Elemental mercury exposure is associated with neurologic manifestations, which can improve after source removal with time. Autoimmune complications from mercury intoxication are rarely reported and may lead to worsening or persistent neurologic symptoms. A 2-year-old girl, in addition to her parents and sibling, developed cough and congestion initially attributed to a respiratory infection. For the next month, the child experienced intermittent episodes of sweating and increased fussiness, then later developed a pruritic erythematous rash to her distal extremities. She was hospitalized and, after toxicology testing revealed elevated whole blood (11 mcg/L) and urine mercury concentrations (79 mcg/g Cr), was treated with oral dimercaptosuccinic acid (DMSA). The source of mercury exposure was later identified as an accidental spill of elemental mercury that occurred in her residence weeks before the onset of her symptoms. Her family temporarily moved away from their residence while mercury remediation was initiated, but continued episodes of altered mental status necessitated hospital readmission. A lumbar puncture was performed, additional chelation with N-acetylcysteine was administered, and an autoimmune encephalitis panel was sent to a reference laboratory. The patient's repeat urine mercury concentration was undetectable, but she had still not returned to her baseline mental status. The autoimmune encephalitis panel was positive for contactin-associated protein 2 (CASPR2) IgG antibodies. After treatment with intravenous immunoglobulin, high-dose methylprednisolone, and oral prednisolone, her mental status gradually improved and returned to baseline over the next several weeks. CASPR2-IgG autoimmune encephalitis is a rare complication of elemental mercury intoxication, characterized by neuropsychiatric symptoms that persist despite traditional chelation treatment and systemic clearance of mercury. Treatment of affected patients may involve the administration of intravenous immunoglobulin and high-dose corticosteroids.

Iron oxide nanoparticles (IONPs) exhibit remarkable anti-tumoral activity, largely mediated by the generation of reactive oxygen species (ROS). Although certain IONPs can induce ferroptosis, the determinants underlying cell-type-specific sensitivity remain poorly understood. Here, we provide novel mechanistic insight by demonstrating that lysosomal acidity and plasticity critically regulate iron mobilization, ROS compartmentalization, and the ferroptotic response triggered by dimercaptosuccinic acid-coated IONPs (DMSA‑IONPs) in MDA‑MB‑231 breast cancer and U87MG glioma cells. DMSA-IONPs generate ROS in both cell models, however, their subcellular localization markedly differed. In MDA-MB-231 cells, highly acidic lysosomes retained redox-active iron (Fe[2][+]), leading to localized ROS accumulation, lysosomal enlargement and pronounced lipid peroxidation, ultimately inducing ferroptosis, which was reverted by the anti-ferroptosis drug Ferrostatin-1. In contrast, the less acidic lysosomes of U87MG cells released iron into the cytosol and mitochondria, resulting in diffuse ROS production without lipid peroxidation and conferring resistance to ferroptosis despite higher nanoparticle uptake. While IONP‑mediated ROS generation via iron mobilization and Fenton‑like reactions is well established, our findings identify lysosomes as critical determinants of cellular responses to IONPs exposure. Specifically, lysosomal acidity and endolysosomal trafficking govern ferroptotic sensitivity to IONPs by controlling the site of ROS accumulation. Our results demonstrate that IONP-induced ferroptosis depends not only on total ROS levels but also on ROS subcellular distribution, with ROS accumulated in lysosomes triggering lipid peroxidation of these organelles. These insights highlight the importance of evaluating lysosomal physiology across tumor type to optimize nanoparticle-based ferroptosis therapies, particularly for tumors resistant to apoptosis.

Heavy metals in food present significant health risks; however, consumer-level solutions for reducing exposure remain limited. This study presents a novel consumer-focused solution in which succimer (an FDA-approved chelation therapy) is stably grafted onto the surface of a wooden spoon. Using a standard coupling reaction, succimer is covalently attached to lignin in the wood matrix through ester bond formation. Succimer-functionalized spoons elicit improved metal retention compared to the pristine wooden spoon. To demonstrate the efficacy of this food contact device, we tested its use during cooking foods from various sources. The treated spoon removed up to 89.1% of heavy metals from white rice and 97.9% from brown rice, with no significant reduction in iron content, suggesting selective surface chelation. In vivo assays using C. elegans models confirm that the DMSA-functionalized spoon does not induce observable toxicity, suggesting that the spoon remains environmentally safe after surface-modification. Consequently, this low-cost, single-use utensil offers an accessible strategy to reduce dietary exposure to toxic metals during food preparation. Its simplicity and scalability make it particularly promising for global applications in regions where food contamination and access to purification technologies are persistent challenges.

