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The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body. Specifically, acetylcholinesterase (AChE), the enzyme that normally and constantly breaks down acetylcholine, is inhibited by the organophosphate substance.
Organophosphate-induced delayed neuropathy (OPIDN), also called organophosphate-induced delayed polyneuropathy (OPIDP), is a neuropathy caused by killing of neurons in the central nervous system, especially in the spinal cord, as a result of acute or chronic organophosphate poisoning.
Health effects of pesticides may be acute or delayed in those who are exposed. [1] Acute effects can include pesticide poisoning, which may be a medical emergency. [2] Strong evidence exists for other, long-term negative health outcomes from pesticide exposure including birth defects, fetal death, [3] neurodevelopmental disorder, [4] cancer, and neurologic illness including Parkinson's disease ...
Organophosphate insecticides are acetylcholinesterase inhibitors, which disrupt the transmission of nerve signals in exposed organisms, with fatal results. The risk of human death through organophosphate poisoning [32] was obvious from the start and led to efforts to lower toxicity against mammals while not reducing efficacy against insects ...
Organophosphate poisoning is not common in the developed world. Most cases of terbufos poisoning occur in the developing world, where protection against pesticides is scarce, but compounds such as terbufos are widespread, uncontrolled by a government and readily available for farmers.
In the treatment of organophosphate toxicity, cholinesterase reactivators such as Pralidoxime reactivate inhibited AChE at peripheral nicotinic receptors.Since AChE mediates effects on both nicotinic and muscarinic receptors, cholinesterase reactivators are co-administered with muscarinic antagonists, primarily atropine.
Sulfotep causes an organophosphate poisoning. This means that it had an effect on the activity of cholinesterase. There are differences for the indications of a sulfotep poisoning between inhalation, ingestion, intake by the skin and intake by the eyes.
This results in abnormal accumulation of ACh within the nervous system. Diazinon, although a thiophosphoric ester, shares a common mechanism of toxicity with other organophosphate insecticides such as chlorpyrifos, malathion and parathion, and is not very effective against the organophosphate-resistant insect populations. [citation needed]