The ability to acquire iron drives microbial fitness in marine environments where iron solubility is extremely low. Iron uptake via the siderophore aerobactin plays an important role in Vibrio fischeri colonization in the light organ of the Hawaiian bobtail squid. To date, the contribution of aerobactin to this mutualistic relationship has not been demonstrated quantitatively. Here we report a revised total synthesis of aerobactin, characterize its stability and iron-binding properties, and demonstrate its importance to Vibrio-squid mutualism. Synthetic aerobactin was characterized by nuclear magnetic resonance (NMR) and high-resolution mass spectrometry and iron binding was measured via the Chrome Azurol S (CAS) assay. Stability experiments in artificial seawater showed that aerobactin degrades slowly, with a half-life on the order of weeks. The activity of synthetic aerobactin was then demonstrated by growth recovery experiments with wild-type V. fischeri ES114 and mutant strains deficient in aerobactin biosynthesis (ΔiucABCD), its outer-membrane aerobactin receptor (ΔiutA), and in the inner-membrane importer (ΔfhuCDB). Available iron was controlled in cell culture experiments by the addition of 2,2'-bipyridine (BPY) or citrate to experimental growth media, with bathocuproine disulfonic acid (BCDS) included as a membrane-impermeable, and poor iron-sequestering control. Exogenous aerobactin restored growth in iron-limited environments in a concentration-dependent manner, particularly in the biosynthesis-deficient mutant. Additionally, we report that BPY inhibits V. fischeri ES114 growth with a broad MIC range (128-256 μM) that highlights its capacity to disrupt the intracellular iron pool. Together, these findings support the use of AB-FeCit as the optimal media system for testing siderophore-dependent growth in V. fischeri and link synthetic aerobactin and iron availability to bacterial growth in a model marine mutualism.
Chronic exposure to copper ions, Cu(II), induces organ-specific oxidative damage and mitochondrial dysfunction, with distinct temporal and biochemical profiles across tissues. This study evaluated the protective effects of vitamin E (α-tocopherol) against Cu(II)-induced phospholipid and protein oxidation, redox imbalance, and bioenergetic disruption in rats. Cu(II) treatment led to early lipid peroxidation in the brain, heart, and lung, followed by delayed oxidative damage in the liver and kidney. Vitamin E effectively prevented phospholipid oxidation in all organs, but its protection against protein oxidation and mitochondrial respiratory impairment was organ-specific and time-dependent. Mitochondrial respiration declined in brain and heart tissues, with partial recovery in the heart after prolonged vitamin E supplementation. Electron transport chain activity was altered by Cu(II), notably with increased complex I activity in the liver and decreased complex I and II activity in the lung and kidney. Vitamin E failed to prevent these changes in most tissues. Glutathione modulation revealed adaptive redox responses in the lung and oxidative depletion in kidney. These findings highlight the complexity of Cu(II)-induced oxidative damage and the limited but significant protective role of vitamin E, emphasizing the need for targeted antioxidant strategies to preserve mitochondrial integrity and cellular function under metal-induced stress.
Mine tailings contribute to environmental heavy metal contamination through the formation of acid mine drainage (AMD). Microbially-mediated processes such as iron and sulfur redox cycling influence metal mobility. Here, we applied an integrated metagenomic and metaproteomic approach to profile microbial communities across vertical geochemical gradients in legacy copper/nickel tailings in Sudbury, Ontario, Canada. From 43 samples, we recovered 454 non-redundant metagenome-assembled genomes (MAGs), revealing diverse populations within the Actinobacteriota, Desulfobacterota, and uncultured lineages such as Candidatus Eremiobacterota and SZUA-79. Functional profiling identified 301 putative iron- and sulfur-cycling MAGs, including those within the Ca. Eremiobacterota and SZUA-79 phyla. A custom set of Hidden Markov Models (HMMs) was used to annotate metal resistance genes, which were widespread and diverse, but whose abundances did not correlate with measured Cu, Ni, or Fe concentrations. This observation suggests that resistance traits are broadly encoded in these microbial communities regardless of environmental metal concentrations. Proteomic data confirmed in situ expression of selected metal resistance genes and iron/sulfur metabolism genes, although protein recovery was limited due to the difficult nature of mine tailings as an extraction matrix. Our findings highlight both the depth of microbial diversity in metal resistance and metal biogeochemical cycling in mining waste, as well as the technical challenges that currently limit genomic and proteomic sequencing coverage in low-biomass, metal-rich matrices.