Lead (Pb) is a heavy metal that causes hepatotoxicity even in trace amounts. This study investigated the therapeutic potential of coriander extract-loaded selenium nanoparticles (coriander@Se-NPs) against Pb toxicity in a mouse model, comparing its efficacy to the benchmark standard chelator, DMSA. The effectiveness of coriander extract, coriander@Se-NPs, and synthetic chelator (DMSA) was evaluated. The study groups contain: a control group receiving distilled water, a Pb toxicity group given Pb-acetate at 150 mg/kg, a positive control group treated with DMSA after Pb exposure, and two groups receiving coriander extract or coriander@Se-NPs after Pb exposure, both at 200 mg/kg daily for three weeks. Our results demonstrated that the coriander@Se-NPs significantly reduced hepatic Pb concentrations (83.90%) and restored antioxidant enzyme activities (SOD and CAT) more effectively than DMSA. Notably, coriander@Se-NPs exhibited potent anti-inflammatory and anti-apoptotic effects, evidenced by a 12.5-fold reduction in IL-6 and the suppression of Caspase 3 to sub-normal levels (0.399-fold). Furthermore, the coriander@Se-NPs treatment stabilized Beclin 1 levels, suggesting a restoration of cellular autophagy homeostasis. These findings indicate that coriander@Se-NPs provide a superior, multi-modal protective shield against heavy metal poisoning compared to traditional synthetic chelators, DMSA, highlighting their potential as a high-efficacy nanomedicine for clinical toxicology. Further studies are needed to explore its potential clinical applications and mechanisms.

Chronic, sub-toxic, multi-metal accumulation stemming from environmental exposure in daily life is a common phenomenon in modern humans and has been linked to numerous diseases. Toxic metals found in leukemia patients have recently been linked to chemoresistance and poor survival. To reverse chemoresistance, depletion of metal ions by chelators has been suggested as a possible adjuvant to chemotherapy. However, existing animal models for metal accumulation are largely unsuitable for this type of cancer research. We developed a novel accelerated model for chronic, sub-toxic, multi-metal accumulation in rats, in which a mixture of 11 metals was administered orally, followed by an equilibration period of at least five weeks to allow the metal ions to settle into their target organs in a chronic-like distribution, without overt toxicity. The model was characterized in terms of metal ion levels in urine, feces, serum, and organs. We surveyed seven chelators with different properties, seeking a compound that would specifically remove highly toxic metals, while exerting a minimal effect on essential elements. Our studies pointed to Monoisoamyl-dimercaptosuccinic acid (MiADMSA), an exploratory chelator with promising properties, as the most suitable for this purpose. Different treatment regimens, aimed at optimizing the clinical application of the chelator, were explored and characterized. Repeated monthly cycles of 5 treatments per cycle led to efficient removal of inorganic arsenic, cadmium, vanadium, and cobalt from rat organs. Our study shows that MiADMSA is a promising chelator that may be efficient in treating chronic metal accumulation, and potentially as an adjuvant to chemotherapy.

