The effect of co-administration of selenium and DMPS in inorganic mercury intoxication in mice

2011 ◽  
Vol 49 (1) ◽  
pp. 319 ◽  
Author(s):  
Gianpaolo Guzzi ◽  
Paolo Pigatto ◽  
Anna Ronchi ◽  
Claudio Minoia
Keyword(s):  
Inorganic Mercury ◽  
Mercury Intoxication

Being alive after a severe inorganic mercury intoxication

2009 ◽  
Vol 169 (5) ◽  
pp. 625-628 ◽  
Author(s):  
Nilgun Erkek ◽  
Saliha Senel ◽  
Avni Sarac ◽  
Ulker Ertan ◽  
Can Demir Karacan
Keyword(s):  
Inorganic Mercury ◽  
Mercury Intoxication

An Association of Mercury with Selenium in Inorganic Mercury Intoxication

1985 ◽  
Vol 4 (6) ◽  
pp. 637-642 ◽  
Author(s):  
T. Aoi ◽  
T. Higuchi ◽  
R. Kidokoro ◽  
R. Fukumura ◽  
A. Yagi ◽  
...  
Keyword(s):  
Trace Element ◽  
Inorganic Mercury ◽  
Energy Dispersive ◽  
X Rays ◽  
X Ray ◽  
Tubular Cells ◽  
Molecular Ratio ◽  
Renal Tubular Cells ◽  
Mercury Intoxication ◽  
Renal Tubular

1 Energy dispersive X-ray analysis was performed on the renal tubular cells of two patients with inorganic mercury intoxication. 2 Some lysosomes of these cells consisted of unusual matrices of aggregated electron-dense grains which were positive for mercury, selenium and sulphur. 3 Though maps of the specific X-rays of both mercury and selenium coincided exactly with these lysosomes, the molecular ratio of selenium to mercury ranged between zero and 2.9. 4 It is unlikely that the trace element of selenium and exogenous inorganic mercury are deposited in the lysosomes independent of each other, but rather their coexistence in the characteristic lysosomes strongly suggests a compound formed by binding mercury to the SeH residues of selenoprotein.

Inorganic mercury intoxication: A case report

2016 ◽  
Vol 259 ◽  
pp. e20-e24 ◽  
Author(s):  
Daniel Dias ◽  
José Bessa ◽  
Susana Guimarães ◽  
Maria Elisa Soares ◽  
Maria de Lourdes Bastos ◽  
...  
Keyword(s):  
Case Report ◽  
Inorganic Mercury ◽  
Mercury Intoxication

scholarly journals Chronic Neurological Disease Due to Methylmercury Poisoning

2018 ◽  
Vol 45 (6) ◽  
pp. 620-623 ◽  
Author(s):  
Alan C. Jackson
Keyword(s):  
Neurological Disease ◽  
Inorganic Mercury ◽  
Northwestern Ontario ◽  
Mercury Intoxication ◽  
Neurological Features ◽  
Methylmercury Poisoning ◽  
Characteristic Features ◽  
The Brain ◽  
Nerve Disease ◽  
Visual Field Constriction

AbstractOrganic mercury, especially methylmercury, poisoning causes chronic neurological disease predominantly affecting the brain. There have been documented exposures from eating fish from contaminated waters in Japan and in northwestern Ontario and in Iraq from eating bread made from seed wheat treated with methylmercuric fungicide. The neurological disease is called Minamata disease in Japan. Visual field constriction due to involvement of the calcarine cortex, sensory disturbance due to involvement of the somatosensory cortex, and cerebellar ataxia due to involvement of granule cell neurons of the cerebellum are common and characteristic features due to methylmercury poisoning. Other neurological features include dysarthria, postural and action tremor, cognitive impairment, and hearing loss and dysequilibrium. In contrast, peripheral nerve disease is more characteristic of inorganic mercury intoxication. Similarly, psychosis is more typical of exposure to inorganic mercury, which has been documented in the felt hat industry (“mad hatter”). Laboratory tests (e.g., on blood and hair and toenail samples) are of limited value in the assessment of chronic neurological disease due to mercury poisoning because they may not reflect remote neuronal injury due to mercury. Methylmercury also causes injury to fetal brains during development. There is no effective treatment.

