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RARE DISEASE
Mercury poisoning
Mercury poisoning
Mercury poisoning
Synonyms: Hydrargyria, Mercurialism, Mercury intoxication
Synonyms: Hydrargyria, Mercurialism, Mercury intoxication
Synonyms: Hydrargyria, Mercurialism, Mercury intoxication
Drug discovery
5
drugs
With orphan designations
Overview
Mercury poisoning arises from exposure to elemental, inorganic, or organic mercury, targeting the nervous, renal, and gastrointestinal systems. Symptoms range from tremors and cognitive deficits (elemental/organic) to corrosive injury and kidney failure (inorganic). Diagnosis relies on blood, urine, and hair analysis. Treatment prioritizes decontamination, chelation (DMSA, DMPS), dialysis, and supportive care [1][6][8][19].
Therapies
Chelation: DMSA (oral) or DMPS (IV) for inorganic/organic forms; dimercaprol for severe cases [2][3][17].
Decontamination: Activated charcoal (oral ingestion), whole-bowel irrigation, and skin/eye cleansing [1][3][6].
Supportive care: Hemodialysis for renal failure, mechanical ventilation for respiratory distress [1][3][8].
Categories: rare disorders due to toxic effects
Research Papers
980 drug discovery papers about Mercury poisoning, with 1 first-in-class and 8 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
980 drug discovery papers about Mercury poisoning, with 1 first-in-class and 8 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
categories:
Small molecules
antibodies
2026-09-28 | Acrodynia and CASPR2 Autoimmunity in Elemental Mercury Toxicity.
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.
2025-09-28 | Interleukin-17A: A Bright Target for Toxicological Mechanisms and Mitigation of Toxic Elements in the Environment
Science and other peer-reviewed studies recognize cadmium (Cd), arsenic (As), mercury (Hg), and fluoride (F) as highly hazardous toxic elements that threaten global health. However, understanding their toxic mechanisms and effective mitigation remains a global challenge. Growing evidence suggests that interleukin-17A (IL-17A) not only plays a role in inflammatory and immune diseases but may also be the brightest target in the mechanisms of toxic injury and its mitigation. This review summarizes IL-17A signaling in toxic element poisoning, highlighting distinct effects on apoptosis, autophagy, and pyroptosis: fluorine promotes cell death, cadmium shows dose-dependent regulation of IL-17A-mediated apoptosis, and arsenic and mercury may inhibit pyroptosis and IL-17A secretion. Moreover, interventions such as riboflavin, bifidobacterium, melatonin (MLT), Ginkgo biloba extract (GBE), lentinan, and taxifolin, were discussed for their protective effects via IL-17A modulation. This provides novel insights into IL-17A signaling, health risks, and therapeutic approaches against toxic elements.
2017-09-28 | An Enigmatic Case of Acute Mercury Poisoning: Clinical, Immunological Findings and Platelet Function
Severe mercury intoxication is very rare in developed countries, but still occurs as the result of volatile substance abuse, suicide attempts, occupational hazards, or endemic food ingestion as reported in the cases of public health disasters in Iraq and in Minamata Bay, Japan. Here, we describe the dramatic physical and cognitive decline of a 23-year-old patient caused by a severe methyl mercury intoxication of unknown origin. We show serial magnetic resonance imaging (MRI) of the patient's brain, as well as ex vivo analyses of blood and cerebrospinal fluid including multicolor flow cytometric measurements, functional assays of hemostaseologic efficacy and evaluation of regulatory effector molecules. Together with the clinical history, our findings show the progressive neuronal degeneration accompanying the deterioration of the patient. Moreover, the ex vivo analyses display alterations of thrombocyte function and coagulation, as well as an immunological milieu facilitating autoimmunity. Despite the successful reduction of the methyl mercury concentration in the patient's blood with erythrocyte apheresis and chelator therapy, his condition did not improve and led to a persistent vegetative state. This case illustrates the neurotoxicity of methyl mercury following severe intoxication for the first time by serial MRI. Data on immune-cell and thrombocyte function as well as on coagulation in mercury poisoning reveal potential implications for anticoagulation and immunomodulatory treatment.
2017-08-22 | Methylmercury Causes Blood-Brain Barrier Damage in Rats via Upregulation of Vascular Endothelial Growth Factor Expression.
Clinical manifestations of methylmercury (MeHg) intoxication include cerebellar ataxia, concentric constriction of visual fields, and sensory and auditory disturbances. The symptoms depend on the site of MeHg damage, such as the cerebellum and occipital lobes. However, the underlying mechanism of MeHg-induced tissue vulnerability remains to be elucidated. In the present study, we used a rat model of subacute MeHg intoxication to investigate possible MeHg-induced blood-brain barrier (BBB) damage. The model was established by exposing the rats to 20-ppm MeHg for up to 4 weeks; the rats exhibited severe cerebellar pathological changes, although there were no significant differences in mercury content among the different brain regions. BBB damage in the cerebellum after MeHg exposure was confirmed based on extravasation of endogenous immunoglobulin G (IgG) and decreased expression of rat endothelial cell antigen-1. Furthermore, expression of vascular endothelial growth factor (VEGF), a potent angiogenic growth factor, increased markedly in the cerebellum and mildly in the occipital lobe following MeHg exposure. VEGF expression was detected mainly in astrocytes of the BBB. Intravenous administration of anti-VEGF neutralizing antibody mildly reduced the rate of hind-limb crossing signs observed in MeHg-exposed rats. In conclusion, we demonstrated for the first time that MeHg induces BBB damage via upregulation of VEGF expression at the BBB in vivo. Further studies are required in order to determine whether treatment targeted at VEGF can ameliorate MeHg-induced toxicity.
2006-10-15 | Amelioration of Mercury-Induced Autoimmunity by 4-1BB
Abstract In certain strains of mice, subtoxic doses of HgCl2 (mercuric chloride; mercury) induce a complex autoimmune condition characterized by the production of antinucleolar IgG Abs, lymphoproliferation, increased serum levels of IgG1/IgE Abs, and deposition of renal immune complexes. 4-1BB is an important T cell costimulatory molecule that has been implicated in T cell proliferation and cytokine production, especially production of IFN-γ. To elucidate T cell control mediated by the 4-1BB signaling pathway in this syndrome, we assessed the effect of administering agonistic anti-4-1BB mAb on mercury-induced autoimmunity. Groups of A.SW mice (H-2s) received mercury/control Ig or mercury/anti-4-1BB or PBS alone. Anti-4-1BB mAb treatment resulted in a dramatic reduction of mercury-induced antinucleolar Ab titers, serum IgG1/IgE induction, and renal Ig deposition. These effects may be related to the present finding that anti-4-1BB mAb decreases B cell numbers and function. The anti-4-1BB mAb-treated mercury group also showed a marked reduction in Th2-type cytokines but an increase in Th1-type cytokines and chemokines. Increased IFN-γ production due to anti-4-1BB mAb treatment appears to be responsible for the observed B cell defects because neutralization of IFN-γ in vivo substantially restored B cell numbers and partly restored IgG1/IgE. Collectively, our results indicate that 4-1BB mAb can down-regulate mercury-induced autoimmunity by affecting B cell function in an IFN-γ-dependent manner and thus, preventing the development of autoantibody production and tissue Ig deposition.
small molecules
2026-09-03 | Mercury-associated minimal change disease induced by whitening cream: a case report.
