[Neurotoxicology of pesticides]

Brain Nerve. 2015 Jan;67(1):39-48. doi: 10.11477/mf.1416200085.
[Article in Japanese]

Abstract

Pesticides have been used for many years for preventing, destroying, repelling, or mitigating pests such as insects, rodents, and weeds. However, most pesticides are not completely specific for pests and can also induce damage to the human nervous system. In particular, insecticides often directly targets the nervous system by affecting major targets such as the neuro-transmitter metabolism, neuronal receptors, and ion channels; acetylcholine (ACh) esterase for organo-phosphates and carbamates, nicotinic ACh receptor for neonicotinoids, γ-aminobutyric acid receptors/chloride channels for organochlorides and fipronil, and voltage-gated sodium channel for pyrethroids. Additional targets include sites in the sodium channels, glutamate-gated chloride channels, and octopamine and ryanodine receptors. Several pesticides also produce adverse neurological effects indirectly by disrupting the general cellular mechanisms that support the high metabolic activity of the nervous system. Nowadays, more potent pesticides are being developed as replacements for the older, harmful ones. Pesticide neurotoxicity in humans may involve the central or peripheral nervous system or both and may induce typical neuronal damage in case of acute poisoning even by new agents. However, whether effect of exposure to pesticides at below acute-poisoning threshold level remains unclear. Moreover, neurotoxicology for behavioral and higher-brain function remains an unresolved and a challenging problem.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Animals
  • Chloride Channels
  • Humans
  • Nervous System / drug effects*
  • Neurons / drug effects*
  • Pesticides / toxicity*
  • Receptors, Nicotinic / drug effects
  • Sodium Channels / drug effects

Substances

  • Chloride Channels
  • Pesticides
  • Receptors, Nicotinic
  • Sodium Channels
  • glutamate-gated chloride channels