Metals and metalloids play essential roles in cancer biology, influencing redox balance, epigenetic regulation, immune responses, and cell death throughout tumour development, progression, and resistance to therapy. Despite this broad biological relevance, the systematic clinical integration of metallomics into oncology remains in its early stages. This review introduces the Cancer Metallome Continuum, a framework illustrating how metallomic reprogramming evolves from cancer initiation through progression to therapy-resistant states, and evaluates the analytical, systems-level, and translational approaches needed to test it. In early stages of cancer, toxic metals such as As, Cd, hexavalent chromium [Cr(VI)], and Ni induce oxidative stress, epigenetic modifications, and DNA repair defects. During progression, dyshomeostasis of essential metals creates tumour-specific dependencies. For example, Fe accumulation can support tumour growth, while tumour cells concurrently engage antiferroptotic programs; Cu contributes to angiogenesis and kinase signalling, and Zn transporter networks regulate apoptosis and immune responses. Under treatment pressure, tumours adapt by rewiring metal transporters, upregulating metallothionein buffering, and suppressing metal-dependent cell death pathways, including ferroptosis and cuproptosis. Translational advances include selenium-based prognostic panels with replicated evidence in breast cancer (SCAN-B) and colorectal cancer (CORSA), Cu-chelation trials, and spatially resolved metallodrug imaging. The strongest human evidence currently supports Se-based prognostic panels (replicated across breast and colorectal cancer cohorts) and the feasibility of biomarker-guided Cu depletion (a Phase II single-arm trial), while spatial integration and artificial intelligence/machine learning applications remain at the proof-of-concept or emerging stages. Clinical translation will require tighter control of preanalytical variability, prospective multicentre validation, and standardized reporting.
Cyclometalated Iridium(III) complexes have emerged as one of the most versatile classes of photosensitizers for photodynamic therapy (PDT), owing to their tunable photophysics, high phosphorescence quantum yields, and intrinsic capacity for real-time optical imaging. However, the clinical translation of conventional PDT remains limited by nonspecific activation, poor selectivity, and off-target phototoxicity. The dynamic and heterogeneous tumour microenvironment (TME)- defined by anomalous pH, elevated Glutathione (GSH) levels, malfunctioned redox homeostasis, enzyme overexpression, and irregular vascularization, which thus offers an opportunity to engineer next-generation photosensitizers that respond selectively to these cancer-specific stimuli. This review aims to explore recent advances in stimuli-responsive and theranostic cyclometalated iridium(III) systems designed to achieve anticancer activity in a spatiotemporal manner. We discuss the molecular design principles and mechanistic bases of TME-, redox-, enzyme-, and light-triggered activation, along with emerging multi-stimuli architectures that enhance the robustness in complexes. The review further focuses on the way Ir(III) Complexes unite therapy and diagnostics. Due to their inherent luminescence, redox characteristics, and excited-state behaviour, these complexes enable simultaneous imaging, ROS production, microenvironment sensing, and real-time monitoring of treatment responses. By correlating structural features with activation pathways and biological outcomes, the review seeks to provide a mechanistic framework for designing smart Ir(III)-based PDT agents with improved selectivity, reduced systemic toxicity, and enhanced therapeutic precision.