Mercury-associated minimal change disease (M-MCD) is a rare form of secondary minimal change disease (MCD) caused by chronic mercury exposure. Given its rarity and nonspecific clinical presentation, M-MCD is frequently underrecognized in clinical practice. We report the case of a 32-year-old woman who presented with nephrotic syndrome following 4 months of applying a skin-whitening cream. Markedly elevated urinary mercury concentrations were detected, and renal biopsy confirmed MCD with immunoglobulin M (IgM) deposition. The patient received four courses of sodium dimercaptopropane sulfonate chelation therapy combined with glucocorticoids. Complete remission of proteinuria was achieved within 1 month, accompanied by normalization of urinary mercury levels. This case underscores the necessity of obtaining a detailed exposure history in patients with unexplained nephrotic syndrome, particularly among young women using skin-whitening cosmetics. Prompt recognition of mercury exposure and timely chelation therapy are essential for achieving remission; adjunctive glucocorticoids may be considered in selected patients with severe disease or suspected immune- mediated injury.
2026-08-23 | Giovanni Antonio Scopoli's De Hydrargyro Idriensi Tentamina (1761): Mercury Mining, Mercurialism, and Preventive Reasoning in Eighteenth-Century Occupational Medicine.
Giovanni Antonio Scopoli (1723-1788), a physician-naturalist of the Enlightenment, is primarily remembered for his contributions to botany and entomology. Less attention has been paid to his medical work De hydrargyro Idriensi Tentamina physico-chymico-medica (1761), written during his fifteen years of service as physician at the mercury mines of Idrija (present-day Slovenia). Its third section, De morbis fossorum hydrargyri, offers a detailed occupational-medical account of disorders and diseases among mercury miners and smelter workers, including tremor, salivation, stomatitis, respiratory disorders, and other conditions associated with mining labor. This article reassesses Scopoli's work within the history of occupational medicine, comparing his site-specific approach with the broader nosology of Bernardino Ramazzini and the later reform-oriented tradition associated with 19th-century industrial medicine. Rather than presenting Scopoli as a neglected founder of the discipline, we argue that the Tentamina represents a distinctive 18th-century form of occupational-medical inquiry: a monographic, workplace-based, clinically grounded study that linked toxic exposure, working conditions, and prevention before the emergence of modern industrial toxicology. The work remains substantially unknown in Anglophone historiography and deserves wider recognition as a significant example of pre-industrial occupational-medical inquiry.
2026-07-22 | A Multi-Analyte-Responsive, Multi-Organ-Imaging, Dual-NIR-Emissive Fluorescent Probe for Visualizing Pyroptosis-Mediated Hg2+-Induced Hepatorenal Dysfunction.
Mercury ions (Hg2+) are highly toxic heavy metals that are widely distributed in the environment and pose a serious threat to both ecosystems and human health. After entering the body, mercury preferentially accumulates in the liver and kidneys, underscoring the importance of early detection of acute and chronic hepatorenal injuries. Although fluorescent probes have been widely explored for disease diagnosis, most existing systems cannot achieve simultaneous in vivo imaging of the liver and kidneys, nor can they monitor multiple pathological parameters during hepatorenal injury, thus limiting their utility in evaluating Hg2+-induced multiorgan damage. In this study, we developed a multifunctional fluorescent probe, VPO, with high sensitivity and good biocompatibility, which can be used to monitor polarity, viscosity, and ONOO- levels in cells. Using VPO, we observed, for the first time, a significant increase in ONOO- during pyroptosis, accompanied by an elevated mitochondrial viscosity and reduced polarity. In addition, VPO successfully enabled the real-time visual monitoring of these changes in mercury-exposed cells, zebrafish, and mice. Moreover, its multiresponsive property enabled the evaluation of the therapeutic efficacy of N-acetylcysteine (NAC) against Hg2+-induced hepatorenal injury. NAC alleviated hepatic and renal mitochondrial oxidative stress, as well as pyroptosis-related inflammatory signaling, by reversing Hg2+-induced biomarker abnormalities. In summary, these findings demonstrate that VPO provides a comprehensive platform for the early diagnosis, therapeutic evaluation, and mechanistic investigation of mercury poisoning.
2026-07-16 | ASSESSMENT OF HEAVY METAL–INDUCED OXIDATIVE STRESS AND THE PROTECTIVE ROLE OF POLYHERBAL FORMULATIONS IN WISTAR RATS
Heavy metal toxicity is a major health problem in the world since it has caused extensive pollution in the environment and prolonged human exposure. Due to prolonged human exposure and widespread environmental pollution, heavy metal poisoning is a serious global health concern. Lead, cadmium, mercury, and arsenic are metals that build up in the body and are hazardous primarily through oxidative stress, inflammation, and apoptosis. Damage to endogenous antioxidant systems and excessive generation of reactive oxygen and nitrogen species lead to lipid peroxidation, protein oxidation, DNA damage, and progressive organ failure. Although chelation therapy is commonly used to reduce metal burden, its long-term usage is limited by low specificity, security concerns, and inability to prevent oxidative tissue damage. Due to their multi-targeted antioxidant, anti-inflammatory, and cytoprotective properties, polyherbal formulations are now regarded as potentially useful treatment methods. Additionally, polyherbal combinations have been shown in Wistar rat models to rescue antioxidant enzyme activities, restore low glutathione levels, control essential molecular pathways in adulthood, such as Nrf2, NF-KB, and MAPK, and protect important organs including the brain, liver, and kidney. This paper summarizes the cytotoxic effects of heavy metals in relation to oxidative stress and discusses the benefits, drawbacks, and potential of polyherbal formulations as a preventative measure. The findings suggest that polyherbal techniques may be utilized in the future as an alternative or supplement to lessen toxicity caused by heavy metals.
