PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Developmental neurotoxicity of the organophosphorus insecticide chlorpyrifos: from clinical findings to preclinical models and potential mechanisms.

Abstract Organophosphorus (OP) insecticides are pest-control agents heavily used worldwide. Unfortunately, they are also well known for the toxic effects that they can trigger in humans. Clinical manifestations of an acute exposure of humans to OP insecticides include a well-defined cholinergic crisis that develops as a result of the irreversible inhibition of acetylcholinesterase (AChE), the enzyme that hydrolyzes the neurotransmitter acetylcholine (ACh). Prolonged exposures to levels of OP insecticides that are insufficient to trigger signs of acute intoxication, which are hereafter referred to as subacute exposures, have also been associated with neurological deficits. In particular, epidemiological studies have reported statistically significant correlations between prenatal subacute exposures to OP insecticides, including chlorpyrifos, and neurological deficits that range from cognitive impairments to tremors in childhood. The primary objectives of this article are: (i) to address the short- and long-term neurological issues that have been associated with acute and subacute exposures of humans to OP insecticides, especially early in life (ii) to discuss the translational relevance of animal models of developmental exposure to OP insecticides, and (iii) to review mechanisms that are likely to contribute to the developmental neurotoxicity of OP insecticides. Most of the discussion will be focused on chlorpyrifos, the top-selling OP insecticide in the United States and throughout the world. These points are critical for the identification and development of safe and effective interventions to counter and/or prevent the neurotoxic effects of these chemicals in the developing brain. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
PMID
Related Publications

Inhibition of hen brain acetylcholinesterase and neurotoxic esterase by chlorpyrifos in vivo and kinetics of inhibition by chlorpyrifos oxon in vitro: application to assessment of neuropathic risk.

Comparative effects of oral chlorpyrifos exposure on cholinesterase activity and muscarinic receptor binding in neonatal and adult rat heart.

Longitudinal assessment of occupational exposures to the organophosphorous insecticides chlorpyrifos and profenofos in Egyptian cotton field workers.

Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds.

Assessment of the neurotoxic potential of chlorpyrifos relative to other organophosphorus compounds: a critical review of the literature.

Authors

Mayor MeshTerms
Keywords

acetylcholinesterase

brain

chlorpyrifos

development

learning

memory

Journal Title journal of neurochemistry
Publication Year Start




PMID- 28791702
OWN - NLM
STAT- In-Process
DA  - 20170809
LR  - 20170809
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 142 Suppl 2
DP  - 2017 Aug
TI  - Developmental neurotoxicity of the organophosphorus insecticide chlorpyrifos:
      from clinical findings to preclinical models and potential mechanisms.
PG  - 162-177
LID - 10.1111/jnc.14077 [doi]
AB  - Organophosphorus (OP) insecticides are pest-control agents heavily used
      worldwide. Unfortunately, they are also well known for the toxic effects that
      they can trigger in humans. Clinical manifestations of an acute exposure of
      humans to OP insecticides include a well-defined cholinergic crisis that develops
      as a result of the irreversible inhibition of acetylcholinesterase (AChE), the
      enzyme that hydrolyzes the neurotransmitter acetylcholine (ACh). Prolonged
      exposures to levels of OP insecticides that are insufficient to trigger signs of 
      acute intoxication, which are hereafter referred to as subacute exposures, have
      also been associated with neurological deficits. In particular, epidemiological
      studies have reported statistically significant correlations between prenatal
      subacute exposures to OP insecticides, including chlorpyrifos, and neurological
      deficits that range from cognitive impairments to tremors in childhood. The
      primary objectives of this article are: (i) to address the short- and long-term
      neurological issues that have been associated with acute and subacute exposures
      of humans to OP insecticides, especially early in life (ii) to discuss the
      translational relevance of animal models of developmental exposure to OP
      insecticides, and (iii) to review mechanisms that are likely to contribute to the
      developmental neurotoxicity of OP insecticides. Most of the discussion will be
      focused on chlorpyrifos, the top-selling OP insecticide in the United States and 
      throughout the world. These points are critical for the identification and
      development of safe and effective interventions to counter and/or prevent the
      neurotoxic effects of these chemicals in the developing brain. This is an article
      for the special issue XVth International Symposium on Cholinergic Mechanisms.
CI  - (c) 2017 International Society for Neurochemistry.
FAU - Burke, Richard D
AU  - Burke RD
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
FAU - Todd, Spencer W
AU  - Todd SW
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
FAU - Lumsden, Eric
AU  - Lumsden E
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
FAU - Mullins, Roger J
AU  - Mullins RJ
AD  - Department of Diagnostic Radiology, University of Maryland School of Medicine,
      Baltimore, Maryland, USA.
FAU - Mamczarz, Jacek
AU  - Mamczarz J
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
FAU - Fawcett, William P
AU  - Fawcett WP
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
FAU - Gullapalli, Rao P
AU  - Gullapalli RP
AD  - Department of Diagnostic Radiology, University of Maryland School of Medicine,
      Baltimore, Maryland, USA.
FAU - Randall, William R
AU  - Randall WR
AD  - Department of Pharmacology, University of Maryland School of Medicine, Baltimore,
      Maryland, USA.
FAU - Pereira, Edna F R
AU  - Pereira EFR
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
AD  - Department of Pharmacology, University of Maryland School of Medicine, Baltimore,
      Maryland, USA.
FAU - Albuquerque, Edson X
AU  - Albuquerque EX
AD  - Division of Translational Toxicology, Department of Epidemiology and Public
      Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.
AD  - Department of Pharmacology, University of Maryland School of Medicine, Baltimore,
      Maryland, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
OTO - NOTNLM
OT  - acetylcholinesterase
OT  - brain
OT  - chlorpyrifos
OT  - development
OT  - learning
OT  - memory
EDAT- 2017/08/10 06:00
MHDA- 2017/08/10 06:00
CRDT- 2017/08/10 06:00
PHST- 2017/04/13 [received]
PHST- 2017/05/16 [revised]
PHST- 2017/05/18 [accepted]
AID - 10.1111/jnc.14077 [doi]
PST - ppublish
SO  - J Neurochem. 2017 Aug;142 Suppl 2:162-177. doi: 10.1111/jnc.14077.