Biological Trace Element Research最新文献

Using nanotechnology in zinc supplementation may increase efficiency, reducing offered amounts and, therefore, allowing for lower cost and minimized environmental damage due to Zn contamination. This study aims to evaluate the kinetics of zinc, derived from micro- and nanometric zinc oxide, by radiolabeling this mineral through neutron activation. Eight Santa Ines ewes, around 10 months old and 23.6 ± 2.0 kg of body weight, were split into two treatments. After adaptation, they were transferred to metabolism evaluation cages, receiving capsules containing 50 mg of ⁶⁵ZnO (with average 54.85 kBq of ⁶⁵Zn), micro- or nanometric, on a single oral dose. After the capsules' ingestion, collections of blood samples were made (0.25h, 0.5h, 1h, 2h, 6h, 14h, 24h, and every 24h thereafter), whereas feces and urine collections were made daily through the tenth day, when the animals were euthanized, and their tissues and gastrointestinal contents collected for ⁶⁵Zn counts and Zn measurement. The nanometric ⁶⁵ZnO treatment presented a biological half-life 12h longer than the micrometric ⁶⁵ZnO, although without statistical difference. The nanometric ⁶⁵ZnO also had higher recovery rates in feces throughout the experiment (p < 0.0001). Generally, the ⁶⁵Zn distribution in the tissues was similar, with the spleen being the only exception, showing higher counts in the micrometric ⁶⁵ZnO group (p < 0.05). In conclusion, our results suggest that ZnO nanoparticles may be as efficient as its micrometric counterpart, although further studies are needed to evaluate the differences found in the spleen, large intestine counts, and biological half-life.

Metal-organic frameworks (MOFs) are highly versatile porous crystalline polymers with diverse structural compositions, high porosity, and biocompatibility, which guarantees their significant potential in various biomedical applications, including drug delivery, magnetic resonance imaging (MRI), and biosensing. However, despite these promising features, MOFs' application is considerably hindered by main challenges such as toxicity and biocompatibility. This review aims to provide a comprehensive understanding of MOF-associated toxicity, and the challenges involved in their biomedical applications. We first addressed the different routes of MOFs exposure, such as oral ingestion, inhalation, skin, and intravenous routes, and their potential contribution to MOF-associated toxicity. Further, we focused on drug delivery systems, MRI contrast agents, and biosensors, along with their key challenges, like how toxicity issues affect their efficacy and safety. The key biological mechanisms involved in MOF-induced toxicity were also critically examined, such as oxidative stress, mitochondrial dysfunction, and autophagy disruption. Moreover, we evaluated how MOFs' toxicity prolife is influenced by their physicochemical properties such as MOFs' composition, size and shape, surface characteristics, biodegradability, and stability. The current advancements were also illustrated to address these challenges and to minimize the toxicity with enhancement in therapeutic performance, such as the development of stimuli-responsive drug delivery systems and MOF-based composites with better biocompatibility and efficacy. Overall, this review enlightens the need for novel strategies to overcome the current challenges in MOFs' biomedical applications. Future research should focus on the evaluation of systematic toxicity and development of novel, suitable MOF-based composites to ensure their safety and efficacy.

The study analyzed radionuclide accumulation in Urtica dioica (stinging nettle) leaves, focusing on both natural and anthropogenic radionuclides. Samples of soil and leaves were measured for specific activity of key radionuclides (strontium-90, cesium-137, thorium-232, potassium-40, radium-226) using the MKGB-01 "RADEK" spectrometer-radiometer. All nettle samples from the Voronezh region met radiation safety standards. Correlation analysis revealed a strong relationship between the specific activity of anthropogenic radionuclides (strontium-90, cesium-137) and natural radionuclides (potassium-40, radium-226) in soil and leaves, with thorium-232 showing a medium degree of correlation. Since it is currently not possible to assess the contribution of radionuclide uptake in stinging nettle leaves from aerosols, we propose the only mechanism for the uptake of natural and anthropogenic radionuclides, which is solely through the plant's root system. Increased specific activity of these radionuclides in soil led to higher concentrations in the medicinal plant material. Notably, cesium-137 and potassium-40 accumulated intensively in nettle leaves, highlighting their unique uptake from soil. The study of radionuclide accumulation coefficients in nettle leaves suggests physiological mechanisms regulating radionuclide penetration and selective accumulation in plant tissues. Using Urtica dioica's ability to accumulate radioactive elements can enhance understanding of the biological behavior of medicinal plants in various ecosystems.