2026-06-01 | Integrative Oncology: A Systems-Based Multidisciplinary Approach Rooted in Agad Tantra Principles
The progressive accumulation of environmental toxins and long-term chemical bio-concentration across trophic levels presents a critical pathodynamic challenge within modern integrative medicine. This chapter delivers a comprehensive systems-biology evaluation of environmental toxicity, chronic poison exposure (Dūṣīviṣa), and complex metabolic imbalances (Āma) viewed through the operational frameworks of classical Agadatantra. Tracing textual guidelines across the Caraka Saṃhitā and Suśruta Saṃhitā, the study analyzes the mechanisms by which heavy metals (such as mercury and lead) and lipophilic pesticide residues accumulate inside tissue channels (Srotas) to trigger systemic inflammation and oncogenic cellular changes. Bridging these traditional views with current biomedical science, these classical pathodynamic pathways are cross-examined against modern ecotoxicology paradigms, including chemical biomagnification cascades, placental-fetal toxin transfer, and xenobiotic-induced oxidative stress. Ultimately, this work provides an evidence-aligned multidisciplinary model using target-specific Ayurvedic anti-toxic purification protocols (Viṣaghna Chikitsā) and cellular cleansing strategies to remove deep-seated lipophilic compounds and support chronic disease management within modern oncology frameworks. Keywords: Agadatantra, Integrative Oncology, Ecotoxicology, Biomagnification, Dushivisha, Xenobiotics, Environmental Toxin, Lipophilic Clearance.
proteins
2026-02-01 | Effect of metallothionein-1 on liver function in rats with mercuric chloride poisoning
Objective To investigate the protective effect of exogenous metallothionein-1 (MT-1) against liver injury induced by mercuric chloride poisoning in Brown-Norway rats. Methods Male Brown-Norway rats (n = 42) were randomly divided into six groups (n = 7 per group), including normal control, model control, positive control, and low-, medium-, and high-dose MT-1 groups. Except for the rats in the normal control group, the rats in all other groups received subcutaneous injections of 1 mg/mL mercuric chloride solution (1.0 mg/kg) every other day for 14 days (7 injections total). The positive control group rats were intramuscularly injected with 2.5 mg/mL sodium 2, 3-dimercapto-1-propanesulfonate (DMPS) at 5 mL/kg every 2 days. Rats in the low-, medium-, and high-dose MT-1 groups received MT-1 via oral gavage at concentrations of 0.032, 0.080, and 0.160 mg/mL (5 mL/kg body weight), respectively, once daily. The normal control and model control groups received equivalent volumes of 9 g/L sodium chloride solution (mass-volume concentration). After the experiment, rat body weight and liver wet weight were measured, and the liver index was calculated. Gross pathological changes of the liver were observed, and serum alanine aminotransferase (ALT), γ-glutamyl transferase (GGT), bilirubin, total protein, globulin, and albumin-to-globulin ratio were determined as indicators of liver function. Results Compared with the normal control group, the mercuric chloride-treated groups of rats showed varying degrees of poisoning symptoms, including reduced body weight, increased liver index, significant elevation in serum ALT, GGT, and total bilirubin levels, and significantly reduced total protein and albumin/globulin ratio. Compared with the model control group, the medium and high dose MT-1 groups and the DMPS group showed a significant lower serum ALT and GGT levels (P < 0.05). All MT-1 dose groups demonstrated significantly higher total protein levels (P < 0.05), and the high-dose MT-1 group also showed a significant recovery in albumin/globulin ratio and total bilirubin level (both P < 0.05). Conclusions Exogenous high-dose MT-1 could alleviate some mercuric chloride-induced liver function abnormalities, with comparable efficacy to DMPS, while also improving total protein level in the model rats.
2023-09-07 | In silico explorations of bacterial mercuric reductase as an ecofriendly bioremediator for noxious mercuric intoxications
Mercury is a major pollutant in the environment due to its high concentration in the soil. In this study, a mercuric reductase was extracted from Pseudomonas aeruginosa. The sequence of the enzyme was retrieved from the literature and structural homologs were identified. The protein bonded with Mercuric compounds and their interaction was briefly studied. Autodock Vina was used to perform a molecular docking with the target protein. Results showed that the sequence consists of most of the random coil 44.74% followed by α-helix and B-turns. Moreover, the protein was predicted to have a FAD/NAD(P)-binding domain. The virulence factor prediction using different approaches of Virulentpred and VICMpred suggested that P00392 is non-toxic. Next, the mutational analyses were performed to predict the active site residues in the resulting models and to determine mutants. The results show that the enzyme is involved in the bioremediation of mercury by using in-silico techniques. Finally, molecular docking studies were conducted on the best-selected model to find the active site residues and to generate a pattern of interaction to understand the mode of action of the substrate and its catalytic activity which refers to the binding with mercury.
2023-06-29 | MORPHOLOGICAL CHANGES IN THE PERIPHERAL NERVES IN TRAUMA, MERCURY INTOXICATION, HYPOTHYROIDISM, AND THEIR CORRECTION
Traumatic peripheral nerve injury (PNI) significantly impacts patients' quality of life, and its treatment necessitates a multidisciplinary approach.Additionally, different non-traumatic factors such as environmental toxicants and endocrine disorders can significantly affect the regenerative capacity of damaged nerves.The aim of this study was to assess the morphological changes in the recovery of the damaged peripheral nerve, considering the impact of environmental heavy metal intoxication (mercury) and hypothyroidism, including their treatment.The study involved a total of 90 white rats divided into three groups, each group further subdivided into subgroups (a and b).All rats underwent surgical cutting of the sciatic nerve.Subgroup Ia underwent sciatic nerve injury alone, while subgroups IIa and IIIa were additionally subjected to experimental mercurialism and hypothyroidism, respectively.Subgroups Ib, IIb, and IIIb received treatments with Cerebrolysin, Thiotriazoline, and L-Thyroxine+Miacalcic, respectively, in addition to the traumatic nerve injury and experimental influences.The damaged nerves were then examined using both light and electron microscopy assessments.The findings of the study suggest that there are general patterns of de -and regeneration of the damaged peripheral nerve in the context of nootropic administration, experimental mercury intoxication, hypothyroidism, and their correction.In all groups, degeneration was observed, but a noteworthy delay in degenerative processes was observed specifically in cases involving delayed surgical nerve connection, mercurialism, and hypothyroidism, possibly due to the inhibition of Schwann cells.This led to a delayed regeneration process.However, the regeneration of the damaged nerve was significantly accelerated when the experimental pathological condition was corrected.
2021-12-29 | Dithiolated peptides incorporating bis(tryptophan)s for cooperative mercury(II) binding.
The indole side chain of tryptophan is a versatile π-donor that can participate in various types of cation-π interactions. An understanding of how it may contribute as an auxiliary binding group in mercury(II) complexes can provide valuable insights toward the design of effective chelators for optimal mercury immobilization. In this study, we investigate how the incorporation of two tryptophan residues in model dicysteinyl peptides might participate in peptide-mercury(II) complex stabilization. Two pentapeptides consisting of a Cys-Trp-Cys sequence motif containing a second tryptophan residue at the N-terminal (BT1) or C-terminal (BT2) were designed. An analogous cyclohexapeptide (BT3) was included to evaluate how tryptophan residues, restricted in constrained peptidic turn motifs, might take part in mercury(II) complexation. Their interactions with mercury(II) were investigated by spectroscopic methods and computational modeling. UV-vis studies indicate the formation of 1:1 dithiolated mercury(II) complex, which is corroborated by ESI-MS analysis. Spectroscopic studies reveal that the tryptophan indole group(s) in BT1 and BT3 can participate in mercury(II) cation-π interactions. Optimized 1:1 mercury(II)-BT3 structures indicate that both indole rings are very close to the mercury(II) coordination site and could stabilize it by shielding it from ligand exchange. These findings provide some useful insights toward use of aromatic donor groups as hydrophobic shields in designing more effective metal chelating agents.
