 0.25 mg AFB₁/kg body weight administered during the final week. Analysis of the sampled tissues showed that hepatic mRNA abundances of four selenoproteins (Selenoh, Selenok, Selenos, and Sephs2) and 8-oxoguanine DNA glycosylase (Ogg1) were increased across all three dietary Se levels (P < 0.05). In contrast, mRNA abundances of Gpx1, Selenof, Selenoo, Selenot, Selenow, and Txnrd3 were significantly increased at only one or two Se levels (P < 0.05). Notably, Selenoh mRNA abundance positively correlated with dietary Se levels without AFB₁ exposure (R² = 0.22, P = 0.04), while Ogg1 mRNA abundance negatively correlated with serum 8-hydroxydeoxyguanosine concentrations in the AFB₁-treated groups (R² = 0.19, P = 0.04). Selenoh and Sephs2 protein levels were increased by Se intake (P < 0.05), but not by AFB₁ exposure. Conclusively, hepatic Selenoh mRNA was more sensitive to short-term, low AFB₁ exposure than its protein and showed a positive response to dietary Se intake in mice, emphasizing its potential as a valuable biomarker in assessing the Se-AFB₁ interaction.

Selenium (Se) is an essential trace element in bone metabolism. Armillaria (AM) has the ability to enrich Se and exhibits the potential for treating osteoporosis. The aim of this study was to evaluate the effect of Se-enriched Armillaria (AM-Se) on osteoporosis in ovariectomized rats. AM-Se was prepared by adding sodium selenite to the liquid fermentation medium of AM. Forty 8-week-old female Sprague-Dawley rats were randomly divided into five groups as follows: (1) Sham operation group (SHAM), (2) Ovariectomy group (OVX), (3) OVX + Estradiol group (E2, 9 µg/kg/day), (4) OVX + AM (AM, 0.4 g/kg/day), and (5) OVX + AM-Se (AM-Se, 0.4 g/kg/day). A rat postmenopausal osteoporosis (PMOP) model was established by bilateral ovariectomy. After 12 weeks of treatment, the results showed that AM or AM-Se alleviated OVX-induced bone trabecular loss, maintained biomechanical properties, and regulated bone metabolism indicators and sex hormone levels in rats. The expression of estrogen receptor α was significantly increased in the hypothalamus, pituitary, and tibia of rats treated with AM or AM-Se. AM-Se is more effective than AM in the treatment of PMOP, and the mechanism involved is related to estrogen-like effects.

Homeostasis is the regulatory mechanism for the expression of all genes, the function of all metabolic pathways, the utilization of any essential trace element (TEs), while its disruptions lead to many pathological states. The pathologies include cardiovascular disease, anaemia, diabetes, neurological disorders, and cell death. For this, copper and zinc are two of the major TEs involved in controlling the physiological and pathological processes in both humans and animals. Zinc deficiency, for instance, is linked with decreased body weight, decreased ability to metabolize glucose, and impaired immune function. By contrast, deficiency of copper can lead to several neurological disorders, oxidative stress, mitochondrial dysfunction, and changes in lipid metabolism. On the other hand, there excessive exposure can have adverse effects on health, including the development of epilepsy, neuronal excitability, genotoxic effects, and cellular toxicity. Moreover, dual biological functions of zinc further complicate the understanding of their roles in both health and disease. Such as, zinc has a neuromodulatory function and helps to control excitably in neurons, but sometimes zinc in the synapse, inhibit the functioning of inhibitory neurotransmitter and cause damage to the neurons. Likewise, in metabolic diseases, particularly diabetes mellitus, there is often dysregulation of the levels of zinc and copper, resulting in steel-like interactions; elevated levels of copper and reduced levels of zinc contribute towards the pathogenesis of both the disease and the progression of dementia. Despite this antagonistic relationship, both trace metals act synergistically as necessary derivatives of superoxide dismutase; therefore, both play a vital role in maintaining cellular antioxidant defense systems. Therefore, this review covers published articles from 1992-2025 with regard to zinc and copper in their dietary and nanoparticle forms in animal and human models to demonstrate their differing roles and how they complement one another, or conflict with one another.