Background and Objectives: Children with febrile urinary tract infections (fUTIs) may be at risk for kidney scarring. Inflammatory biomarkers may predict the risk of scarring. The aim of this study was to investigate the predictive role of PCT, CRP and other markers in scarring in pediatric patients with first fUTI. Materials and Methods: The study was in accordance with the institution's ethics committee (No. 108/2023). Included patients underwent a kidney-ureter-cyst ultrasound (US). The primary outcomes of this study were the associations of procalcitonin (PCT), C-reactive protein (CRP), and white blood cells (WBC) with kidney scarring. The secondary outcomes were the associations of PCT, CRP, and WBC with vesicoureteral reflux (VUR). A p < 0.05 was considered statistically significant. Results: Sixty-five pediatric patients (1-16 years of age) with a first fUTI, from February 2023 to January 2025, were included. Sixteen patients had VUR, and thirteen patients developed kidney scarring. C-reactive protein was significantly elevated in the VUR group (p = 0.026). In a series of logistic regression analyses, abnormal US findings and severe VUR were associated with scarring (p = 0.009 and p = 0.016, accordingly). The optimal cut-off value for PCT in predicting scarring was calculated as 6.05 ng/mL (sensitivity: 36% and specificity: 97%), and for CRP as 3.62 mg/dL (sensitivity: 63.6% and specificity: 62.1%). Conclusions: This study showed a significant difference in CRP levels between the groups with and without VUR. Abnormal US findings and severe VUR were the most significant predictors of kidney scarring. Significant difference was not reached in PCT and WBC levels between the groups with and without VUR or with and without kidney scarring. The small sample size may have influenced the study's outcomes.

Lead toxicity in adults is uncommon and can present with progressive neurological manifestations that mimic neurodegenerative diseases. We describe the case of a 61-year-old man with a several-year history of worsening gait instability, cognitive decline, dysarthria, and involuntary movements in the setting of persistently elevated blood lead levels. The patient's symptoms began in late 2023 with balance difficulties and frequent falls, followed by progressive cognitive impairment, personality changes, and a 100 lb unintentional weight loss. His clinical course was further complicated by chronic non-healing wounds and imaging evidence of renal and hepatic scarring. Extensive neurological evaluation, including CT and MRI of the brain and genetic testing for Huntington's, was unrevealing. The patient was found to have repeatedly elevated blood lead levels, initially in the 30 μg/dL range and later peaking in the 60 μg/dL range, despite cessation of work at the chemical and metal processing facility he had been employed at. Evaluation of potential ongoing sources revealed multiple retained BB fragments in the hand and foot dating back to early adulthood. These were initially considered as possible contributors, but point-of-care testing of the fragments on removal was negative for lead. A fragment in the foot was embedded in the bone and not amenable to removal. Additionally, possible residential exposure was considered, as the patient resided in a mid-20th-century home. He required multiple hospitalizations for progressive neurologic decline and elevated lead levels, during which he received inpatient chelation therapy with succimer. Chelation was associated with partial improvement and modest cognitive stabilization, though his dysarthria and gait ataxia persisted. His outpatient course was complicated by financial barriers that limited sustained chelation therapy, resulting in recurrent elevations of blood lead levels. Ongoing management included serial monitoring of lead levels following chelation, with plans to pursue surgical removal of a retained abdominal wall wire if levels were to rise again, suggesting an endogenous source.

Although heavy metal contamination is an ancient problem, it remains a global concern in isolated areas. Herein, we report the design of a novel thiol-rich Zr(IV) metal-organic framework (BCM-5), assembled from meso-2,3-dimercaptosuccinic acid (Succimer), a commercially available thiol-rich metal-chelating agent used in the treatment of heavy metal poisoning. BCM-5 has been subsequently integrated into porous PVDF-HFP membranes processed via salt-leaching. The non-immobilized BCM-5 and the BCM-5@PVDF-HFP membranes were systematically evaluated for Pb(II), Cd(II), and Hg(II) capture. The results demonstrate that the metal-chelating functionalities of Succimer linker are effectively preserved within the BCM-5 framework, while immobilization of BCM-5 into PVDF-HFP membranes significantly enhances the material's dispersibility and improves its capacity for the efficient capture of the targeted heavy metals. A detailed structural, chemical, and DFT characterization of post-adsorption BCM-5 suggests that metal immobilization proceeds via chemisorption within hydrophobic, hydrophilic, and amphiphilic pore regions of BCM-5, depending on the nature of the heavy metal. Overall, this work introduces a novel approach to use metal-chelator molecules as building blocks for MOFs construction targeted to the recovery of heavy metals, while also detailing strategies for their immobilization into polymeric structures with interconnected macroporosity.