2018-11-28 | A polysaccharide-peptide with mercury clearance activity from dried fruiting bodies of maitake mushroom Grifola frondosa
Mercury is considered to be "a global pollutant" and raises concern worldwide. Once mercury enters the body, it will be distributed all over the body but will accumulate in the brain, kidney and liver. To date, no substance originating from edible fungi capable of adsorbing mercury has been reported. We found that the mushroom Grifola frondosa exhibited mercury adsorption capacity. A polysaccharide-peptide (GFPP), displaying the unique N-terminal amino acid sequence of APPGMHQKQQ and 7 partial sequences with high reliability obtained by LC-MS/MS, was isolated by hot-water extraction of its fruiting bodies followed by ion exchange chromatography and gel filtration chromatography. Two rat models were employed to determine the dose and the duration of HgCl2 treatment (given by acute administration or continuous treatment) to test if G. frondosa could promote mercury elimination. For rats subjected to acute treatment with HgCl2, both GFPP and G. frondosa fruiting bodies (GFFF) could accelerate the decline of blood mercury level, which fell precipitously by 50% on the second day. GFPP and GFFF also promoted elimination of the burden of mercury in the liver and kidneys. For rats receiving continuous HgCl2 treatment, G. frondosa prevented the progressive increase of blood mercury level, and kept the blood mercury level within a relatively stable range.
cell therapies
2024-05-09 | Case Reports of Intravenous Drug Use of Elemental Mercury as an Aphrodisiac: A Call for Surgical Intervention
This report describes two cases of intravenous injection of elemental mercury. The presence of mercury in the environment is due to pollution from power plants and in food, particularly fish, and dental amalgams. One patient succumbed and the other remains asymptomatic two years after the surgical removal of all the injected mercury. Management of intravenous injection of elemental mercury (intended to be an aphrodisiac in these two cases) is discussed here and the need for surgical removal of all accessible mercury has been emphasized. In case no.1, it is difficult to come to any conclusion as we do not have information about the duration of exposure and the volume of mercury injected. In contrast, in case no.2, all the metallic elemental mercury was removed on two occasions and the patient has led an uneventful life showing no clinical signs of mercury poisoning in the follow-up period of two years.
2023-10-14 | Fecal microbiota transplantation in treating methylmercury-poisoned rats: Reconstruction of gut microbiome and modulation of gut-brain axis related metabolites
Abstract Background Methylmercury (MeHg) can bring devastating neurotoxicity to animals and human beings. Gut microbiota has been found to demethylate MeHg while MeHg exposure was found to destroy the diversity and abundance of gut microbiota. Besides, some neurotransmitters such as GABA, glutamate and other metabolites were altered due to MeHg exposure. Fecal microbiota transplantation (FMT) has been successfully applied to treat a series of diseases like Tourette syndrome, irritable bowel syndrome, necrotizing enterocolitis and to treat ulcerative coliti. The objective of this study was to investigate the effects of FMT in treating MeHg-poisoned rats. Results : It was found that FMT for 14 days promoted body weight gain, enhanced demethylation of MeHg and increased fecal excretion of Hg in MeHg-poisoned rats. Furthermore, the gut microbial bacteria associated with demethylation, such as sulfate-reducing bacteria were restored and some metabolites related to neuroactivity through gut-brain axis were increased after FMT, there is also repair of brain derived neurotrophic factor(BDNF)-related factor levels in the intestine, brain and serum. Conclusions : In all, it was showed that FMT can be a effective way in treating MeHg-poisoned rats through the reconstruction of gut microbiota, especially the bacteria that are associated with the demethylation of MeHg. Furthermore, the modulation of metabolites that are related to gut-brain axis after FMT also contributed to the treating of MeHg-poisoning. This study provides a novel way to treat MeHg-poisoning, which may contribute to the health promotion of mercury exposed population and shed lights on the treatment of other neurological diseases like Parkinson’s disease.
2023-07-03 | Strictly-controlled techniques are required in laparoscopic appendectomy for elemental mercury sequestration in the appendix: a case report.
Elemental mercury impaction in the appendix can cause subsequent local and systemic complications. We present a case of a teenage boy who ingested approximately 10 mL of elemental mercury, resulting in residual mercury sequestration in the appendix after conservative management. We performed laparoscopic appendectomy to remove the residual mercury. The patient made a complete clinical recovery without adverse events related to mercury poisoning over the 6-month follow-up. We highlight the advantages of laparoscopic appendectomy, abdominal computed tomography (CT), negative pressure operating rooms, and surgeon protection to improve surgical success rates. This case report adds to the literature on the management of elemental mercury impaction in the appendix and provides valuable insights for clinical decision-making.
2020-04-30 | An Unusual Cause of High Density Radiological Opacities
Metallic mercury poisoning through intravenous injection is rare, especially as part of a suicide attempt. Diagnosis and treatment of the disease are challenging as clinical features are not specific.A 41-year-old male presented with dyspnea, fatigue, loss of weight, and loss of appetite over two months. Routine radiological examination by chest X-ray and CT showed randomly distributed high density opacities with Hounsfield units (HU) around 500 HU all over the body. The diagnosis was then confirmed with a urinary mercury concentration of > 1000 mcg/24 h.The patient's clinical condition was getting worse in spite of chelation therapy and hemodialysis. The patient eventually died because of respiratory failure.Early diagnosis and appropriate treatment are critical for intravenous mercury poisoning especially because there are no specific signs or symptoms. There should be a high level of suspicion in drug abusers. Treatment should involve the combined use of chelating agents and other treatments such as hemodialysis and plasma exchange in advanced clinical settings.
2019-03-13 | Ectopic expression of a bacterial mercury transporter MerC in root epidermis for efficient mercury accumulation in shoots of Arabidopsis plants
Abstract For mercury phytoextraction, we previously demonstrated in Arabidopsis thaliana that a constitutive and ubiquitous promoter-driven expression of a bacterial mercury transporter MerC fused with SYP121, a plant SNARE for plasma membrane protein trafficking increases plant mercury accumulation. To advance regulation of ectopic expression of the bacterial transporter in the plant system, the present study examined whether merC-SYP121 expression driven by a root epidermis specific promoter (pEpi) is sufficient to enhance mercury accumulation in plant tissues. We generated five independent transgenic Arabidopsis plant lines (hereafter pEpi lines) expressing a transgene encoding MerC-SYP121 N-terminally tagged with a fluorescent protein mTRQ2 under the control of pEpi, a root epidermal promoter. Confocal microscopy analysis of the pEpi lines showed that mTRQ2-MerC-SYP121 was preferentially expressed in lateral root cap in the root meristematic zone and epidermal cells in the elongation zone of the roots. Mercury accumulation in shoots of the pEpi lines exposed to inorganic mercury was overall higher than the wild-type and comparable to the over-expressing line. The results suggest that cell-type specific expression of the bacterial transporter MerC in plant roots sufficiently enhances mercury accumulation in shoots, which could be a useful phenotype for improving efficiency of mercury phytoremediation.
antibodies
2026-09-28 | Acrodynia and CASPR2 Autoimmunity in Elemental Mercury Toxicity.
