Biological Trace Element Research最新文献

The increasing popularity of roll-your-own (RYO) tobacco has raised toxicological concerns regarding heavy metal exposure. This study quantified fourteen metals (Fe, Zn, Mn, Cr, Cu, Ni, Cd, Mo, Co, Sb, Pb, As, Hg, and V) in RYO tobacco samples collected from ten provinces in Türkiye using inductively coupled plasma optical emission spectrometry (ICP-OES). Fe exhibited the highest mean concentration (18.11 mg.kg^-1), followed by Zn (10.53 mg.kg^-1) and Mn (5.020 mg.kg^-1), whereas As (0.041 mg.kg^-1), Hg (0.015 mg.kg^-1) and V (0.001 mg.kg^-1) occurred at the lowest concentrations. Statistically significant correlations were observed, including Fe-Hg (r = 0.97, p < 0.001) and Zn-As (r = -0.77, p < 0.01), indicating shared geochemical influences and contrasting uptake patterns. Health risk assessment following USEPA guidelines indicated that all Hazard Quotients (HQ < 1) and Hazard Index (HI = 4.8 × 10^-3) remained below the non-carcinogenic threshold, and Carcinogenic Risk values ranged from 2.50 × 10^-7 to 2.00 × 10^-10 and remained below 10^-6. The results characterize metal exposure levels in RYO tobacco and indicate potential toxic elements as elements requiring continued monitoring due to their toxicological relevance.

The aim of this research was to examine the potential ameliorative effects of chrysin (CHR) against mercuric chloride (HgCl₂)-induced testicular damage in rats. For this purpose, rats were divided into four groups: Control, CHR, HgCl₂ and HgCl₂ + CHR. HgCl₂ was administered intraperitoneally at a dose of 1.23 mg/kg, and CHR was administered orally at a dose of 50 mg/kg for 7 days. Biochemical, molecular and immunohistochemical analyses were performed to determine the effect of treatment-mediated changes in the testicular tissue. Based on the results obtained in testicular tissue, administration of HgCl₂ was observed to lower antioxidant markers, elevate malondialdehyde (MDA) levels, and increase inflammatory marker expression in rat testicular tissue. It also led to reduced testosterone levels. Additionally, there was a decrease in the expression of antiapoptotic B-cell lymphoma 2 (Bcl-2) an apoptosis marker while the levels of Caspase-3 and Bcl-2-associated X protein (Bax) were found to be higher. The endoplasmic reticulum stress marker protein kinase R-like ER kinase (PERK) and the autophagy marker Beclin-1 showed strong immunoreactivity. Additionally, HgCl₂ + CHR treatment were found to significantly reduce oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and autophagy processes in testicular tissue. In conclusion, HgCl₂ administration to rats caused testicular tissue damage compared to the other groups, but CHR treatment alleviated this damage. Overall, this demonstrates the potential ameliorative mechanisms of CHR as a possible agent for HgCl₂-induced testicular damage.

Monitoring toxic elements has a long tradition in Slovenia due to historical mining. More recently, attention has shifted to essential elements, since both deficiencies and excesses can harm health. Regular monitoring of (non-)essential elements supports risk assessment and policymaking. While urine and blood are common biomonitoring matrices, hair offers a non-invasive alternative that reflects exposure over several months, though standardised methodologies for hair analysis remain limited. This study aimed to develop and validate a sensitive and robust analytical method for the determination of 29 elements in human hair, addressing key challenges in sample preparation and contamination control. We developed a sensitive and robust method for the determination of 29 elements (Ag, Al, As, Ba, Ca, Cd, Co, Cr, Cu, Fe, Hg, K, Mg, Mn, Mo, Na, Ni, P, Pb, Rb, S, Sb, Se, Sn, Sr, Ti, U, V, and Zn) in 3 cm segments of human hair that involves a washing procedure with acetone and Milli-Q water, microwave digestion with 65% HNO₃, and analysis with Triple Quadrupole Inductively Coupled Plasma Mass Spectrometry (ICP-MS/MS). Evaluation of preparation steps revealed stainless-steel scissors as a major contamination source. Glass digestion vessels were unsuitable for several elements due to high detection limits and relative standard deviations. The optimised method reduced analytical variability and improved sensitivity compared to published protocols. This validated method enables reproducible multi-elemental analysis in hair, highlights overlooked contamination risks, and is now applied in human biomonitoring studies to strengthen exposure assessment and standardisation efforts.

