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Monocrotophos toxicity and bioenergetics of muscle weakness in the rat
- Source :
- Toxicology. 277:6-10
- Publication Year :
- 2010
- Publisher :
- Elsevier BV, 2010.
-
Abstract
- Acute organophosphate pesticide poisoning is a common medical emergency with high fatality in agricultural communities of Asia. Organophosphate compounds inhibit acetylcholinesterase and prolonged neuromuscular weakness is a major cause of morbidity and mortality of poisoning. Organophosphate pesticide induced muscle weakness may not only arise from inhibition of acetylcholinesterase but also from non-cholinergic pathomechanisms, particularly mitochondrial dysfunction, affecting the production of sufficient ATP for muscle function. This study examined whether muscle weakness in rats subject to monocrotophos toxicity (0.8LD 50 ) was caused by inhibition of ATP synthesis, by oxidative phosphorylation and glycolysis, in addition to inhibition of muscle acetylcholinesterase. Severe muscle weakness in rats following monocrotophos administration was associated with inhibition of muscle acetylcholinesterase (30–60%) but not with reduced ATP production. The rats rapidly recovered muscle strength with no treatment. The ability of rats to spontaneously reactivate dimethyoxy phosphorylated acetylcholinesterase and efficiently detoxify organophosphates may prevent severe inhibition of muscle acetylcholinesterase following acute severe monocrotophos poisoning. This may protect rodents against the development of prolonged muscle weakness induced by organophosphates.
- Subjects :
- Insecticides
medicine.medical_specialty
Oxidative phosphorylation
Biology
Toxicology
chemistry.chemical_compound
Internal medicine
medicine
Animals
Glycolysis
Rats, Wistar
Energy charge
Muscle, Skeletal
Muscle Weakness
Organophosphate
Muscle weakness
Acetylcholinesterase
Rats
Endocrinology
chemistry
Monocrotophos
Toxicity
Female
medicine.symptom
Energy Metabolism
Subjects
Details
- ISSN :
- 0300483X
- Volume :
- 277
- Database :
- OpenAIRE
- Journal :
- Toxicology
- Accession number :
- edsair.doi.dedup.....0511aa925a1c74401dac8e0d9323dc2b