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.
2025-09-28 | Interleukin-17A: A Bright Target for Toxicological Mechanisms and Mitigation of Toxic Elements in the Environment
Science and other peer-reviewed studies recognize cadmium (Cd), arsenic (As), mercury (Hg), and fluoride (F) as highly hazardous toxic elements that threaten global health. However, understanding their toxic mechanisms and effective mitigation remains a global challenge. Growing evidence suggests that interleukin-17A (IL-17A) not only plays a role in inflammatory and immune diseases but may also be the brightest target in the mechanisms of toxic injury and its mitigation. This review summarizes IL-17A signaling in toxic element poisoning, highlighting distinct effects on apoptosis, autophagy, and pyroptosis: fluorine promotes cell death, cadmium shows dose-dependent regulation of IL-17A-mediated apoptosis, and arsenic and mercury may inhibit pyroptosis and IL-17A secretion. Moreover, interventions such as riboflavin, bifidobacterium, melatonin (MLT), Ginkgo biloba extract (GBE), lentinan, and taxifolin, were discussed for their protective effects via IL-17A modulation. This provides novel insights into IL-17A signaling, health risks, and therapeutic approaches against toxic elements.
2017-09-28 | An Enigmatic Case of Acute Mercury Poisoning: Clinical, Immunological Findings and Platelet Function
Severe mercury intoxication is very rare in developed countries, but still occurs as the result of volatile substance abuse, suicide attempts, occupational hazards, or endemic food ingestion as reported in the cases of public health disasters in Iraq and in Minamata Bay, Japan. Here, we describe the dramatic physical and cognitive decline of a 23-year-old patient caused by a severe methyl mercury intoxication of unknown origin. We show serial magnetic resonance imaging (MRI) of the patient's brain, as well as ex vivo analyses of blood and cerebrospinal fluid including multicolor flow cytometric measurements, functional assays of hemostaseologic efficacy and evaluation of regulatory effector molecules. Together with the clinical history, our findings show the progressive neuronal degeneration accompanying the deterioration of the patient. Moreover, the ex vivo analyses display alterations of thrombocyte function and coagulation, as well as an immunological milieu facilitating autoimmunity. Despite the successful reduction of the methyl mercury concentration in the patient's blood with erythrocyte apheresis and chelator therapy, his condition did not improve and led to a persistent vegetative state. This case illustrates the neurotoxicity of methyl mercury following severe intoxication for the first time by serial MRI. Data on immune-cell and thrombocyte function as well as on coagulation in mercury poisoning reveal potential implications for anticoagulation and immunomodulatory treatment.
2017-08-22 | Methylmercury Causes Blood-Brain Barrier Damage in Rats via Upregulation of Vascular Endothelial Growth Factor Expression.
Clinical manifestations of methylmercury (MeHg) intoxication include cerebellar ataxia, concentric constriction of visual fields, and sensory and auditory disturbances. The symptoms depend on the site of MeHg damage, such as the cerebellum and occipital lobes. However, the underlying mechanism of MeHg-induced tissue vulnerability remains to be elucidated. In the present study, we used a rat model of subacute MeHg intoxication to investigate possible MeHg-induced blood-brain barrier (BBB) damage. The model was established by exposing the rats to 20-ppm MeHg for up to 4 weeks; the rats exhibited severe cerebellar pathological changes, although there were no significant differences in mercury content among the different brain regions. BBB damage in the cerebellum after MeHg exposure was confirmed based on extravasation of endogenous immunoglobulin G (IgG) and decreased expression of rat endothelial cell antigen-1. Furthermore, expression of vascular endothelial growth factor (VEGF), a potent angiogenic growth factor, increased markedly in the cerebellum and mildly in the occipital lobe following MeHg exposure. VEGF expression was detected mainly in astrocytes of the BBB. Intravenous administration of anti-VEGF neutralizing antibody mildly reduced the rate of hind-limb crossing signs observed in MeHg-exposed rats. In conclusion, we demonstrated for the first time that MeHg induces BBB damage via upregulation of VEGF expression at the BBB in vivo. Further studies are required in order to determine whether treatment targeted at VEGF can ameliorate MeHg-induced toxicity.
2006-10-15 | Amelioration of Mercury-Induced Autoimmunity by 4-1BB
Abstract In certain strains of mice, subtoxic doses of HgCl2 (mercuric chloride; mercury) induce a complex autoimmune condition characterized by the production of antinucleolar IgG Abs, lymphoproliferation, increased serum levels of IgG1/IgE Abs, and deposition of renal immune complexes. 4-1BB is an important T cell costimulatory molecule that has been implicated in T cell proliferation and cytokine production, especially production of IFN-γ. To elucidate T cell control mediated by the 4-1BB signaling pathway in this syndrome, we assessed the effect of administering agonistic anti-4-1BB mAb on mercury-induced autoimmunity. Groups of A.SW mice (H-2s) received mercury/control Ig or mercury/anti-4-1BB or PBS alone. Anti-4-1BB mAb treatment resulted in a dramatic reduction of mercury-induced antinucleolar Ab titers, serum IgG1/IgE induction, and renal Ig deposition. These effects may be related to the present finding that anti-4-1BB mAb decreases B cell numbers and function. The anti-4-1BB mAb-treated mercury group also showed a marked reduction in Th2-type cytokines but an increase in Th1-type cytokines and chemokines. Increased IFN-γ production due to anti-4-1BB mAb treatment appears to be responsible for the observed B cell defects because neutralization of IFN-γ in vivo substantially restored B cell numbers and partly restored IgG1/IgE. Collectively, our results indicate that 4-1BB mAb can down-regulate mercury-induced autoimmunity by affecting B cell function in an IFN-γ-dependent manner and thus, preventing the development of autoantibody production and tissue Ig deposition.
small molecules
2026-09-03 | Mercury-associated minimal change disease induced by whitening cream: a case report.
Mercury-associated minimal change disease (M-MCD) is a rare form of secondary minimal change disease (MCD) caused by chronic mercury exposure. Given its rarity and nonspecific clinical presentation, M-MCD is frequently underrecognized in clinical practice. We report the case of a 32-year-old woman who presented with nephrotic syndrome following 4 months of applying a skin-whitening cream. Markedly elevated urinary mercury concentrations were detected, and renal biopsy confirmed MCD with immunoglobulin M (IgM) deposition. The patient received four courses of sodium dimercaptopropane sulfonate chelation therapy combined with glucocorticoids. Complete remission of proteinuria was achieved within 1 month, accompanied by normalization of urinary mercury levels. This case underscores the necessity of obtaining a detailed exposure history in patients with unexplained nephrotic syndrome, particularly among young women using skin-whitening cosmetics. Prompt recognition of mercury exposure and timely chelation therapy are essential for achieving remission; adjunctive glucocorticoids may be considered in selected patients with severe disease or suspected immune- mediated injury.