Extracorporeal Regional Complexing Haemodialysis Treatment of Acute Inorganic Mercury Intoxication

1990 ◽  
Vol 9 (3) ◽  
pp. 137-141 ◽  
Author(s):  
P.J. Kostyniak ◽  
H.B. Greizerstein ◽  
J. Goldstein ◽  
M. Lachaal ◽  
P. Reddy ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Suicide Attempt ◽  
Inorganic Mercury ◽  
Chelating Agent ◽  
White Female ◽  
Mercury Poisoning ◽  
Arterial Blood ◽  
Mercury Intoxication ◽  
Haemodialysis Treatment

A 70-year-old white female presented approximately 24 h after ingesting three 475 mg tablets (1.425 g) of mercuric chloride in a suicide attempt. Acute renal failure necessitated the initiation of haemodialysis approximately 4 d after the ingestion. Treatment with BAL (2,3-dimercaptopropanol) resulted in only small increases in mercury output into dialysate. A new procedure involving the extracorporeal infusion of the chelating agent dimercaptosuccinic acid (DMSA) into the arterial blood line during haemodialysis was initiated. This procedure of Extracorporeal Regional Complexing Haemodialysis (ERCH) had been effective in increasing methylmercury removal in patients poisoned by contaminated grain. The first DMSA-ERCH procedure was performed 6 d after poisoning. There was a dramatic increase in mercury output into the dialysate. During three treatment sessions of 80 min each, 1189 μg of mercury were removed from the patient. The dialysed mercury represented the only mercury output since the patient was anuric and not producing faeces. DMSA-ERCH appears to be much more effective than BAL and haemodialysis in the treatment of acute inorganic mercury poisoning. The long interval between poisoning and initiation of treatment probably contributed to the patients ultimate demise, 28 d after poisoning. Efficacy of the DMSA-ERCH procedure for inorganic mercury poisoning is likely to be improved as the interval between exposure and treatment is reduced.

scholarly journals From Molecules to Behavior in Long-Term Inorganic Mercury Intoxication: Unraveling Proteomic Features in Cerebellar Neurodegeneration of Rats

2021 ◽  
Vol 23 (1) ◽  
pp. 111
Author(s):  
Leonardo Oliveira Bittencourt ◽  
Victória Santos Chemelo ◽  
Walessa Alana Bragança Aragão ◽  
Bruna Puty ◽  
Aline Dionizio ◽  
...  
Keyword(s):  
Purkinje Cells ◽  
Inorganic Mercury ◽  
Nervous System Development ◽  
Proteomic Profile ◽  
Mercury Toxicity ◽  
Adult Rats ◽  
Motor Functions ◽  
Proteomic Approach ◽  
Mercury Intoxication

