Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

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Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

Organophosphorus (OPs) compounds are widely used as insecticides, plasticizers, and fuel additives. These compounds potently inhibit acetylcholinesterase (AChE), the enzyme that inactivates acetylcholine at neuronal synapses, and acute exposure to high OP levels can cause cholinergic crisis in humans and animals. Evidence further suggests that repeated exposure to lower OP levels insufficient t...

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Side effects of organophosphorus compounds: delayed neurotoxicity.

Many organophosphorus compounds produce a chronic toxicity that has been classified as a dying-back process in which the long axons are particularly affected. Recent evidence indicates that an essential first step in the production of the lesion is the phosphorylation of a protein that is able to hydrolyse substrates such as phenyl phenylacetate. The esterase activity of the protein is inhibite...

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[Structure-reactivity relationships and delayed neurotoxicity of organophosphorus compounds].

A correlation has been found between the reactivity in the alkaline hydrolysis reaction of a new series of organophosphates and their ability or disability to produce the clinical manifestations of delayed neurotoxicity in hen. At a dose of 1000 mg/kg only compounds exceeding a lower limit of reactivity (about 6x10-2 M-1S-1) are active.

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Studies on the delayed neurotoxicity of organophosphorus compounds- (I).

Delayed neurotoxicity experiments of an organophosphorus compound, TOCP, on hens and quails were carried out. The animals were orally exposed with TOCP in dose of 400 mg/kg, and maintained for 25 and 50 days under observation, respectively. They were sacrificed and dissected at different periods after the exposure, and the histopathological examinations were made on those animals. During the pe...

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Protein adducts as biomarkers of exposure to organophosphorus compounds.

Exposure to organophosphorus (OP) compounds can lead to serious neurological damage or death. Following bioactivation by the liver cytochromes P450, the OP metabolites produced are potent inhibitors of serine active-site enzymes including esterases, proteases and lipases. OPs may form adducts on other cellular proteins. Blood cholinesterases (ChEs) have long served as biomarkers of OP exposure ...

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ژورنال

عنوان ژورنال: Frontiers in Neuroscience

سال: 2017

ISSN: 1662-453X

DOI: 10.3389/fnins.2016.00590