Cd is a ubiquitous and toxic heavy metal, characterized by environmental persistence and bioaccumulation, which presents high risks to agricultural production and human health. In this review, natural countermeasures against Cd toxicity are systematically categorized into inorganic substances, active natural products, and microorganisms. We discuss these compounds as protectants and the shared and distinct mechanisms by which they reduce metal toxicity, including competitive uptake, chelation, antioxidant enhancement, and gene regulation. A comprehensive review of studies published in recent years highlights the great influence on protective efficacy by compound-specific mechanisms, including the role of essential metals in competitive uptake and induction of particular antioxidant pathways through phyto-chemical exposure. Despite this, major knowledge gaps are still left to be filled, especially concerning the combined impact of treatments and their performances under field conditions or long-term sustainability. The aim of the present study is to explain the mechanisms for their protective effects, and these results offer an overview to contribute to developing environmentally friendly methods for Cd phytoremediation. This literature review comprehensively summarizes the up-to-date comprehension of natural protection against Cd, and will provide an insight for the subsequent investigations on the practical applications in agriculture, environmental treatment, and public health to ensure food system safety and land reduction of pollutants from the contaminated environment.

Cadmium (Cd), a toxic metal, poses significant threats to ecological and human health due to its neurotoxic and gut toxicity effects. However, the mechanisms by which Cd disrupts brain-gut axis interactions remain unclear, and strategies to mitigate these effects are limited. Melatonin (MT), known for its anti-inflammatory and antioxidant properties, has shown promise in counteracting heavy metal toxicity. This study investigated the protective mechanisms of MT against Cd-induced toxicity in adult zebrafish using histopathological analysis, 16 S rRNA sequencing, RNA-sequencing, and qRT-PCR. Results showed that MT significantly alleviated Cd-induced structural damage in brain spongiosa and restored intestinal villi integrity. 16 S rRNA sequencing revealed that MT reduced pathogenic bacteria and increased beneficial bacteria in the gut microbiota. Transcriptomic analysis identified 31 differentially expressed genes (DEGs) in brain, KEGG enrichment analysis showed these DEGs are associated with neurodegenerative diseases pathways. Concurrently, 8 DEGs in gut were linked to oxidative phosphorylation signaling pathways. Correlation analysis showed pathogenic Legionella and Aeromonas were positively correlated with htr2b, il21r.2, il2rb, il21r.2, cyp46a1.3 cyp2ad3, cyp46a1.3 in brain, Candidatus_Protochlamydia was positively correlated with il7r, drd3 in gut, those are down regulated DEGs, whereas beneficial Acinetobacter and Achromobacter were positively correlated with cyp2 × 8 in gut, this is up regulated DEG. These suggests that Legionella, Candidatus_Protochlamydia, Achromobacter and Acinetobacter may be key bacterial that mediate the MT reduction in neurotoxicity and immunotoxicity induced by Cd. These findings highlight MT's potential to mitigate Cd-induced toxicity by modulating the gut microbiota, offering therapeutic insights for reducing Cd toxicity risks in aquaculture.

Tellurium, long considered a toxic element, now represents a unique platform for biomedical nanomaterials. Its fundamental paradox lies in its dual nature: depending on the form and dose, it exhibits both potent pro-oxidant activity against tumor cells and pathogens, and pronounced antioxidant properties. Tellurium nanoparticles (TeNPs) serve as a tool for managing this duality. This review systematizes modern methods of TeNPs synthesis, including laser ablation as a source of high-purity particles, and details the mechanisms of their biological action - from redox activity and modulation of calcium signaling to the targeted suppression of signaling pathways. Particular attention is paid to the application of TeNPs as antimicrobial and anticancer agents, and as modulators of central nervous system functions, where particle size determines the shift from neurotoxicity to neuroprotection. The analysis suggests the potential of TeNPs for creating new therapeutic platforms, although challenges related to their narrow therapeutic window and long-term safety remain.

