Evidence for a Neuromuscular Disorder in Methylmercury Poisoning

Rustam, H.; Burg, R. von; Amin-Zaki, Laman; Hassani, Soghra

doi:10.1080/00039896.1975.10666674

Cited by 41 publications

(12 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the Iraqi episode of poisoning, ~14% of the patients presented with a neuromuscular weakness resembling myasthenia gravis; its origin was not determined Bakir et al, 1980), nor was a definitive diagnosis of myasthenia gravis made. Motor dysfunction in MeHg-poisoned humans includes ataxia, muscle weakness, and inability to walk; these observations are consistent with clinical signs of neuromuscular-like disorders, suggesting that MeHg impacts MN function to some extent (Eto, 1997, Eto et al, 2002; Dietrich et al, 2005, Rustam et al, 1975). Additionally, MN-directed disease, including amyotrophic lateral sclerosis, has been reported after exposure to inorganic Hg (Adams et al, 1983; Praline et al, 2007; Rooney, 2011).…”

Section: Effects Of Mehg On Motor Efferentssupporting

confidence: 69%

Effects of methylmercury on spinal cord afferents and efferents—A review

2017

View full text Add to dashboard Cite

Methylmercury (MeHg) is an environmental neurotoxicant of public health concern. It readily accumulates in exposed humans, primarily in neuronal tissue. Exposure to MeHg, either acutely or chronically, causes severe neuronal dysfunction in the central nervous system and spinal neurons; dysfunction of susceptible neuronal populations results in neurodegeneration, at least in part through Ca2+-mediated pathways. Biochemical and morphologic changes in peripheral neurons precede those in central brain regions, despite the fact that MeHg readily crosses the blood-brain barrier. Consequently, it is suggested that unique characteristics of spinal cord afferents and efferents could heighten their susceptibility to MeHg toxicity. Transient receptor potential (TRP) ion channels are a class of Ca2+-permeable cation channels that are highly expressed in spinal afferents, among other sensory and visceral organs. These channels can be activated in numerous ways, including directly via chemical irritants or indirectly via Ca2+ release from intracellular storage organelles. Early studies demonstrated that MeHg interacts with heterologous TRPs, though definitive mechanisms of MeHg toxicity on sensory neurons may involve more complex interaction with, and among, differentially-expressed TRP populations. In spinal efferents, glutamate receptors of the N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and possibly kainic acid (KA) classes are thought to play a major role in MeHg-induced neurotoxicity. Specifically, the Ca2+-permeable AMPA receptors, which are abundant in motor neurons, have been identified as being involved in MeHg-induced neurotoxicity. In this review, we will describe the mechanisms that could contribute to MeHg-induced spinal cord afferent and efferent neuronal degeneration, including the possible mediators, such as uniquely expressed Ca2+-permeable ion channels.

show abstract

Section: Effects Of Mehg On Motor Efferentssupporting

confidence: 69%

Effects of methylmercury on spinal cord afferents and efferents—A review

2017

View full text Add to dashboard Cite

show abstract

“…The inhibition of muscarinic receptor binding induced by in vivo exposure to cadmium is similar to that seen by parallel in vitro studies (Hedlund et al 1979). In addition, the concentrations of lead and mercury that are effective in inhibiting muscarinic receptors in vitro approximate those which occur in metal poisoning of the brain (Rustam et al 1975;Aronstam and Eldefrawi 1979). However, in one study, lead-treated animals have been found to exhibit no changes in the level of the striatal dopamine receptor (Govoni et al 1979).…”

Section: Discussionmentioning

confidence: 96%

“…The toxic effects of lead and mercury are especially pronounced at the neurological level (Felton et al 1972;Rustam et al 1975). The tremor, poor coordination and other movement disturbances caused by compounds containing these heavy metals, suggested that they may in part exert their effects by way of interference with nerve function.…”

Section: Introductionmentioning

confidence: 99%

The inhibition of cerebral high affinity receptor sites by lead and mercury compounds

Bondy

Agrawal

1980

Arch Toxicol

View full text Add to dashboard Cite

Abstract. The effect of various concentrations of several lead and mercury compounds upon various high affinity receptor sites within discrete brain regions has been measured. The specific binding of radioactive spiroperidol and quinuclidinyl benzilate to striatal and cortical membranes respectively, was much more severely inhibited in the presence of tri-n-butyl lead acetate than by lead acetate. This suggested that the hydrophobic organic lead derivative was able to interfere with receptor structure more readily than the lead acetate. On the other hand mercuric chloride was more effective in blocking these two neurotransmitter receptor sites than was the organic methylmercuric chloride. This implied that sulfhydryl groups may be within, or proximal to the allosteric binding site. The relative ineffectiveness of all heavy metal compounds studied in blocking the glycine, GABA or the diazepam receptors indicated that the mechanism of binding may not be similar with different receptor proteins. Since micromolar concentrations of some lead and mercury compounds suffice to severely inhibit neurotransmitter binding sites, such a direct interference with postsynaptic events may in part account for the neurological consequences of heavy metal poisoning.

show abstract

“…The manifestations in vivo of massive chronic mercury poisoning are often conspicuous. It is known that high concentrations of methyl-Hg (5 pM) in vivo can exert toxic actions on excitable tissue (20). However, during distribution of small amounts of mercury, effects that are less pronounced than those associated with acute and massive chronic poisoning could be exerted on tissues in the body.…”

mentioning

confidence: 98%

Effects of mercuric ions on isolated guinea-pig ileum

Moberg

1986

Acta Odontologica Scandinavica

View full text Add to dashboard Cite

The possible physiological significance of low concentrations of Hg2+ in the guinea-pig ileum has been investigated. Responses to nerve stimulation by single electrical shocks, acetylcholine (ACh), and histamine (Hi) and the response to ACh of a depolarized preparation were examined. A stimulant effect of Hg2+, in the concentration range of 10 nM-1 microM, dominated in intestine accommodated in biological saline solution. This excitatory effect was probably mainly due to stimulation of a depolarization-coupled initiation of the contraction. The inhibitory effect of Hg2+, 10 nM-1 microM, observed in depolarized muscle was presumably due to a decreased Ca2+ availability for the contractile process. In the higher concentration range, 1-100 microM, a probably direct action on the contractile elements causing irreversible deterioration of the preparation seems to be present.

show abstract

Evidence for a Neuromuscular Disorder in Methylmercury Poisoning

Cited by 41 publications

References 13 publications

Effects of methylmercury on spinal cord afferents and efferents—A review

Effects of methylmercury on spinal cord afferents and efferents—A review

The inhibition of cerebral high affinity receptor sites by lead and mercury compounds

Effects of mercuric ions on isolated guinea-pig ileum

Contact Info

Product

Resources

About