Histochemical Demonstration of Calcium Accumulation in Muscle Fibres after Experimental Organophosphate Poisoning

  title={Histochemical Demonstration of Calcium Accumulation in Muscle Fibres after Experimental Organophosphate Poisoning},
  author={Robert H. Inns and N J Tuckwell and J. E. Bright and Timothy Clive Marrs},
  journal={Human \& Experimental Toxicology},
  pages={245 - 250}
The LD50 of subcutaneously-injected sarin (GB: isopropyl methylphosphonofluoridate) in mice was 172 μg kg-1. Mice were treated with sarin at doses between 25 and 150 μg kg-1, administered subcutaneously. After sacrifice of the animals, the diaphragms were removed and stained for acetylcholinesterase activity and the presence of ionized calcium. Calcium was found in the diaphragms of those mice to which sarin had been administered at doses of 50 μg kg-1 or above. Calcium accumulation was not… Expand
A Histochemical Study of Changes Observed in the Mouse Diaphragm after Organophosphate Poisoning
It was concluded that sarin produced myopathic changes preceded by calcium accumulation, which were rapidly regressing by 5 d and histological appearances were normal by 14 d. Expand
Biochemical Changes Associated with Muscle Fibre Necrosis after Experimental Organophosphate Poisoning
These biochemical markers will prove useful for investigating the possible relationships between the different neuromuscular syndromes occurring in the course of an OP poisoning and potential therapeutic or protective pharmacological measures. Expand
Inhalation toxicity studies of thimet (phorate) in male Swiss albino mouse, Mus musculus: I. Hepatotoxicity.
  • M. Morowati
  • Biology, Medicine
  • Environmental pollution
  • 1997
The results suggest the inhalation of Thimet (Phorate) at the recommended field dose could affect the liver of Mus musculus and both prehepatic and hepatocellular hyperbilirubinaemia. Expand
Success of pyridostigmine, physostigmine, eptastigmine and phosphotriesterase treatments in acute sarin intoxication.
Phosphotriesterase and physostigmine were the most effective treatments against sarin intoxication and protected the brain AChE activities measured 24 h after sarin exposure, respectively, while eptastigmine did not provide any protection from sarin toxicity. Expand
Effects of Organophosphates on Skeletal Muscle
Much of the morbidity and mortality associated with organophosphorus intoxication is due to the effects of these compounds on skeletal muscle and in particular the muscles of respiration. Expand
Biochemical and histopathological changes in serum creatinine and kidney induced by inhalation of Thimet (Phorate) in male Swiss albino mouse, Mus musculus.
  • M. Mohssen
  • Medicine, Biology
  • Environmental research
  • 2001
Investigation of biochemical and histopathological changes in serum creatinine level and kidney of male Swiss albino mouse exposed to the recommended field dose of Thimet suggests impairment of the glomerular function and tubular damage in the kidneys. Expand
Chapter 13 Organophosphate and carbamate poisoning
Electrophysiological studies help to resolve the functional mechanism of OP and CM toxicity and interaction of OPs with other proteins explains inter-individual differences in sensitivity to OP toxicity. Expand
Organophosphate-Induced Intermediate Syndrome
The intermediate syndrome (IMS) following organophosphorus (OP) insecticide poisoning was first described in the mid-1980s and it is now emerging that the degree and extent of muscle weakness may vary following the onset of the IMS, whilst repetitive firing is observed during the acute cholinergic syndrome. Expand
Intermediate Syndrome in Organophosphate Poisoning
The clinical recognition of IMS is no longer problematic for most medical workers in the field, and considerable progress toward the elucidation of the underlying mechanisms has been made in the 10 years following the initial description. Expand
Chapter 40 – Skeletal Muscle
This chapter describes OP nerve agent-induced alterations in structural and functional properties of the muscle, cytotoxicity biomarkers, muscle involvement in tolerance development and in intermediate syndrome, and various strategies in the prevention and treatment of myopathy. Expand


Biochemical and histochemical alterations following acute soman intoxication in the rat.
It can be concluded that soman-induced acute toxicity is directly related to the rate and degree of AChE inhibition and a significant amount of soman binds to non-AChE enzymes with serine sites such as BuChE and carboxylesterases. Expand
Evidence of necrosis in human intercostal muscle following inhalation of an organophosphate insecticide.
Results indicate that acute organophosphate exposure through inhalation can lead to skeletal muscle fiber damage in humans, similar to results obtained by ingestion. Expand
The reversible carbamate, (-)physostigmine, reduces the size of synaptic end plate lesions induced by sarin, an irreversible organophosphate.
Pretreatment of rats with atropine and the reversible esterase inhibitor physostigmine [-)PHY, prior to injection of a lethal dose of the irreversible organophosphate sarin, protects 100% of the animals from lethality and shows that damage to the end plate region of voluntary muscles is also strikingly limited by the same pretreatment. Expand
Myopathic changes in diaphragm of rats fed pyridostigmine bromide subchronically.
It is concluded that subchronic feeding of pyridostigmine bromide induces primarily myopathic rather than neurogenic changes in the diaphragm and that some mechanism of accommodation may be activated that minimizes continued muscle injury. Expand
Paraoxon-induced myopathy: Muscle specificity and acetylcholine involvement
Evidence suggests there may be a critical period of inhibition of ChE activity to initiate the myopathic process and a possible nerve-mediated muscle necrosis in rats treated with Paraoxon. Expand
Pesticide Induced Muscle Necrosis: Mechanisms and Prevention
The nerve agent soman, as well as other organophosphates such as paraoxon and phospholine in concentrations that caused cholinergic symptoms induced a progressive dose-related necrosis in ratExpand
Acute tabun toxicity; biochemical and histochemical consequences in brain and skeletal muscles of rat.
Male Sprague-Dawley rats injected with an acute non-lethal dose of ethyl N,N-dimethylphosphoramidocyanidate (tabun) showed onset of hypercholinergic activity within 10-15 min, and the inhibition of BuChE and CarbE can serve as a protective mechanism against tabun toxicity by reducing the amount available for AChE inhibition. Expand
Agonist-induced myopathy at the neuromuscular junction is mediated by calcium
The results favor the hypothesis that esterase inhibition leads to an agonist-induced myopathy, which is mediated by Ca++ and requires an intact AChR, and could be prevented by inactivating the acetylcholine receptors with alpha- bungarotoxin or by removing Ca++ from the bath with EGTA. Expand
Release of Calcium in the Myoneural Junction
The objective of the investigations was to demonstrate histochemically this release of calcium in muscle fibres, and to suggest that muscular activity results in liberation of bound calcium. Expand
A simple pocedure for localizing calcium ions in tissues and in cells with glyoxal bis (2-hydroxy-anil) (GBHA) has been described. The GBHA molecule, in alcoholic solution made alkaline with NaOH,Expand