Phosphorus (P) is central to biology, yet it remains unclear whether P limitation acts as an isolated nutrient constraint or as a perturbation to a dynamical elemental network. We tested this using the rainbow trout liver cell line RTL-W1 by manipulating phosphorus supply (0%, 10%, and 100% of normal supply; P0, P10, and P100) and quantifying proliferation, protein content, metabolic activity, membrane integrity, and multielement composition. Phosphorus supply significantly altered cell proliferation and protein accumulation, with higher P supporting greater growth. Metabolic activity was affected by P supply, whereas membrane integrity remained largely stable, indicating altered allocation rather than generalized cellular damage. Compositional ionomic analysis revealed that phosphorus perturbation restructured the multielement network. At Day 3, treatment effects were strongest for P, K, and S. By Day 6, additional elements, including Sr and Mn, exhibited coordinated shifts relative to the P100 reference. Compositional data analysis showed that elemental imbalances shifted through time, consistent with flux rebalancing in an open system rather than static homeostasis. If phosphorus limitation were mechanistically independent, multielement composition would remain stable aside from P itself. Instead, phosphorus perturbation induced coordinated shifts across the ionome, consistent with rebalancing in open material systems.
Mutations in the copper (Cu) transporter ATP7A cause a spectrum of X-linked diseases, including Menkes Disease, Occipital horn syndrome, and distal hereditary motor neuropathy (dHMNX). We previously generated a conditional knock-in mouse model of dHMNX expressing Atp7aT985I, the murine orthologue of the human T994I variant identified in dHMNX patients. Although Atp7aT985I mice did not develop overt motor degeneration, affected males showed a trend toward reduced Cu levels in the peripheral nervous system (PNS). The high-affinity copper transporter Ctr1, encoded by Slc31a1, regulates Cu uptake, and ubiquitous heterozygosity for Slc31a1 (Ctr1+/-) has been reported to limit Cu availability in the nervous system without impairing motor performance. In this study, we genetically restricted Cu availability in Atp7aT985I mice by crossing them with Ctr1+/- animals. Atp7aT985I/Ctr1+/- males exhibited significantly reduced Cu levels in both the central nervous system and PNS compared to wild-type littermates. At 6 months of age, behavioural testing and histopathological assessment revealed mild motor deficits and axonal loss, preferentially affecting small-caliber fibres exclusively in the Cu-restricted Atp7aT985Imales. Tandem mass tag-based proteomics of sciatic nerve identified significant changes linked to energy metabolism, cytoskeletal integrity, and cellular stress responses. Together, these data show that limiting Cu availability unmasks a dHMNX-like phenotype in Atp7aT985I/Ctr1+/- mice, demonstrate the critical role of Cu availability in maintaining peripheral axons and suggest that reduced Cu in motor neurons contributes to axonal degeneration in dHMNX.
Chromatin remodeling by SWI/SNF complexes is essential for transcriptional regulation, yet how distinct SWI/SNF subcomplexes contribute to cellular stress responses remains incompletely understood. Here, we identify a specific role for the PBAF subunit Baf180 in regulating metal-responsive transcription and adaptation to metal stress in proliferating myoblasts. While knockdown (KD) of the BAF-specific subunit Baf250a or the ncBAF-specific subunit Brd9 significantly impairs myoblast proliferation, KD of the PBAF-specific subunit Baf180 has no effect under basal conditions. Notably, supplementation with copper (Cu) or zinc (Zn) restores proliferative capacity in Baf250a- and Brd9-deficient myoblasts. In contrast, Baf180-depleted myoblasts exhibit impaired proliferation upon metal exposure, accompanied by selective dysregulation of genes involved in Cu and Zn homeostasis. Transcriptomic and chromatin profiling further reveal that loss of Baf180 alters the activity of metal-regulatory transcription factor 1 (MTF1), including reduced chromatin occupancy at metal-responsive loci. Together, these findings support a model in which PBAF promotes metal-responsive gene regulation to maintain metal homeostasis and sustain myoblast proliferation, uncovering a previously unrecognized link between nucleosome remodeling and metal homeostasis during muscle cell proliferation.