Milk is a daily source of essential nutrients, but the presence of trace metals raises significant health concerns about the quality of dairy products. This study investigated the presence of and human health exposure to potentially toxic elements (PTEs) in raw cow milk produced in the Caribbean region of Colombia, during both dry and rainy seasons. A total of 100 samples were collected from farms in five zones and analysed for toxic metal(loid)s, including Pb, Cr, Hg and As. Metal(loid) concentrations were generally higher during the rainy season, except for Hg, which showed elevated concentrations during the dry season. During the rainy season, values increased by factors of 20, 44, 3 and 0.5 for Pb, Cr, As and Hg, respectively. The year-round median concentrations of Pb, Cr, As and Hg in milk were 2.23, 44, 2.93 and 0.18 µg/L, respectively. The hazard index (HI) was higher than 1 in both adults and children, indicating a significant health risk of exposure to metal(loid)s in the milk-consuming population. Frequent milk consumption posed no public health concern for carcinogenic risk related to Pb and As across age groups. However, the estimated carcinogenic risk for Cr exceeded the USEPA guidance reference value for both children (1.7·10^-4) and adults (4.8·10^-4) indicating a potential public health concern across all age groups. In conclusion, it is essential not to underestimate the health risks associated with frequent milk consumption. Immediate action and stricter regulations on consumption are urgently needed to prevent potential public health emergencies.

This study examined the effects of syringic acid (SA) against testicular toxicity induced by cadmium (CAD). In the study, once daily for 7 days, the control and CAD groups were administered sterile distilled water, while the CAD + SA and SA groups were administered 25 mg/kg SA. Additionally, on the first day of the study, saline solution was administered intraperitoneally to the control and SA groups, and 1.5 mg/kg CdCl₂ was administered intraperitoneally to the CAD and CAD + SA groups. In blood, serum aspartate transaminase (AST) and alanine aminotransferase (ALT) enzyme activity, testosterone, creatine, and urea levels were evaluated. Spermatological parameters, including sperm motility, sperm viability, sperm concentration, and abnormal sperm, were evaluated. Histopathological examination and immunohistochemical analysis (inducible nitric oxide synthase (iNOS), cyclin D1, cannabinoid receptor1 (CB1)) were performed on testicular tissue. The testosterone value of the CAD group was significantly lower compared to the control and SA groups (p < 0.0083). In the CAD + SA group, sperm motility, sperm vitality, and sperm concentration were significantly increased compared to the CAD group. In contrast, the percentages of abnormal sperm (head and tail) were significantly decreased in the CAD + SA group compared to the CAD group (p < 0.0083). The rate of iNOS positivity in the SA and CAD + SA groups was similar to those in the control group. However, iNOS positivity was significantly higher in the testicles of the CAD group compared to the remaining groups (p < 0.0083). In conclusion, SA can be used as a preventative agent against testicular toxicity caused by CAD.