Cerebral ischemia-reperfusion injury is a prevalent complication following blood flow restoration in ischemic stroke, which induces severe neurological dysfunction via intricate oxidative stress and inflammatory cascades. Cerium oxide nanoparticles (CeO₂NPs), endowed with unique Ce³⁺/Ce⁴⁺ valence transition properties, exhibit mimetic activities of superoxide dismutase and catalase, enabling efficient scavenging of reactive oxygen species and attenuation of inflammatory responses. This study aimed to investigate the protective effects and underlying molecular mechanisms of CeO₂NPs against cerebral ischemia-reperfusion injury. First, the physicochemical properties and toxicity of CeO₂NPs were systematically characterized: dynamic light scattering (DLS) showed a polydispersity index (PDI) of 0.28 and a ζ-potential of -24.9 mV; transmission electron microscopy (TEM) confirmed a particle size range of 2-6 nm; X-ray photoelectron spectroscopy (XPS) quantification demonstrated 100% Ce coverage on the particle surface. The Morris water maze test indicated no significant neurotoxicity at a dose of 0.4 mg/kg. Subsequently, the therapeutic efficacy was evaluated using a MCAO mouse model. Behavioral assessments revealed that 24 h after reperfusion, the CeO₂NPs-treated group exhibited behavioral performance more comparable to the normal group. Combined with histopathological analysis of brain tissues, these findings confirmed that CeO₂NPs significantly improved neurological function and alleviated brain tissue damage. Proteomics analysis further uncovered that CeO₂NPs mitigate oxidative damage and inflammation primarily by regulating the mitochondrial-mediated apoptotic pathway and superoxide dismutase-related oxidative stress responses. In conclusion, 2-6 nm CeO₂NPs hold great promise as an effective neuroprotective agent for the treatment of cerebral ischemia-reperfusion injury, with their mechanism of action involving multiple cellular protective pathways.

Recent advances in the field of nanotechnology have paved the way for novel biomedical applications of nanomaterials. Nanoscale vanadates possess unique properties and have been reported to elicit anti-aging, antibacterial, anti-cancer and antioxidant effects. Likewise, they are potentially applied as bioimaging, drug delivery, theranostic or would healing agents, as well as biosensors. In this review, we highlight and critically discuss biomedical applications of vanadate nanostructures. This review article aims at identifying molecular hallmarks of vanadate nanomaterial-mediated cytotoxicity. Our analysis reveals that depending on size, morphology, composition, concentration, and external conditions (pH, irradiation, etc.) nanoscale vanadates induce oxidative stress, mitochondrial dysfunction, and lysosomal damage, culminating in cell death. Notably, besides apoptosis, nanosized vanadates trigger immunogenic non-apoptotic cell death pathways (ferroptosis and necroptosis) primarily due to overproduction of reactive oxygen species (ROS). Thus, our review demonstrates that nanostructured vanadates are multifaceted pharmacological agents with a wide spectrum of diverse biological applications. Our analysis demonstrates that redox activity of nanostructured vanadates is a key factor determining biological responses to them. Thus, more studies should focus on elucidating the biologically-relevant redox mechanisms of nanosized vanadates.

Dysregulated zinc homeostasis is a common feature of diabetes mellitus (DM), exacerbating β-cell dysfunction, impairing glycemic control, and promoting vascular, renal, neural, and cognitive complications. This review summarizes experimental and clinical evidence on hyperzincuria and impaired intestinal zinc absorption in type 1 (T1DM) and type 2 (T2DM) DM, focusing on their mechanisms and implications for revising dietary zinc recommendations. Experimental models showed tissue-specific zinc depletion, with pancreas, liver, and femur zinc levels reduced by 17-50%, while kidney, muscle, and intestine show variable changes depending on DM duration and dietary zinc. Radiolabeled zinc studies report a 53% reduction in intestinal uptake, while early-stage of DM may compensatory increase absorption up to ~ 70%. However, prolonged hyperglycemia and zinc transporter dysregulation (ZIP4/ZIP7/ZIP14 down, ZnT1/5/7 and metallothioneins up) cause persistent intracellular and systemic zinc depletion. Persistent urinary zinc (UZn) loss, a marker of disrupted zinc homeostasis in diabetes, increases 3- to 14-fold in T1DM models, 5- to 6-fold in db/db mice, and is 1.6- to 5-fold higher in humans with T1DM and 1.4- to 7-fold higher in T2DM. Hyperzincuria in DM is primarily driven by hyperglycemia-induced osmotic diuresis and glycosuria, exacerbated by diabetic nephropathy, proteinuria, and the use of certain antidiabetic and antihypertensive medications. Current zinc RDAs (8 mg/day for women, 11 mg/day for men) may be insufficient in diabetes, and a 30-50% higher intake could help restore zinc balance, improve glycemic control, and reduce the risk of complications. However, these estimates are based on experimental and observational data, and well-designed clinical studies are needed to confirm the optimal zinc intake in DM.