PURPOSE: 99mTc-dimercaptosuccinic acid (DMSA) renal scintigraphy with single-photon emission computed tomography (SPECT) provides unique information regarding cortical functional integrity. However, it has never been tested whether the cortical functional integrity on DMSA SPECT can predict 1-year graft function. This study investigated whether early DMSA SPECT-derived quantitative parameters predict graft function at 1 year post-KT. METHODS: Consecutive KT recipients from June 2022 to August 2024 who underwent DMSA SPECT at 2 weeks post-KT were included. Serum creatinine measurement and estimated glomerular filtration rate [eGFR] calculation were performed at 2 weeks (on the same day of DMSA SPECT; early eGFR) and at 1 year post-KT (follow-up eGFR). The correlation of DMSA imaging parameters with graft function was assessed by analyzing its linear correlations with early and follow-up eGFR, along with other clinical variables. The patients were classified as those having either low or high follow-up eGFR (< 60 mL/min/1.73 m2 and ≥ 60 mL/min/1.73 m2, respectively). Multivariable analyses were performed to identify imaging and clinical variables that are independently associated with low follow-up eGFR. RESULTS: Total 90 KT recipients were finally included in the present analysis. They included 50 males and 40 females, with deceased-donor KT in 62 (69%). Patients with low follow-up eGFR (n = 36; 40%) had significantly higher donor’s age, lower graft weight normalized to body surface area and lower early eGFR. Among imaging parameters, planar and SPECT % injected dose (%ID), functional cortical volume, maximum and mean standardized uptake value (SUV), and SUV volume were significantly lower in patients with low follow-up eGFR. In multivariable analysis, high donor age (≥ 48 years old; odds ratio [95% confidence interval], 4.69 [1.59–13.82]), low early eGFR (< 60 mL/min/1.73 m2; 3.89 [1.33–11.42]), and low SPECT %ID (< 8.6%; 3.64 [1.25–10.55]) were independently associated with low follow-up eGFR. CONCLUSION: Cortical functional integrity measured by DMSA renal SPECT early after KT could predict graft function at 1 year, independently from other clinical factors including laboratory renal function test.

Lead toxicity is an uncommon but clinically important cause of unexplained anaemia. Its heterogeneous haematological manifestations can mimic autoimmune haemolytic anaemia, resulting in diagnostic uncertainty and delayed recognition. A 49-year-old woman presented with a three-week history of worsening abdominal pain and lethargy. She had a background of inclusion body myositis treated with long-term intravenous immunoglobulin and recent initiation of mycophenolate mofetil. Initial investigations demonstrated severe anaemia with reticulocytosis but minimal biochemical evidence of haemolysis. A weakly positive direct antiglobulin test (IgG 1+, C3d negative) raised suspicion for autoimmune haemolysis. The initial peripheral blood film was reported as showing marked red cell agglutination without additional abnormalities. Progressive anaemia prompted extensive investigations, including infectious, immunological, and haematological workups, all of which were unremarkable. Bone marrow aspirate demonstrated atypical plasma cells, prompting re-examination of the peripheral blood film, which revealed Pappenheimer bodies and basophilic stippling. Further history identified ingestion of an unlabelled health supplement, and toxicology testing confirmed markedly elevated blood lead levels. Chelation therapy with succimer led to clinical and haematological improvement. Public health investigation subsequently confirmed the supplement as the source of lead and mercury exposure. This case highlights lead toxicity as an important but under-recognised mimic of autoimmune haemolytic anaemia. Careful review of peripheral blood morphology and a thorough exposure history are essential when evaluating unexplained anaemia with an inconclusive haemolysis workup.

A 4-month-old infant with a small right kidney underwent a 99m Tc-DMSA scan showing unjustifiable findings including global cortical loss in the left kidney, increased liver and bowel uptake. Retrospective review revealed reuse of a sterile needle contaminated with residual 99m Tc-MIBI, compromising scan quality and falsely elevating right kidney function. A repeat scan showed normal left kidney uptake and significantly reduced right kidney function. This case highlights the importance of employing safe techniques with disposable equipment, thorough workflow review, and transparent error reporting in nuclear medicine to ensure accurate diagnosis and patient safety.