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Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase.

Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase. Research Abstract Details 

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  • Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase. Abstract Text:

    floria pancettiFloria Pancetti,cristina olmosCristina Olmos,alexies dagnino-subiabreAlexies Dagnino-Subiabre,carlos rozasCarlos Rozas,bernardo moralesBernardo Morales,floria pancettiFloria Pancetti,cristina olmosCristina Olmos,alexies dagnino-subiabreAlexies Dagnino-Subiabre,carlos rozasCarlos Rozas,bernardo moralesBernardo Morales,

    Organophosphate pesticides have been classically described as inhibitors of acetylcholinesterase (AChE) activity in insects and invertebrates. However, there is now more evidence supporting the hypothesis that these compounds also act through noncholinergic pathways, especially those related to cognitive processes. The enzyme acylpeptide hydrolase was identified as a new target for organophosphate pesticides. This enzyme is more sensitive than AChE to some organophosphates (OP), including dichlorvos, which is the parent compound for metrifonate, a therapeutic agent used in the treatment of cognitive impairment associated to Alzheimer's disease. Therefore, there is some doubt as to whether the mechanism of action of this drug is mediated by a potentiation of cholinergic transmission. However, the direct action of acylpeptide hydrolase in cognitive processes and the physiological and molecular mechanisms underlying subacute exposure to OP have yet to be demonstrated. This review deals with evidence demonstrating the existence of mechanisms of actions of OP, which are independent of cholinergic pathway potentiation and which have an effect on cognitive processes. In addition, the possible participation of the enzyme acylpeptide hydrolase in these processes is also discussed. Finally, the possibility of using this enzyme activity as a new biomarker for exposure to OP is considered.

    Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase. Publishing Authors By Initials

    f pancettiF Pancetti,c olmosC Olmos,a dagnino-subiabreA Dagnino-Subiabre,c rozasC Rozas,b moralesB Morales,f pancettiF Pancetti,c olmosC Olmos,a dagnino-subiabreA Dagnino-Subiabre,c rozasC Rozas,b moralesB Morales,

    For similar abstracts research abstracts see: abstracts research

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    Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of toxicology and environmental health. Pa

    VOLUME: 10

    Page Numbers: 623-30

    Journal Abbreviation:

    ISSN: 1521-6950

    DAY: 30

    MONTH: Dec

    YEAR: 2007

    Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase. Information

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    LANGUAGE: eng

    NlmUniqueID: 9802627

    Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase. Keywords Mesh Terms:

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    Grant and Affiliation Information for Noncholinesterase effects induced by organophosphate pesticides and their relationship to cognitive processes: implication for the action of acylpeptide hydrolase.

    AFFILIATION: Laboratory of Environmental Neurotoxicology, Department of Biological Sciences, Faculty of Medicine, Universidad Católica del Norte, Coquimbo, Chile. pancetti@ucn.cl

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Toxicol Environ Health B Cri

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