Biometals最新文献

Prolonged exposure to mancozeb (MZ), a frequently used fungicide, may cause oxidative stress damage to several organs; however, the mechanism of toxicity remains obscure. So, the present work sought to assess the contribution of some biometals, including Mn, Zn, Ca, and Fe, to the subacute hepatic and renal injury prompted by MZ-mediated oxidative stress and to evaluate the protective impact of naringin (NAR), a citrus-derived flavonoid, against this toxicity. Twenty-eight male Wistar rats were divided into four groups (n = 7) as follows: (1) control, (2) NAR (20 mg/kg bwt), (3) MZ (250 mg/kg bwt), and (4) NAR + MZ. The daily oral intake of MZ for 54 days induced marked hematological alterations, elevation in some hepatorenal markers, and alteration of the redox status of both liver and kidney tissues. There were marked histopathological alterations in both liver and kidney tissues that were confirmed by the immunohistochemical staining, which demonstrated strong iNOS and Bax along with weak Bcl-2 immunoexpression. The repeated exposure to MZ significantly increased the levels of Mn and decreased the levels of Ca, Zn, and Fe in both liver and kidney tissues, which attributed to upregulation of the mRNA levels of MT-1, CYP1A1, and casp-3 genes. On the other hand, the co-administration of NAR with MZ significantly reversed these toxic effects via improving the hematological profile, restoring antioxidant enzyme activity, and mitigating both hepatorenal function and structure. The data indicated that NAR had considerable protective effects against MZ-induced hepatorenal damage, mostly through enhanced antioxidant capacity, preservation of trace element equilibrium, and modulation of oxidative, inflammatory, and apoptotic pathways.

Sulfate is known to protect microalgae from Cr(VI) toxicity in seawater. We investigated whether varying sulfate levels could lead to a change in the most toxic chromium species for freshwater and marine algae. For Cr(VI), reducing medium sulfate by 125-fold lowered the EC50 for C. vulgaris from 17.9 to 1.5 µM, and for D. tertiolecta from 413.9 to 18.3 µM. In contrast, Cr(III) toxicity appeared largely independent of sulfate: the EC50 values ranged for C. vulgaris from 5.0 to 4.0 µM, and for D. tertiolecta from 30.8 to 11.5 µM. The Cr(VI):SO₄^2- and Cr(III):SO₄^2- ratios were calculated to compare the toxicity of the chromium species to the microalgae in terms of dependence on ambient sulfate. Total growth inhibition occurred at Cr(VI):sulfate ratios greater than 1:20 for both algae, while toxicity disappeared below 1:2000 (C. vulgaris) and 1:200 (D. tertiolecta). For Cr(III), both complete and negligible inhibition was observed across a wide range of ratios (1:2000 - 1:20). These findings suggest that seawater sulfate-mediated protection may not be effective against Cr(III). In marine cultures, Cr(III) was more toxic than Cr(VI), contradicting conventional assumptions about the greater toxicity of hexavalent chromium.

Rapid industrialization and technological advancements have led to extensive environmental contamination of lead, disrupting the ecological balance and posing significant risks to biodiversity and ecosystem functionality. Lead remains a critical concern due to its high toxicity, persistence, and ability to bioaccumulate, which can elicit oxidative and metabolic disruptions. Lead toxicity impairs haematological, biochemical, and structural parameters, ultimately compromising hepatic, renal, neurological, and reproductive functions. This review integrates the current understanding of the mechanistic pathways involved in lead-induced toxicity, with a specific focus on oxidative stress and apoptosis. Lead exposure disrupts redox homeostasis, characterized by an increase in reactive oxygen species (ROS) and a reduction in antioxidant defenses, notably superoxide dismutase, catalase, and glutathione levels. Concurrently, it triggers apoptotic signalling via mitochondrial dysfunction, thereby elevating the expression of pro-apoptotic mediators (e.g., Bax, caspases) while suppressing the anti-apoptotic factor Bcl-2. Furthermore, this review discusses emerging strategies for prevention and therapy, highlighting the protective effects of natural phytochemicals and antioxidant-based interventions that may alleviate cellular and tissue damage associated with lead exposure.

