Accelerated Uptake of Mercury by Brain caused by 2,3‐ Dimercaptopropanol (BAL) After Injection into the Mouse of a Methylmercuric Compound

Berlin, Maths; Jerksell, L G; Nordberg, Gunnar F.

doi:10.1111/j.1600-0773.1965.tb00356.x

Cited by 58 publications

(2 citation statements)

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“…The decreased amount of mercury in the kidney after DDC treatment may thus depend on a complex formation and a more uniform distribution of the complex. A similar theory may explain the redistribution of mercury demonstrated with both inorganic mercury and methyl mercuric compounds and other chelating agents (BERLIN et al 1965;BERLIN I& LE-WANDER 1969;MAGOS 1968;NORSETH 1973a). The red cell depot of mercury in the rats is, however, unchanged, indicating that this assumption is either incorrect, or that there is a different binding in red cells as compared to the kidney.…”

Section: Discussionmentioning

confidence: 92%

The Effect of Diethyldithiocarbamate on Biliary Transport, Excretion and Organ Distribution of Mercury in the Rat after Exposure to Methyl Mercuric Chloride

Norseth

1974

Acta Pharmacologica et Toxicologica

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Diethyldithiocarbamate (DDC) and disulfiram decrease the biliary excretion of methyl mercuric compounds. The biliary mercury excretion returns to normal after a time period which is dependent on the dose of the inhibiting compound. For some doses of DDC the excretion of mercury increases above control values following the period of inhibition. DDC treatment increases brain, muscle and fur content of mercury. There is an increased retention of mercury in the liver, but decreased amounts of mercury in the kidney. Mercury in red cells is not affected. Faecal excretion of mercury decreases as expected because of decreased biliary excretion. The urinary excretion of mercury also decreases, but the mechanism is not clear. Changes in the excretion and organ distribution pattern indicate similar mechanisms for DDC treatment as for bile duct ligation, but DDC probably also changes the organ distribution and excretion by complex formation with some methyl mercuric compound.

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Section: Discussionmentioning

confidence: 92%

The Effect of Diethyldithiocarbamate on Biliary Transport, Excretion and Organ Distribution of Mercury in the Rat after Exposure to Methyl Mercuric Chloride

Norseth

1974

Acta Pharmacologica et Toxicologica

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“…Hence, this does not indicate, as suggested by the authors, that baseline concentrations of gadolinium were elevated or that gadolinium was being removed from excess tissue reservoirs in these patients related to previous gadolinium-based contrast agent administration. It is also important to consider that if, as was suggested in the aforementioned paper, chelation therapy does remove gadolinium from tissue stores, there have historically been extensive conflicting reports as to whether chelation therapy may actually mobilise heavy metals deposited in bone into the circulation and subsequently lead to increased deposition in soft tissues, such as the brain and heart [71][72][73][74]. Whilst urine heavy metal concentrations can be helpful in assessing the impact of chelation therapy [75,76]; it is essential that these are not considered in isolation as an indicator of therapeutic efficacy.…”

Section: Clinical Studiesmentioning

confidence: 99%

Gadolinium-based contrast agents – what is the evidence for ‘gadolinium deposition disease’ and the use of chelation therapy?