2026-08-23 | Giovanni Antonio Scopoli's De Hydrargyro Idriensi Tentamina (1761): Mercury Mining, Mercurialism, and Preventive Reasoning in Eighteenth-Century Occupational Medicine.
Giovanni Antonio Scopoli (1723-1788), a physician-naturalist of the Enlightenment, is primarily remembered for his contributions to botany and entomology. Less attention has been paid to his medical work De hydrargyro Idriensi Tentamina physico-chymico-medica (1761), written during his fifteen years of service as physician at the mercury mines of Idrija (present-day Slovenia). Its third section, De morbis fossorum hydrargyri, offers a detailed occupational-medical account of disorders and diseases among mercury miners and smelter workers, including tremor, salivation, stomatitis, respiratory disorders, and other conditions associated with mining labor. This article reassesses Scopoli's work within the history of occupational medicine, comparing his site-specific approach with the broader nosology of Bernardino Ramazzini and the later reform-oriented tradition associated with 19th-century industrial medicine. Rather than presenting Scopoli as a neglected founder of the discipline, we argue that the Tentamina represents a distinctive 18th-century form of occupational-medical inquiry: a monographic, workplace-based, clinically grounded study that linked toxic exposure, working conditions, and prevention before the emergence of modern industrial toxicology. The work remains substantially unknown in Anglophone historiography and deserves wider recognition as a significant example of pre-industrial occupational-medical inquiry.
2026-07-22 | A Multi-Analyte-Responsive, Multi-Organ-Imaging, Dual-NIR-Emissive Fluorescent Probe for Visualizing Pyroptosis-Mediated Hg2+-Induced Hepatorenal Dysfunction.
Mercury ions (Hg2+) are highly toxic heavy metals that are widely distributed in the environment and pose a serious threat to both ecosystems and human health. After entering the body, mercury preferentially accumulates in the liver and kidneys, underscoring the importance of early detection of acute and chronic hepatorenal injuries. Although fluorescent probes have been widely explored for disease diagnosis, most existing systems cannot achieve simultaneous in vivo imaging of the liver and kidneys, nor can they monitor multiple pathological parameters during hepatorenal injury, thus limiting their utility in evaluating Hg2+-induced multiorgan damage. In this study, we developed a multifunctional fluorescent probe, VPO, with high sensitivity and good biocompatibility, which can be used to monitor polarity, viscosity, and ONOO- levels in cells. Using VPO, we observed, for the first time, a significant increase in ONOO- during pyroptosis, accompanied by an elevated mitochondrial viscosity and reduced polarity. In addition, VPO successfully enabled the real-time visual monitoring of these changes in mercury-exposed cells, zebrafish, and mice. Moreover, its multiresponsive property enabled the evaluation of the therapeutic efficacy of N-acetylcysteine (NAC) against Hg2+-induced hepatorenal injury. NAC alleviated hepatic and renal mitochondrial oxidative stress, as well as pyroptosis-related inflammatory signaling, by reversing Hg2+-induced biomarker abnormalities. In summary, these findings demonstrate that VPO provides a comprehensive platform for the early diagnosis, therapeutic evaluation, and mechanistic investigation of mercury poisoning.
2026-07-16 | ASSESSMENT OF HEAVY METAL–INDUCED OXIDATIVE STRESS AND THE PROTECTIVE ROLE OF POLYHERBAL FORMULATIONS IN WISTAR RATS
Heavy metal toxicity is a major health problem in the world since it has caused extensive pollution in the environment and prolonged human exposure. Due to prolonged human exposure and widespread environmental pollution, heavy metal poisoning is a serious global health concern. Lead, cadmium, mercury, and arsenic are metals that build up in the body and are hazardous primarily through oxidative stress, inflammation, and apoptosis. Damage to endogenous antioxidant systems and excessive generation of reactive oxygen and nitrogen species lead to lipid peroxidation, protein oxidation, DNA damage, and progressive organ failure. Although chelation therapy is commonly used to reduce metal burden, its long-term usage is limited by low specificity, security concerns, and inability to prevent oxidative tissue damage. Due to their multi-targeted antioxidant, anti-inflammatory, and cytoprotective properties, polyherbal formulations are now regarded as potentially useful treatment methods. Additionally, polyherbal combinations have been shown in Wistar rat models to rescue antioxidant enzyme activities, restore low glutathione levels, control essential molecular pathways in adulthood, such as Nrf2, NF-KB, and MAPK, and protect important organs including the brain, liver, and kidney. This paper summarizes the cytotoxic effects of heavy metals in relation to oxidative stress and discusses the benefits, drawbacks, and potential of polyherbal formulations as a preventative measure. The findings suggest that polyherbal techniques may be utilized in the future as an alternative or supplement to lessen toxicity caused by heavy metals.
2026-06-01 | Integrative Oncology: A Systems-Based Multidisciplinary Approach Rooted in Agad Tantra Principles
The progressive accumulation of environmental toxins and long-term chemical bio-concentration across trophic levels presents a critical pathodynamic challenge within modern integrative medicine. This chapter delivers a comprehensive systems-biology evaluation of environmental toxicity, chronic poison exposure (Dūṣīviṣa), and complex metabolic imbalances (Āma) viewed through the operational frameworks of classical Agadatantra. Tracing textual guidelines across the Caraka Saṃhitā and Suśruta Saṃhitā, the study analyzes the mechanisms by which heavy metals (such as mercury and lead) and lipophilic pesticide residues accumulate inside tissue channels (Srotas) to trigger systemic inflammation and oncogenic cellular changes. Bridging these traditional views with current biomedical science, these classical pathodynamic pathways are cross-examined against modern ecotoxicology paradigms, including chemical biomagnification cascades, placental-fetal toxin transfer, and xenobiotic-induced oxidative stress. Ultimately, this work provides an evidence-aligned multidisciplinary model using target-specific Ayurvedic anti-toxic purification protocols (Viṣaghna Chikitsā) and cellular cleansing strategies to remove deep-seated lipophilic compounds and support chronic disease management within modern oncology frameworks. Keywords: Agadatantra, Integrative Oncology, Ecotoxicology, Biomagnification, Dushivisha, Xenobiotics, Environmental Toxin, Lipophilic Clearance.