Methylmercury (MeHg) contamination can cause damage to the salivary glands, which is associated with oxidative stress and glandular dysfunction. Açaí (Euterpe oleracea Martius), a fruit rich in antioxidants, emerges as a natural alternative to mitigate the toxic effects of MeHg. This study aimed to evaluate whether clarified açaí juice exerts a protective effect on the major salivary glands of rats intoxicated with MeHg. Wistar rats were allocated into four groups: control, MeHg-exposed (0.04 mg/kg/day), açaí-supplemented (0.01 L/kg/day), and MeHg-exposed with açaí supplementation. The compounds were administered by orogastric gavage for 60 days. Subsequently, total saliva was collected to determine antioxidant capacity, lipid peroxidation, and amylase activity, while submandibular and parotid glands were analyzed to total mercury (Hg) levels, antioxidant capacity, and lipid peroxidation. Our results showed that açaí supplementation did not reduce Hg accumulation in the salivary glands. However, MeHg exposure significantly decreased antioxidant capacity in both glands, whereas açaí supplementation mitigated this reduction, maintaining values comparable to the control group. Lipid peroxidation was elevated in the MeHg group in both glands, but this alteration was attenuated by açaí. In saliva, MeHg exposure lowered antioxidant capacity and elevated lipid peroxidation levels, both of which were attenuated by açaí supplementation. Moreover, MeHg altered salivary protein concentration and reduced amylase activity, while açaí supplementation counteracted these effects. These results demonstrate that açaí's antioxidant constituents confer protective effects against MeHg-induced oxidative damage and functional impairment in salivary glands and saliva, underscoring its potential as a natural protective agent against Hg toxicity.

Ferric carboxymaltose (FCM) and ferric derisomaltose (FDI) are key for treating iron deficiency anemia. However, FCM has been shown to raise serum fibroblast growth factor (FGF)-23 levels, causing hypophosphatemia and alterations in bone turnover in some patients. To date, it is unknown if FCM and FDI also affect bone mineralization. This study examined FDI and FCM effects on bone mineralization and FGF-23 in healthy mice, avoiding disease confounders. Male 12-week-old C57BL/6 J mice received single or weekly FDI, FCM, or placebo injections for 4 weeks.Repeated FDI and FCM injections affected body weight, blood counts, and caused significant liver iron accumulation and high serum iron. Both reduced most bone parameters by µCT; however, FCM showed falsely high bone density due to iron clusters in the bone marrow. Histology revealed greater bone volume loss with FCM than FDI (-36% FCM, p < 0.01; vs - 24% FDI, p < 0.05), predominantly from suppressed bone formation. Both iron formulations also led to a prominent increase in osteoid and FGF-23 (intact and C-terminal), raising the i:cFGF-23 ratio. A single dose led to similar, but milder effects than repeated dosing. In summary, repeated high doses of both, FDI and FCM, in healthy mice increased the i:cFGF-23 ratio and osteoid production, while reducing bone formation and volume.

To examine inflammatory biomarkers as potential mediators in the association between urinary metal exposure and advanced Cardiovascular-Kidney-Metabolic Syndrome (CKM) risk in US adults, and to evaluate urinary metals' association with risk and their predictive value. Analysis included 6249 NHANES participants. Restricted Cubic Spline (RCS) explored dose-response relationships. Multivariable and piecewise logistic regression assessed associations between specific metals and advanced CKM risk at different exposure levels. Receiver Operating Characteristic (ROC) curves evaluated predictive performance. Mediation analysis tested the role of inflammatory biomarkers. Generalized Weighted Quantile Sum (gWQS) regression and machine learning (ML) models further assessed metal mixture effects and mechanisms. Restricted cubic spline analysis indicated linear associations between all urinary metal levels and advanced CKM risk. Elevated levels of the Multi-Metal Inflammatory Index (MMII), cadmium (Cd), and cobalt (Co) were significantly associated with increased risk of advanced CKM: each 1-unit increase was associated with a 122%, 28%, and 14% higher risk, respectively. This association was significant only at higher exposure levels. ROC analysis showed good predictive performance. Inflammatory biomarkers, including WBC, NENO, SIRI, AISI, MHR, and NHR, mediated the associations between MMII/Cd/Co and advanced CKM risk. gWQS and ML analyses confirmed the adverse associations of MMII, Cd, and Co, ranking their importance as MMII > Cd > Co. Higher levels of MMII, Cd, and Co are significantly associated with increased advanced CKM risk among US adults, with inflammatory biomarkers playing a key mediating role. These findings highlight a notable public health consideration.