Besides its traditional uses for epilepsy/migraine, topiramate has demonstrated remarkable antioxidant and anti-apoptotic features. In this study, we investigated the potential role of topiramate in mitigating cadmium-induced nephrotoxicity in rats, focusing on oxidative stress, apoptosis, and autophagy. Twenty-four male Wistar rats were randomly allocated into control, topiramate, cadmium, and cadmium + topiramate groups. Nephrotoxicity was induced by oral cadmium chloride (5 mg/kg/day) for 2 months, while topiramate (50 mg/kg/day) was co-administered orally. Renal injury, oxidative stress indices, autophagy-, and apoptosis-related proteins were examined using histopathology, ELISA, and immunohistochemistry. This study showed significant renal damage, manifested as multiple histological aberrations, elevated blood urea nitrogen and serum creatinine, along with elevated renal expression of kidney injury molecule-1 (KIM-1). Topiramate co-treatment reduced blood urea nitrogen and serum creatinine by 37.7% and 39%, respectively, and lowered KIM-1 by 36.9%, while lowering the endothelial/glomerular/tubular/interstitial (EGTI) histopathological damage score by 52.9%. Mechanistically, topiramate mitigated cadmium-induced nephrotoxicity by suppressing renal pro-oxidants and augmenting several antioxidant signals, including sirtuin 1 (SIRT1), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and heme oxygenase 1 (HO-1) by 71.3%, 120.8%, and 78.7%, respectively. It also alleviated autophagy impairment by reducing sequestosome-1/protein 62 (SQSTM-1/p62) accumulation by 52.2% while activating AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) pathway. Additionally, topiramate curtailed apoptosis, as evidenced by increased B cell lymphoma 2 (Bcl-2) protein levels and lowered Bcl-2-associated x protein (Bax) expression and caspase-3 activity. Collectively, promoting SIRT1/Nrf2 antioxidant pathway, enhancing AMPK/mTOR-directed autophagy, and dampening renal apoptosis were involved in topiramate's protection against cadmium nephrotoxicity.

The presence of hazardous heavy metals (HMs) in the environment is well established, and numerous studies have explored their involvement in brain-related disorders. However, their potential impact on neuroinflammation, disease severity, and cognitive function in schizophrenia (SZ) remains largely unexplored. Therefore, this study aimed to investigate the potential pathophysiological role of environmental HMs in SZ. A total of 40 SZ patients and 40 healthy controls (HCs) were recruited from AIIMS Jodhpur, India. Blood samples were analyzed for lead (Pb), cadmium (Cd), arsenic (As), aluminium (Al), and TNF-α using atomic absorption spectroscopy and ELISA, while TNF-α gene expression was quantified using RT-qPCR. Patients exhibited notably elevated concentrations of Cd and Pb while decreased levels of As with median (IQR), 0.9 (0.40-1.72); 1.11 (0.59-1.26); and 0.73 (0.46-0.89) compared to HCs with median (IQR), 0.75 (0.46-1.06); 0.11 (0.04-0.18); and 0.92 (0.65-1.60) respectively. A significant positive relationship between TNF-α gene expression and blood As (ρ = 0.33, p < 0.05) and a negative association between Pb and Al (ρ = -0.34; p < 0.05) were reported in the patient group. Cognitive focus test scores were significantly lower in patients than in controls (p < 0.001). Cd levels negatively correlated with Stroop Word, Stroop Color, Color-Word, and Stroop Total scores (ρ =  - 0.28, - 0.36, - 0.28, - 0.33), indicating cognitive dysfunction. Additionally, PANSS score correlated negatively with Stroop Word (ρ =  - 0.36) and Stroop Total (ρ =  - 0.35), while PANSS Total scores showed negative correlations with Stroop Total (ρ =  - 0.33) and Stroop Color (ρ =  - 0.34), linking higher disease severity to poorer cognitive performance. In conclusion, these findings provide novel insights into SZ pathophysiology, highlighting the neurotoxic impact of heavy metals on TNF-α regulation, neuroinflammation, and cognition. The relationship between cognitive function with Cd and disease severity underscores the importance of early intervention and environmental risk mitigation to protect brain function and overall health.

Kashin-Beck disease (KBD) is a chronic osteoarticular disease. Chondroitin sulfate A-selenium nanoparticles (CSA-SeNP), a polysaccharide-based nanoparticle, have shown promise in facilitating cartilage repair, but the mechanism remains unclear. Given our previous findings of downregulated AMPK-mTOR pathway and autophagy in KBD chondrocytes, this study explored the effects of CSA-SeNP on the AMPK-mTOR pathway and autophagy levels in KBD chondrocytes. KBD chondrocytes were treated with CSA-SeNP and AMPK inhibitors alone or in combination. We found that CSA-SeNP promoted autolysosome content and autophagic flux and upregulated the AMPK-mTOR pathway and autophagy markers, while reducing apoptosis in KBD chondrocytes. It effectively alleviated oxidative stress, as evidenced by decreased ROS level and MDA concentration, along with increased activities of antioxidant enzymes (SOD, CAT, and T-AOC). Concurrently, it also improved mitochondrial function, including elevated ATP content, enhanced SDH and ATPase activities, and restored mitochondrial membrane potential. However, co-treatment of KBD chondrocytes with CSA-SeNP and AMPK inhibitor resulted in levels of autolysosome content, autophagic flow, AMPK-mTOR pathway activity, autophagy markers, apoptosis, oxidative stress, and mitochondrial function that were intermediate between those observed with respective treatment with CSA-SeNP or AMPK inhibitor. In summary, CSA-SeNP could effectively activate AMPK-mTOR pathway to promote autophagy process, reduce oxidative stress and apoptosis, and improve mitochondrial function, thereby repairing KBD chondrocytes. This study may provide new insights into the potential of CSA-SeNP as a therapeutic agent for KBD.