Cisplatin is a DNA-targeting chemotherapeutic. Here we investigate how the cisplatin-damaged gene (CDG) loci are linked to specific protein-driven signalling pathways. A human high mobility group protein 1 box a-based affinity probe has been constructed and 1,2-cisplatin-crosslinked DNA has been isolated before high throughput gene sequencing. Cisplatin damage to specific genes has been mapped in human lung cancer cells, and a total of 16 216 CDGs mapped with fold-enrichment >1.5. Surprisingly, bioinformatics analysis demonstrates that cisplatin targets most of the human protein kinase (PK) and phosphatase genes and is involved in 300 important cell signalling pathways (-log p > 4). The most associated key signalling pathways are sperm motility and protein kinase A. Notably, cisplatin damaged 85% (440) of human PK genes and 81% (110) of human protein phosphatase genes. This implies that cisplatin may disrupt protein phosphorylation signalling genome-wide, evidenced by a significant decrease in expression of a series of key PK genes.
A method for quantitative speciation analysis of residual gadolinium in skin following gadolinium-based contrast agent exposure was developed for the first time. Polyethersulfone was identified as a suitable filter material for these compounds, allowing complete recovery of spiked contrast agents. In contrast, decreasing recoveries with increasing charge of the compound were observed for regenerated cellulose and cellulose triacetate as filter materials. The developed method entailed the utilization of bead beating for tissue homogenization, and the release of yttrium from ceramic beads was shown to result in the gadolinium transmetalation of a linear gadolinium-based contrast agent. A three-step centrifugation of homogenized skin samples, followed by filtration, was performed to extract hydrophilic species for analysis. In combination with using the respective europium chelates as internal standards, this approach enabled the complete recovery of macrocyclic contrast agents from spiked tissue. Quantitative speciation analysis of the biological extracts was conducted by means of anion exchange chromatography hyphenated to inductively coupled plasma-mass spectrometry. This analytical strategy applied to rat skin tissue after repeated administration of macrocyclic contrast agents showed that about a quarter of the residual gadolinium in skin tissue was present in the aqueous extract one month after the last injection. The majority of this water-soluble gadolinium was confirmed by speciation analysis to be the intact administered contrast agent. The presented methodological framework can serve as a first step towards exhaustive speciation analysis of residual gadolinium in skin matrix.
Isotopes of calcium (Ca) in blood and urine have been introduced as a potential clinical tool for monitoring bone mineral balance (BMB). While several works support the ability of Ca isotope composition (δ44/42Ca) to capture a shift in BMB in response to external forcings (e.g. bed rest) or disease (e.g. osteoporosis), the influence of an individual's demographic, health status, diet or lifestyle on δ44/42CaUrine/Blood remains largely unconstrained. To gauge the effects of several variables among these four broader categories, we present a population study of δ44/42CaUrine from 103 individuals (age 18-76). Age is negatively correlated with δ44/42CaUrine, and we identify three other attributes (active vitamin D deficiency, vegetarian diet, and being post-menopausal) that lead to systematic differences in an individual's δ44/42CaUrine. Fluctuations in Ca reabsorption generate significant intra-individual δ44/42CaUrine variability. Within a typical range of reabsorption rates, however, the initial isotope composition (δ44/42CaSerum) exerts the strongest control on inter-individual δ44/42CaUrine variability. Using a simple Rayleigh model to express isotopic fractionation associated with Ca reabsorption in the kidneys, we find that a fractionation factor of 0.99972 reproduces the range of isotope ratios and excretion values for several, healthy individuals across three different studies and nearly a 30-year age span. Importantly, δ44/42CaUrine variations in three post-menopausal women from three separate studies cannot be explained by the same model, pointing to a different mechanistic control of δ44/42CaUrine in these subjects.