Metal ions are involved in many biological functions such as enzyme catalysis, signal transduction and gene expression regulation in biological system. They play multiple roles in the pathogenesis and immune escape mechanism of gastric cancer(GC). This review begins by outlining the fundamental biological roles of metal ions, highlighting its significance in tumor development. We focus on elucidating how metal ions modulate the gastric cancer immune landscape by regulating immune cell functions, and participating in specific signaling pathways. Additionally, the potential of metal ion interference as an emerging therapeutic strategy for tumors is discussed, along with the prospects for applying metal-based nanomaterials in the treatment of gastric cancer. Additionally, we discuss the crosstalk between ferroptosis and cuproptosis mediated by metal ions, which provides a novel perspective for understanding metal ion-dependent tumor cell death. The potential of metal ion interference as an emerging therapeutic strategy and the application prospects of metal-based nanomaterials in gastric cancer treatment are summarized. Finally, we point out key future research needs, including clarifying the dynamics of metal ions in the gastric cancer microenvironment, standardizing metal-related biomarkers for clinical stratification, and optimizing the safety and targeting of metal-based therapies. This review comprehensively summarizes the regulatory roles and mechanisms of metal ions in the gastric cancer immune microenvironment, offering theoretical support for the development of precision therapeutic strategies targeting metal ion homeostasis.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disorder worldwide and is strongly associated with metabolic syndrome. Copper, an essential cofactor for enzymes involved in redox regulation and lipid metabolism, is frequently diminished in MASLD patients. Copper deficiency may exacerbate oxidative stress, inflammation, and hepatocellular damage. The aim of this study was to investigate the impact of dietary copper deficiency on oxidative stress, inflammatory response, and histopathological alterations in mice fed a high-fat diet. Male C57BL/6 J mice (n = 32) were assigned to four groups: control diet (CD), copper-deficient control diet (CD-Cu), high-fat diet (HFD), and copper-deficient high-fat diet (HFD-Cu) for 12 weeks. Biochemical, histological, and molecular parameters were evaluated. Mice in the HFD-Cu group exhibited significantly greater dyslipidemia, elevated transaminases, increased hepatic lipid accumulation, enhanced oxidative stress (reduced SOD1 activity, increased TBARS, protein carbonyls, and GSSG), and higher inflammatory cytokine levels (TNF-α, IL-1β) compared to HFD alone. Histological analysis confirmed more severe macrovesicular steatosis and inflammation in HFD-Cu mice. In conclusion, copper deficiency potentiates the deleterious effects of a high-fat diet, aggravating oxidative stress, inflammation, and hepatic injury. These results highlight the critical role of copper in liver homeostasis and its potential involvement in MASLD progression.

Biological soil crusts (BSCs) play essential roles in arid ecosystems by stabilizing soil and regulating hydrological processes. BSC microbial communities comprise a small number of abundant taxa and a large pool of rare taxa, which differ in their transcriptional capacities. However, the respective contributions of abundant and rare taxa to alkali‑metal homeostasis, a process crucial for maintaining cellular osmotic balance and metabolic activity, remain poorly understood. Here, we integrated metatranscriptomic sequencing with chemical fractionation analysis of Na⁺ and K⁺ to compare transcriptional patterns and influencing factors between rare and abundant microbial taxa in moss‑dominated (MD) and lichen‑dominated (LD) crusts. Our results indicated that abundant bacteria expressed the Na⁺/H⁺ antiporter nhaA and the trk/ktr K⁺ uptake protein, particularly in MD crusts. In contrast, rare taxa expressed diverse genes, including Na⁺/H⁺ antiporter nhaB, nhaC, and nhaD, K⁺-stimulated Na⁺-pyrophosphatase nsaA, and kup K⁺ uptake. Abundant fungi dominated expression of the NHE‑type Na⁺/H⁺ antiporter nha1, while rare fungi expressed a variety of genes. Analysis of the integrated co-occurrence network indicated that abundant bacterial and fungal taxa displayed greater node degree and connectivity relative to rare taxa, and were dominant in both microbial co-occurrence links and the expression of key Na⁺/K⁺ uptake and transport genes. The expression of these genes was more strongly correlated with bioavailable Na and K fractions, particularly carbonate- and oxide-bound forms, than with soil pH or electrical conductivity. These findings indicate that bioavailable Na and K contents induce distinct transcriptional responses in abundant and rare taxa, thereby regulating key alkali-metal homeostasis within BSC microbial communities.

Metals are critical in anaerobic digestion, but their co-occurrence effects on microbiome structure and function are underexplored. This study hypothesized that exposure of methanogenic granules to a trace element (TE) mixture alongside molybdenum (Mo), tungsten (W) or selenium (Se)-would alter (i) extracellular polymeric substances (EPS) protein and carbohydrate content, (ii) microbial composition and function (iii) methanogenic pathways.To test this, anaerobic batch reactors (n = 35) were set up in a fed batch mode, with sacrificial reactors (n = 14) used to collect biomass for analyses, including DNA: RNA co-extraction, amplicon sequencing, and determination of the concentrations of total and soluble metals, Scanning Electron Microscopy- Energy Dispersive X-ray (SEM-EDX) and EPS extraction over a 24-day period.The results reveal that, Mo and W increased the concentration of soluble Fe in abiotic controls, enhancing Fe and S retention. The presence of W, Mo, W + Se, and Se had a positive effect on methane production, with W + Se and W enhancing acetoclastic methanogenesis. Additionally, Se increased EPS protein and carbohydrate contents in the biomass. Shifts in the microbiome composition were mainly driven by Mo and Se, with typically dominant Anaerolineacaeae, Capriciproducens, Macelibacteroides and Clostridium sensu stricto 5 taxa. Functional potential suggested an enrichment of nucleotide metabolism and, importantly, Vitamin (B12, B6 and B9) metabolic potential.These finding inform Anaerobic digestion (AD) stakeholders about the impacts of Fe, W, Mo, and Se co-dosing on process performance and microbiome structure and function, offering insights to optimize biogas production through tailored metal supplementation combinations, given demonstrations at lab and pilot scales.