proteins
2026-02-01 | Effect of metallothionein-1 on liver function in rats with mercuric chloride poisoning
Objective To investigate the protective effect of exogenous metallothionein-1 (MT-1) against liver injury induced by mercuric chloride poisoning in Brown-Norway rats. Methods Male Brown-Norway rats (n = 42) were randomly divided into six groups (n = 7 per group), including normal control, model control, positive control, and low-, medium-, and high-dose MT-1 groups. Except for the rats in the normal control group, the rats in all other groups received subcutaneous injections of 1 mg/mL mercuric chloride solution (1.0 mg/kg) every other day for 14 days (7 injections total). The positive control group rats were intramuscularly injected with 2.5 mg/mL sodium 2, 3-dimercapto-1-propanesulfonate (DMPS) at 5 mL/kg every 2 days. Rats in the low-, medium-, and high-dose MT-1 groups received MT-1 via oral gavage at concentrations of 0.032, 0.080, and 0.160 mg/mL (5 mL/kg body weight), respectively, once daily. The normal control and model control groups received equivalent volumes of 9 g/L sodium chloride solution (mass-volume concentration). After the experiment, rat body weight and liver wet weight were measured, and the liver index was calculated. Gross pathological changes of the liver were observed, and serum alanine aminotransferase (ALT), γ-glutamyl transferase (GGT), bilirubin, total protein, globulin, and albumin-to-globulin ratio were determined as indicators of liver function. Results Compared with the normal control group, the mercuric chloride-treated groups of rats showed varying degrees of poisoning symptoms, including reduced body weight, increased liver index, significant elevation in serum ALT, GGT, and total bilirubin levels, and significantly reduced total protein and albumin/globulin ratio. Compared with the model control group, the medium and high dose MT-1 groups and the DMPS group showed a significant lower serum ALT and GGT levels (P < 0.05). All MT-1 dose groups demonstrated significantly higher total protein levels (P < 0.05), and the high-dose MT-1 group also showed a significant recovery in albumin/globulin ratio and total bilirubin level (both P < 0.05). Conclusions Exogenous high-dose MT-1 could alleviate some mercuric chloride-induced liver function abnormalities, with comparable efficacy to DMPS, while also improving total protein level in the model rats.
2023-09-07 | In silico explorations of bacterial mercuric reductase as an ecofriendly bioremediator for noxious mercuric intoxications
Mercury is a major pollutant in the environment due to its high concentration in the soil. In this study, a mercuric reductase was extracted from Pseudomonas aeruginosa. The sequence of the enzyme was retrieved from the literature and structural homologs were identified. The protein bonded with Mercuric compounds and their interaction was briefly studied. Autodock Vina was used to perform a molecular docking with the target protein. Results showed that the sequence consists of most of the random coil 44.74% followed by α-helix and B-turns. Moreover, the protein was predicted to have a FAD/NAD(P)-binding domain. The virulence factor prediction using different approaches of Virulentpred and VICMpred suggested that P00392 is non-toxic. Next, the mutational analyses were performed to predict the active site residues in the resulting models and to determine mutants. The results show that the enzyme is involved in the bioremediation of mercury by using in-silico techniques. Finally, molecular docking studies were conducted on the best-selected model to find the active site residues and to generate a pattern of interaction to understand the mode of action of the substrate and its catalytic activity which refers to the binding with mercury.
2023-06-29 | MORPHOLOGICAL CHANGES IN THE PERIPHERAL NERVES IN TRAUMA, MERCURY INTOXICATION, HYPOTHYROIDISM, AND THEIR CORRECTION
Traumatic peripheral nerve injury (PNI) significantly impacts patients' quality of life, and its treatment necessitates a multidisciplinary approach.Additionally, different non-traumatic factors such as environmental toxicants and endocrine disorders can significantly affect the regenerative capacity of damaged nerves.The aim of this study was to assess the morphological changes in the recovery of the damaged peripheral nerve, considering the impact of environmental heavy metal intoxication (mercury) and hypothyroidism, including their treatment.The study involved a total of 90 white rats divided into three groups, each group further subdivided into subgroups (a and b).All rats underwent surgical cutting of the sciatic nerve.Subgroup Ia underwent sciatic nerve injury alone, while subgroups IIa and IIIa were additionally subjected to experimental mercurialism and hypothyroidism, respectively.Subgroups Ib, IIb, and IIIb received treatments with Cerebrolysin, Thiotriazoline, and L-Thyroxine+Miacalcic, respectively, in addition to the traumatic nerve injury and experimental influences.The damaged nerves were then examined using both light and electron microscopy assessments.The findings of the study suggest that there are general patterns of de -and regeneration of the damaged peripheral nerve in the context of nootropic administration, experimental mercury intoxication, hypothyroidism, and their correction.In all groups, degeneration was observed, but a noteworthy delay in degenerative processes was observed specifically in cases involving delayed surgical nerve connection, mercurialism, and hypothyroidism, possibly due to the inhibition of Schwann cells.This led to a delayed regeneration process.However, the regeneration of the damaged nerve was significantly accelerated when the experimental pathological condition was corrected.
2021-12-29 | Dithiolated peptides incorporating bis(tryptophan)s for cooperative mercury(II) binding.
The indole side chain of tryptophan is a versatile π-donor that can participate in various types of cation-π interactions. An understanding of how it may contribute as an auxiliary binding group in mercury(II) complexes can provide valuable insights toward the design of effective chelators for optimal mercury immobilization. In this study, we investigate how the incorporation of two tryptophan residues in model dicysteinyl peptides might participate in peptide-mercury(II) complex stabilization. Two pentapeptides consisting of a Cys-Trp-Cys sequence motif containing a second tryptophan residue at the N-terminal (BT1) or C-terminal (BT2) were designed. An analogous cyclohexapeptide (BT3) was included to evaluate how tryptophan residues, restricted in constrained peptidic turn motifs, might take part in mercury(II) complexation. Their interactions with mercury(II) were investigated by spectroscopic methods and computational modeling. UV-vis studies indicate the formation of 1:1 dithiolated mercury(II) complex, which is corroborated by ESI-MS analysis. Spectroscopic studies reveal that the tryptophan indole group(s) in BT1 and BT3 can participate in mercury(II) cation-π interactions. Optimized 1:1 mercury(II)-BT3 structures indicate that both indole rings are very close to the mercury(II) coordination site and could stabilize it by shielding it from ligand exchange. These findings provide some useful insights toward use of aromatic donor groups as hydrophobic shields in designing more effective metal chelating agents.