Zinc is an essential trace element, yet how graded dietary zinc intake reshapes tissue-specific distributions of zinc and other essential metals remains incompletely understood. This study investigated the impact of dietary zinc ranging from deficiency to high supplementation on the metallomic profile of C57BL/6 J mice. Mice were fed one of five zinc diets for 3 or 6 weeks, after which zinc status and related elements (copper, iron, manganese, calcium, and magnesium) were quantified in serum and multiple tissues by inductively coupled plasma-optical emission spectrometry, alongside expression of zinc transporter and metal-related genes in intestinal segments. Tissue zinc responses differed strongly across organs. Serum zinc increased only after prolonged supplementation, the colon and small intestine showed rapid and pronounced shifts with both deficiency and excess, brain and skeletal muscle regions displayed selective sensitivity, and liver and kidney zinc remained comparatively stable, consistent with strong homeostatic control. Dietary zinc did not deplete tissue copper but instead showed positive associations between zinc and copper in several tissues. We also observed co-ordinated and tissue-dependent relationships between zinc and iron, manganese, calcium, and magnesium, which challenges the traditional view that mineral interactions are uniformly antagonistic. When we integrated elemental and gene expression data and explicitly linked metal responses to measured tissue zinc levels, we identified segment-specific and transporter-specific adaptations that support a model in which dietary zinc reorganizes local and systemic mineral balance. This reorganization reflects both changes in tissue zinc levels and additional regulatory mechanisms in metal transport and storage that are not apparent from whole-tissue zinc measurements alone.
Understanding how chalcogen elements taken up by biological systems change their chemical speciation is essential for elucidating their intracellular behaviour. However, knowledge of the uptake and transformation of selenium and tellurium oxyanions in unicellular algae remains limited. In this study, selenium and tellurium oxyanions in different oxidation states (VI or IV) were added to two unicellular algae, Chlamydomonas reinhardtii and Pseudococcomyxa simplex, and their intracellular accumulation and chemical speciation were systematically investigated. X-ray absorption fine structure analysis revealed that both selenium and tellurium underwent intracellular reduction irrespective of their initial oxidation states. However, the extent of reduction, accumulation efficiency, and final chemical speciation differed markedly depending on both the oxidation state of the added oxyanion and the algal species, indicating shared yet species-dependent intracellular transformation patterns. In particular, tetravalent oxyanions (selenite and tellurite) underwent more rapid reduction and exhibited higher cellular accumulation than the corresponding hexavalent species in both algae, although the extent and kinetics of reduction differed markedly between species. Scanning and transmission electron microscopy demonstrated that selenium was immobilized as spherical elemental nanoparticles, whereas tellurium formed needle-like metallic nanorods within algal cells. Under hexavalent selenate exposure, higher-valent and organoselenium species remained detectable, and the formation of elemental selenium nanoparticles was limited. These results demonstrated speciation- and species-dependent intracellular transformation and accumulation of selenium and tellurium in unicellular algae, providing chemical speciation-based insights into algal chalcogen metabolism and detoxification processes.
In recent years, in addition to their potential diagnostic and therapeutic properties, the immunogenic cell death (ICD) induction activity of iridium(III) and rhenium(I) complexes has been extensively reported. 4-Phenylimidazole (4-PIM), as an indoleamine 2,3-dioxygenase (IDO) inhibitor, can improve the immunosuppressive environment and enhance the efficacy of chemotherapy drugs. In this study, a series of Ir(III)/Re(I)-PIM complexes [Ir-PIM-(1-3) and Re-PIM-(1-3)] by coordination 4-PIM with iridium(III)/rhenium(I) metal centers were designed and synthesized to study their antitumor mechanisms. Among the six complexes screened, four compounds Ir-PIM-(1-3) and Re-PIM-1 showed good antitumor activity against human triple negative breast cancer (MDA-MB-231) cells. And Ir-PIM-(1-3)/Re-PIM-1 exhibited potential IDO inhibitory activity, which can suppress the expression of IDO protein. Further mechanistic studies indicate that Ir-PIM-(1-3)/Re-PIM-1 can effectively enter MDA-MB-231 cells, and induce the depolarization of mitochondrial membrane potential, the elevation of reactive oxygen species, G2/M phase cell cycle arrest and the release of damage-related molecular patterns, exhibiting dual activity in inducing both apoptosis and ICD.