Mercury is a severe environmental pollutant with neurotoxic effects, especially when exposed for long periods. Although there are several evidences regarding mercury toxicity, little is known about inorganic mercury (IHg) species and cerebellum, one of the main targets of mercury associated with the neurological symptomatology of mercurial poisoning. Besides that, the global proteomic profile assessment is a valuable tool to screen possible biomarkers and elucidate molecular targets of mercury neurotoxicity; however, the literature is still scarce. Thus, this study aimed to investigate the effects of long-term exposure to IHg in adult rats’ cerebellum and explore the modulation of the cerebellar proteome associated with biochemical and functional outcomes, providing evidence, in a translational perspective, of new mercury toxicity targets and possible biomarkers. Fifty-four adult rats were exposed to 0.375 mg/kg of HgCl2 or distilled water for 45 days using intragastric gavage. Then, the motor functions were evaluated by rotarod and inclined plane. The cerebellum was collected to quantify mercury levels, to assess the antioxidant activity against peroxyl radicals (ACAPs), the lipid peroxidation (LPO), the proteomic profile, the cell death nature by cytotoxicity and apoptosis, and the Purkinje cells density. The IHg exposure increased mercury levels in the cerebellum, reducing ACAP and increasing LPO. The proteomic approach revealed a total 419 proteins with different statuses of regulation, associated with different biological processes, such as synaptic signaling, energy metabolism and nervous system development, e.g., all these molecular changes are associated with increased cytotoxicity and apoptosis, with a neurodegenerative pattern on Purkinje cells layer and poor motor coordination and balance. In conclusion, all these findings feature a neurodegenerative process triggered by IHg in the cerebellum that culminated into motor functions deficits, which are associated with several molecular features and may be related to the clinical outcomes of people exposed to the toxicant.

scholarly journals Ocular Surface Pathology in Patients Suffering from Mercury Intoxication

Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1326
Author(s):  
Pilar Cañadas ◽  
Yrbani Lantigua ◽  
Amalia Enríquez-de-Salamanca ◽  
Itziar Fernandez ◽  
Salvador Pastor-Idoate ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Cell Density ◽  
Ocular Surface ◽  
Inorganic Mercury ◽  
Principal Component ◽  
Corneal Sensitivity ◽  
Cross Sectional ◽  
Thermal Thresholds ◽  
Mercury Intoxication

Purpose: To report the ocular surface pathology of patients suffering from acute/subacute mercury vapor intoxication. Design: Cross-sectional study. Participants: Male workers intoxicated with inorganic mercury referred for ophthalmic involvement and healthy control subjects. Methods: The following tests were performed: dry eye (DE)-related symptoms indicated by the ocular surface disease (OSDI) index questionnaire; tear osmolarity; analysis of 23 tear cytokine concentrations and principal component and hierarchical agglomerative cluster analyses; tear break-up time (T-BUT); corneal fluorescein and conjunctival lissamine green staining; tear production by Schirmer and tear lysozyme tests; mechanical and thermal corneal sensitivity (non-contact esthesiometry); and corneal nerve analysis and dendritic cell density by in vivo confocal microscopy (IVCM). Results: Twenty-two out of 29 evaluated patients entered the study. Most had DE-related symptoms (OSDI values > 12), that were severe in 63.6% of them. Tear osmolarity was elevated (>308 mOsms/L) in 83.4% of patients (mean 336.23 (28.71) mOsm/L). Corneal and conjunctival staining were unremarkable. T-BUT was low (<7 s) in 22.7% of patients. Schirmer test and tear lysozyme concentration were low in 13.6% and 27.3% of cases, respectively. Corneal esthesiometry showed patient mechanical (mean 147.81 (53.36) mL/min) and thermal thresholds to heat (+2.35 (+1.10) °C) and cold (−2.57 (−1.24) °C) to be significantly higher than controls. Corneal IVCM revealed lower values for nerve density ((6.4 (2.94) n/mm2), nerve branching density (2 (2.50) n/mm2), and dendritic cell density (9.1 (8.84) n/mm2) in patients. Tear levels of IL-12p70, IL-6, RANTES, and VEGF were increased, whereas EGF and IP-10/CXCL10 were decreased compared to controls. Based on cytokine levels, two clusters of patients were identified. Compared to Cluster 1, Cluster 2 patients had significantly increased tear levels of 18 cytokines, decreased tear lysozyme, lower nerve branching density, fewer dendritic cells, and higher urine mercury levels. Conclusions: Patients suffering from systemic mercury intoxication showed symptoms and signs of ocular surface pathology, mainly by targeting the trigeminal nerve, as shown by alterations in corneal sensitivity and sub-basal nerve morphology.

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