2018-11-28 | A polysaccharide-peptide with mercury clearance activity from dried fruiting bodies of maitake mushroom Grifola frondosa
Mercury is considered to be "a global pollutant" and raises concern worldwide. Once mercury enters the body, it will be distributed all over the body but will accumulate in the brain, kidney and liver. To date, no substance originating from edible fungi capable of adsorbing mercury has been reported. We found that the mushroom Grifola frondosa exhibited mercury adsorption capacity. A polysaccharide-peptide (GFPP), displaying the unique N-terminal amino acid sequence of APPGMHQKQQ and 7 partial sequences with high reliability obtained by LC-MS/MS, was isolated by hot-water extraction of its fruiting bodies followed by ion exchange chromatography and gel filtration chromatography. Two rat models were employed to determine the dose and the duration of HgCl2 treatment (given by acute administration or continuous treatment) to test if G. frondosa could promote mercury elimination. For rats subjected to acute treatment with HgCl2, both GFPP and G. frondosa fruiting bodies (GFFF) could accelerate the decline of blood mercury level, which fell precipitously by 50% on the second day. GFPP and GFFF also promoted elimination of the burden of mercury in the liver and kidneys. For rats receiving continuous HgCl2 treatment, G. frondosa prevented the progressive increase of blood mercury level, and kept the blood mercury level within a relatively stable range.
cell therapies
2024-05-09 | Case Reports of Intravenous Drug Use of Elemental Mercury as an Aphrodisiac: A Call for Surgical Intervention
This report describes two cases of intravenous injection of elemental mercury. The presence of mercury in the environment is due to pollution from power plants and in food, particularly fish, and dental amalgams. One patient succumbed and the other remains asymptomatic two years after the surgical removal of all the injected mercury. Management of intravenous injection of elemental mercury (intended to be an aphrodisiac in these two cases) is discussed here and the need for surgical removal of all accessible mercury has been emphasized. In case no.1, it is difficult to come to any conclusion as we do not have information about the duration of exposure and the volume of mercury injected. In contrast, in case no.2, all the metallic elemental mercury was removed on two occasions and the patient has led an uneventful life showing no clinical signs of mercury poisoning in the follow-up period of two years.
2023-10-14 | Fecal microbiota transplantation in treating methylmercury-poisoned rats: Reconstruction of gut microbiome and modulation of gut-brain axis related metabolites
Abstract Background Methylmercury (MeHg) can bring devastating neurotoxicity to animals and human beings. Gut microbiota has been found to demethylate MeHg while MeHg exposure was found to destroy the diversity and abundance of gut microbiota. Besides, some neurotransmitters such as GABA, glutamate and other metabolites were altered due to MeHg exposure. Fecal microbiota transplantation (FMT) has been successfully applied to treat a series of diseases like Tourette syndrome, irritable bowel syndrome, necrotizing enterocolitis and to treat ulcerative coliti. The objective of this study was to investigate the effects of FMT in treating MeHg-poisoned rats. Results : It was found that FMT for 14 days promoted body weight gain, enhanced demethylation of MeHg and increased fecal excretion of Hg in MeHg-poisoned rats. Furthermore, the gut microbial bacteria associated with demethylation, such as sulfate-reducing bacteria were restored and some metabolites related to neuroactivity through gut-brain axis were increased after FMT, there is also repair of brain derived neurotrophic factor(BDNF)-related factor levels in the intestine, brain and serum. Conclusions : In all, it was showed that FMT can be a effective way in treating MeHg-poisoned rats through the reconstruction of gut microbiota, especially the bacteria that are associated with the demethylation of MeHg. Furthermore, the modulation of metabolites that are related to gut-brain axis after FMT also contributed to the treating of MeHg-poisoning. This study provides a novel way to treat MeHg-poisoning, which may contribute to the health promotion of mercury exposed population and shed lights on the treatment of other neurological diseases like Parkinson’s disease.
2023-07-03 | Strictly-controlled techniques are required in laparoscopic appendectomy for elemental mercury sequestration in the appendix: a case report.
Elemental mercury impaction in the appendix can cause subsequent local and systemic complications. We present a case of a teenage boy who ingested approximately 10 mL of elemental mercury, resulting in residual mercury sequestration in the appendix after conservative management. We performed laparoscopic appendectomy to remove the residual mercury. The patient made a complete clinical recovery without adverse events related to mercury poisoning over the 6-month follow-up. We highlight the advantages of laparoscopic appendectomy, abdominal computed tomography (CT), negative pressure operating rooms, and surgeon protection to improve surgical success rates. This case report adds to the literature on the management of elemental mercury impaction in the appendix and provides valuable insights for clinical decision-making.
2020-04-30 | An Unusual Cause of High Density Radiological Opacities
Metallic mercury poisoning through intravenous injection is rare, especially as part of a suicide attempt. Diagnosis and treatment of the disease are challenging as clinical features are not specific.A 41-year-old male presented with dyspnea, fatigue, loss of weight, and loss of appetite over two months. Routine radiological examination by chest X-ray and CT showed randomly distributed high density opacities with Hounsfield units (HU) around 500 HU all over the body. The diagnosis was then confirmed with a urinary mercury concentration of > 1000 mcg/24 h.The patient's clinical condition was getting worse in spite of chelation therapy and hemodialysis. The patient eventually died because of respiratory failure.Early diagnosis and appropriate treatment are critical for intravenous mercury poisoning especially because there are no specific signs or symptoms. There should be a high level of suspicion in drug abusers. Treatment should involve the combined use of chelating agents and other treatments such as hemodialysis and plasma exchange in advanced clinical settings.
2019-03-13 | Ectopic expression of a bacterial mercury transporter MerC in root epidermis for efficient mercury accumulation in shoots of Arabidopsis plants
Abstract For mercury phytoextraction, we previously demonstrated in Arabidopsis thaliana that a constitutive and ubiquitous promoter-driven expression of a bacterial mercury transporter MerC fused with SYP121, a plant SNARE for plasma membrane protein trafficking increases plant mercury accumulation. To advance regulation of ectopic expression of the bacterial transporter in the plant system, the present study examined whether merC-SYP121 expression driven by a root epidermis specific promoter (pEpi) is sufficient to enhance mercury accumulation in plant tissues. We generated five independent transgenic Arabidopsis plant lines (hereafter pEpi lines) expressing a transgene encoding MerC-SYP121 N-terminally tagged with a fluorescent protein mTRQ2 under the control of pEpi, a root epidermal promoter. Confocal microscopy analysis of the pEpi lines showed that mTRQ2-MerC-SYP121 was preferentially expressed in lateral root cap in the root meristematic zone and epidermal cells in the elongation zone of the roots. Mercury accumulation in shoots of the pEpi lines exposed to inorganic mercury was overall higher than the wild-type and comparable to the over-expressing line. The results suggest that cell-type specific expression of the bacterial transporter MerC in plant roots sufficiently enhances mercury accumulation in shoots, which could be a useful phenotype for improving efficiency of mercury phytoremediation.
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Drug Discovery Landscape
5 orphan drug designations for Mercury poisoning.
5 orphan drug designations for Mercury poisoning.
Drug | Therapy type | Orphan designation | Clinical trial status | Sponsor |
|---|---|---|---|---|
Emeramide | small molecules | EMA | NBMI Science Limited | |
Erdosteine | small molecules | EMA | — | Rafifarm SRL |
emeramide | small molecules | FDA | NBMI Science Limited | |
N,N'-bis(2-mercaptoethyl)isophthalamide | small molecules | EMA | NBMI Science Limited | |
Succimer | small molecules | FDA | — | Sanofi Winthrop, Inc. |
“Terminated” – programs with discontinued clinical trials, or with no updates reported for 5 years after completion or 12 years after the last trial started.
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