The title novel cage complexes were prepared using two-stage nucleophilic substitution of their dichloromacrobicyclic precursor and characterized using elemental analysis, MALDI-TOF mass, UV-vis, 1H and 13C{1H} NMR spectra, and single-crystal XRD experiments. Their chemical compositions suggest an existence of 3D-shaped molecules in either neutral or zwitter-ionic forms and molecular drawings were evaluated basing on most likely hydrogen bonds in the crystals. Effect of proton intramolecular transfer on peculiarities of charge distribution was theoretically studied using XRD structures of two forms of a para-amino-meta-carboxyl-terminated complex. Molecular geometries, charge distributions and electrostatic potentials for them were quantum-chemically calculated. Solution circular dichroism (CD) data suggest that the nature and position of terminal biorelevant groups strongly affect their supramolecular interactions with globular proteins, inducing a metal-centered chirality. Intensities of CD outputs on formation of protein-clathrochelate assemblies and positions of their maxima are also affected by the nature of protein host. Four novel iron(II) clathrochelates possess a cytotoxicity against several cancer cell lines in the comparable low-micromolar concentration range. Maximal cytotoxicities against the cancer HeLa, MCF-7, Caco-2, A549, Hep-2, and PC-3 cells, and relatively low cytotoxities against the normal MRC-5 cells were found for heterodifunctionalized meta(para)-amine-para-carboxyl-terminated isomers (being affected by their structural isomerism) and for mono-meta(para)-carboxylochloroclathrochelates. Cell death in cancer HeLa and Hep-2 lines almost equiprobably includes both necrosis and apoptosis. Low-micromolecular concentration of a meta-amine-para-carboxyl-terminated iron(II) clathrochelate affected a cell cycle of Hep-2 cells causing an increase in the fraction inclined in its S-phase. Pathway of their death and cycle phase distribution shift were studied.
Zinc is essential for cellular homeostasis and acts both as a structural element and a secondary messenger in intracellular signalling. While the role of SLC39 (former ZIP) family transporters in breast cancer biology is intensively studied, the signalling function of SLC30 family transporters (former ZnT) remains insufficiently explored. This study investigates the involvement of SLC30 transporters in oestrogen receptor-positive (ER+) breast cancer. Bioinformatic and experimental analyses revealed that SLC30 transporters, particularly SLC30A1, SLC30A5, and SLC30A9, regulate the PTP/AKT/ESR1 pathway, contributing to hormone-independent ESR1 activation. Zn-dependent inhibition of PTP phosphatases modulates kinase signalling, promoting proliferation. Notably, high SLC30 expression correlates with improved survival, but serves as a negative prognostic marker under tamoxifen treatment. Here, we evidence that ESR1 directly represses SLC30 transcription and that zinc transporters form a regulatory feedback loop sustaining ER+ breast tumour progression. These findings position SLC30 transporters as active participants in signalling cascades, offering novel targets for therapeutic intervention in ER+ breast cancer.
The distribution of inorganic elements in brown rice has been vigorously investigated for many years using the most advanced instruments of each era. The present study was a challenge to gain new insights into the distribution of various inorganic elements in brown rice by autoradiography using radioisotopes: 22Na, 45Ca, 54Mn, 55Fe, 60Co, 63Ni, 65 Zn, 90Sr, 203 Hg, and 210 Pb. Autoradiography of tissue sections using the Imaging Plate (IP) fully exploited its advantage of high-throughput imaging, enabling three-dimensional reconstruction that encompassed the entire brown rice grain. Consequently, characteristic distribution patterns of individual elements in the peripheral layer, endosperm, and embryo were identified following radiotracer supplementation to the culture solution. For instance, 63Ni was uniformly distributed within the endosperm during the early stages of development but progressively accumulated in the outer layers and embryo as growth advanced; such a pattern was not observed for 54Mn or 55Fe. To minimize the cost of the experiment, a direct injection method into the node was developed. This approach successfully visualized 203 Hg, demonstrating that its entry into the embryonic tissue is severely restricted irrespective of the developmental stage of the rice grain.