Layne

Wood

2019

Clinical Toxicology

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Introduction: Gadolinium-based contrast agents are widely used for magnetic resonance imaging and, until recently, had been generally considered to have an excellent safety profile in patients with normal renal function. Nephrogenic systemic fibrosis is a well-established disease process involving fibrosis of the skin and internal organs seen in some patients with severely impaired renal function following exposure to these agents. Following reports that individuals with normal renal function may experience gadolinium deposition within brain and bone tissue, the term "gadolinium deposition disease" has been proposed and the use of chelating agents has been recommended to treat this "disease". Objectives: This review will address the clinical evidence for "gadolinium deposition disease" and discuss whether chelation therapy is appropriate for individuals who believe they have this condition. Methods: Electronic databases (PUBMED, Ovid MEDLINE and EMBASE) were searched up to 1 st October 2019 for all studies evaluating clinical signs or symptoms related to potential gadolinium toxicity post-gadolinium-based contrast agent exposure in subjects with normal renal function, or papers evaluating the potential chelation of gadolinium in humans. Does "gadolinium deposition disease" exist as a novel condition? We identified four clinical studies relating to "gadolinium deposition disease", including one that included some discussion of the use of chelation therapy. Two of the clinical studies presented data from anonymous online surveys that recruited participants from support forums for people who self-identified as having gadoliniumbased contrast agent-induced toxicity, with questions focussing on their reported symptoms and signs. The published literature to date has demonstrated that gadolinium deposition within the brain primarily occurs within the dentate nucleus and globus pallidus. These patients did not complain of movement disorders, but instead reported generalised sensory symptoms, which would not be expected to occur with pathology in these areas of the brain. There was considerable selection bias and a lack of available clinical information to exclude alternative medical diagnoses for these series, thus rendering the results difficult to interpret. Role of chelation therapy in patients exposed to gadolinium-based contrast agent: One study reported data from 25 patients who were diagnosed with "gadolinium deposition disease" according to unspecified criteria and were treated with intravenous calcium or zinc trisodium pentetate. The authors reported an increase in urine gadolinium concentrations following administration of the chelating agents, which they attributed to re-chelation of gadolinium from tissue deposits, however, there are insufficient data to be able to substantiate this. Conclusion: There is currently no published information from well-designed clinical studies that support a link between gadolinium deposition and the development of clinical sequelae in patients with normal renal function. Clinic...

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Methylmercury poisoning: Long‐term clinical, radiological, toxicological, and pathological studies of an affected family

Davis

Kornfeld

Mooney

et al. 1994

Annals of Neurology

167

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For 3 months in 1969 a family in the United States that included a pregnant mother consumed pork containing methylmercury. Children, aged 20, 13, and 8 years and a neonate, developed severe neurological signs. Twenty-two years later, the 2 oldest had cortical blindness or constricted visual fields, diminished hand proprioception, choreoathetosis, and attentional deficits. Magnetic resonance images showed tissue loss in the calcarine and parietal cortices and cerebellar folia. The youngest had quadriplegia, blindness, and severe mental retardation until their deaths. The brain of the 8-year-old who died at age 30 showed cortical atrophy, neuronal loss, and gliosis, most pronounced in the paracentral and parietooccipital regions. The total mercury level in formalin-fixed, left occipital cortex was 1,974 ng/gm as measured by atomic absorption. Regional brain mercury levels correlated with extent of brain damage. A control patient had 38.5 ng of mercury/gm in the occipital cortex. Systemic organs in the patient and a control subject had comparable mercury levels. In mercury-intoxicated rats, we found that only 5 to 10% of total brain mercury was lost by formalin fixation. Brain inorganic mercury in the patient ranged from 82 to 100%. Since inorganic mercury crosses the blood-brain barrier poorly, biotransformation of methyl to inorganic mercury may have occurred after methylmercury crossed the blood-brain barrier, accounting for its persistence in brain and causing part of the brain damage.

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Accelerated Uptake of Mercury by Brain caused by 2,3‐ Dimercaptopropanol (BAL) After Injection into the Mouse of a Methylmercuric Compound

Cited by 58 publications

References 4 publications

The Effect of Diethyldithiocarbamate on Biliary Transport, Excretion and Organ Distribution of Mercury in the Rat after Exposure to Methyl Mercuric Chloride

The Effect of Diethyldithiocarbamate on Biliary Transport, Excretion and Organ Distribution of Mercury in the Rat after Exposure to Methyl Mercuric Chloride

Gadolinium-based contrast agents – what is the evidence for ‘gadolinium deposition disease’ and the use of chelation therapy?

Methylmercury poisoning: Long‐term clinical, radiological, toxicological, and pathological studies of an affected family

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