Boron compounds, such as boric acid(BA-H₃BO₃), have been utilized as potential candidates for modulating various biological functions owing to their specific characteristics, such as low toxicity, interaction with biomolecules, and possible roles as antigenotoxic and anticancer agents. On the other hand, mitomycin-C(MMC), a chemotherapeutic drug used for several cancers, may induce genetic damage in the healthy cells of cancer patients. Therefore, this study evaluated whether BA (0.25-2.5 µg/mL) generates protective potential against MMC-induced DNA and chromosome damage. After human lymphocytes were exposed to MMC and BA alone and in combination (BA + MMC), genotoxic and/or mitigating effects were evaluated using chromosomal aberration (CAs), sister chromatid exchange (SCE) (24 and 48 h), and cytokinesis-block micronucleus cytome (48 h) tests. The ameliorative potential of BA against hydrogen peroxide(H₂O₂)-induced DNA damage was also assessed using a comet assay (1 h). MMC significantly increased (p < 0.05) the frequency of abnormal cells, CA/cell, SCE/cell, micronucleus, and nuclear buds and decreased (p < 0.05) the mitotic index compared to the control. However, BA alone did not induce any significant alterations in the incidence of these aberrations. In addition, all the combined treatments of BA + MMC significantly ameliorated (p < 0.05) all of these indices against MMC. In the comet assay, BA significantly diminished (p < 0.05) the tail intensity (%DNA) against H₂O₂. These results revealed that BA does not induce significant genotoxic effects. Moreover, it may exert chemopreventive potential against MMC- and H₂O₂-induced genetic damage. These findings suggest that boric acid is safe and effective at low concentrations in food, medicine, and healthcare applications.

Environmental pollutants, such as zearalenone (ZEA), a mycotoxin from Fusarium graminearum that contaminates cereal crops and animal feed, significantly threaten reproductive health. The main toxicity mechanism of ZEA involves triggering oxidative stress and apoptosis. Zinc (Zn), a critical antioxidant for reproductive health, may counteract ZEA toxicity, but its mechanism of action remains unclear. The objective of the study was to investigate the alleviating effects of Zn supplementation against ZEA-induced testicular toxicity. We combined network toxicology and animal experiments to evaluate Zn's efficacy. Male Kunming mice were divided into Control, ZEA (2 mg/kg), Zn (20 mg/kg) and ZEA + Zn (10/20/40 mg/kg) groups and treated for 28 days. The results revealed that ZEA exhibited marked reductions in sperm quality, accompanied by structural testicular injury to the testis. ZEA diminishes the activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), while simultaneously increasing the levels of malondialdehyde (MDA), which results in oxidative stress. ZEA down-regulates serum levels of testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and impairs steroidogenesis. Significant elevations in ROS levels and apoptotic protein expression were observed in the testicular tissue of the ZEA group. ZEA significantly decreased both the mRNA and protein expression levels of Sirt3 and Foxo3, as well as their immunofluorescence intensity. Zn significantly increased sperm quality, improved testicular morphology, increased Sirt3 and Foxo3 levels, reduced ROS, normalized antioxidant capacity, improved apoptosis, and restored serum hormone levels. These findings emphasize the reproductive risks associated with ZEA, while also highlighting Zn as a possible candidate for developing alleviating effects against mycotoxin-induced reproductive toxicity.