INTRODUCTION:Zinc is an essential trace element with antioxidant and signaling functions critical to cardiac physiology. This study investigated the role of zinc in myocardial ischemia-reperfusion (IR)-induced cardiac damage using a rat model, and whether zinc deficiency induced by intermittent hypoxia (IH) exacerbates cardiac injury. METHODS:Regional IR was performed in isolated rat hearts, and zinc concentrations were measured in coronary effluents. Plasma zinc status was assessed following 14- or 35-day IH exposure (1-min cycles alternating 21% and 5% FiO₂, 8 h/day). The cardioprotective effects of intracoronary zinc administration with the ionophore pyrithione were evaluated based on arrhythmias, infarct size, and contractile recovery. RESULTS:Myocardial IR induced significant zinc release upon reperfusion (615.7 ± 78.2 nM vs. 374.5 ± 40.3 nM pre-reperfusion, P < 0.01). Zinc administration during reperfusion reduced arrhythmia duration (358.0 ± 61.7 sec vs. 559.9 ± 31.6 sec, P < 0.01) and improved myocardial recovery. IH exposure led to reduced plasma zinc levels (10.3 ± 0.5 µM vs. 13.0 ± 1.2 µM, P = 0.057) and significantly increased infarct size following IR (43.9 ± 4.2% vs. 29.2 ± 4.3%, P < 0.05). Zinc-pyrithione treatment during reperfusion abolished the deleterious effects of IH on infarct size. DISCUSSION:IH-induced zinc deficiency exacerbates cardiac vulnerability to IR injury, while zinc restoration through targeted administration mitigates this damage. Zinc's protective effects may involve antioxidant action, calcium homeostasis, and signaling modulation. CONCLUSION:Zinc plays a critical role in limiting IR-induced cardiac damage. Zinc supplementation during reperfusion may offer therapeutic benefit, particularly in conditions associated with chronic IH, such as obstructive sleep apnea.
Zinc (Zn) is a trace element essential for the function of over 10% of the human proteome, yet the average adult body contains only about two grams. Despite its trace status, Zn plays an indispensable role in immune regulation, inflammation control, and redox signalling. Low Zn status is associated with impaired immune function and increased oxidative stress-factors that critically contribute to the pathogenesis of cardiac inflammatory diseases (CIDs), including myocarditis and pericarditis. These conditions are rising in incidence globally, particularly in younger adults, and are linked to viral infections, autoimmune triggers, and post-vaccination inflammatory responses. Zn not only protects cysteine thiol groups from oxidation but also acts as a redox-sensitive secondary messenger via the "Redox Zinc Switch" mechanism-a key process in modulating cellular responses to oxidative stress. In the cardiovascular system, Zn influences antioxidant defence, cytokine regulation, and membrane repair pathways, including cellular responses that are regulated by protein kinase C and metallothioneins. Emerging evidence supports Zn supplementation as a strategy to mitigate myocardial inflammation, reduce cardiac remodelling, and improve outcomes in oxidative stress driven heart diseases. This review synthesizes current knowledge on Zn's biochemical, immunological, and therapeutic roles in cardiac inflammation. We argue that maintaining optimal Zn levels through diet or supplementation represents a promising, accessible intervention to reduce the burden of CIDs and improve cardiovascular resilience in at-risk populations.
Brassica cultivars have the ability to hyperaccumulate thallium when growing on soils contaminated with this element. Earlier research identified the presence of crystalline thallium deposits in the leaves of Brassica oleracea var. acephala. The aim of this study was to investigate the nature of these thallium crystals. A combination of synchrotron-based methods was used involving micro-X-ray fluorescence (µXRF) for the elemental distribution in the leaves and micro-X-ray diffraction mapping (µXDM) for the identification of the crystals. Thallium concentrates along the foliar margins, especially near vascular bundles, and dense congregations of minute thallium-rich crystals are observed in these areas. The thallium speciation is revealed to be nearly exclusively monovalent thallium, whilst the crystals are largely cubic thallium chloride, TlCl(s). The formation of thallium-rich crystals in the form of thallium chloride appears to be a tolerance mechanism similar to that of halophytes, and possibly a way in which excess thallium is expelled from leaves.
