The Neurotoxicity of Pesticides

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Environmental Neuroscience".

Deadline for manuscript submissions: closed (25 May 2023) | Viewed by 6173

Special Issue Editor

Special Issue Information

Dear Colleagues,

Pesticides encompass a broad chemical group that primarily includes herbicides, fungicides, rodenticides, and insecticides. Pesticides play an important role in sustained and economically viable agricultural production to prevent the disease and infestation of crops. However, although pesticides are designed with the intention of targeting a particular pest(s), the impact on the health of non-target species, such as humans, is apparent. For example, the insecticide class includes pyrethroids, carbamates, organochlorines, and the majorly employed organophosphorus pesticides (OPs). OPs target acetylcholinesterase within the central nervous system and neuromuscular junctions with thousands of annual intentional and non-intentional human poisonings. Hence, there is a growing body of scientific evidence that links acute or chronic pesticide exposure to neurotoxicity, more so when the brain is particularly vulnerable, for example, due to damage or incomplete development of the blood–brain barrier. In this Special Issue, we aim to bring together scientific articles and reviews that specifically focus upon the neurotoxicity of pesticides. This will include in vitro (cell-based) studies or those that utilize in vivo animal models, or ex vivo tissue as well as the epidemiology of exposures.  The collective aim of this Special Issue would, therefore, be to provide a comprehensive collection of focused articles that will provide a useful and up-to-date resource for scientists working in this field.

Dr. Wayne Carter
Guest Editor

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Keywords

  • biomarkers of exposure
  • herbicides
  • fungicides
  • insecticides
  • neurotoxicity
  • neurodegeneration
  • organophosphates
  • pesticides

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Published Papers (2 papers)

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Research

20 pages, 4690 KiB  
Article
Differentiated Neurons Are More Vulnerable to Organophosphate and Carbamate Neurotoxicity than Undifferentiated Neurons Due to the Induction of Redox Stress and Accumulate Oxidatively-Damaged Proteins
by Anusha W. Mudyanselage, Buddhika C. Wijamunige, Artur Kocon and Wayne G. Carter
Brain Sci. 2023, 13(5), 728; https://doi.org/10.3390/brainsci13050728 - 26 Apr 2023
Cited by 8 | Viewed by 1881
Abstract
Organophosphate (OP) and carbamate pesticides are toxic to pests through targeted inhibition of acetylcholinesterase (AChE). However, OPs and carbamates may be harmful to non-target species including humans and could induce developmental neurotoxicity if differentiated or differentiating neurons are particularly vulnerable to neurotoxicant exposures. [...] Read more.
Organophosphate (OP) and carbamate pesticides are toxic to pests through targeted inhibition of acetylcholinesterase (AChE). However, OPs and carbamates may be harmful to non-target species including humans and could induce developmental neurotoxicity if differentiated or differentiating neurons are particularly vulnerable to neurotoxicant exposures. Hence, this study compared the neurotoxicity of OPs, chlorpyrifos-oxon (CPO), and azamethiphos (AZO) and the carbamate pesticide, aldicarb, to undifferentiated versus differentiated SH-SY5Y neuroblastoma cells. OP and carbamate concentration-response curves for cell viability were undertaken using 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays and cellular bioenergetic capacity assessed via quantitation of cellular ATP levels. Concentration-response curves for inhibition of cellular AChE activity were also generated and the production of reactive oxygen species (ROS) was monitored using a 2′,7′-dichlorofluorescein diacetate (DCFDA) assay. The OPs and aldicarb reduced cell viability, cellular ATP levels, and neurite outgrowth in a concentration-dependent fashion, from a threshold concentration of ≥10 µM. Neurotoxic potency was in the order AZO > CPO > aldicarb for undifferentiated cells but CPO > AZO > aldicarb for differentiated cells and this toxic potency of CPO reflected its more extensive induction of reactive oxygen species (ROS) and generation of carbonylated proteins that were characterized by western blotting. Hence, the relative neurotoxicity of the OPs and aldicarb in part reflects non-cholinergic mechanisms that are likely to contribute to developmental neurotoxicity. Full article
(This article belongs to the Special Issue The Neurotoxicity of Pesticides)
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23 pages, 3554 KiB  
Article
An Investigation of the Neurotoxic Effects of Malathion, Chlorpyrifos, and Paraquat to Different Brain Regions
by Ekramy Elmorsy, Ayat Al-Ghafari, Huda Al Doghaither, Mohamed Salama and Wayne G. Carter
Brain Sci. 2022, 12(8), 975; https://doi.org/10.3390/brainsci12080975 - 24 Jul 2022
Cited by 12 | Viewed by 3098
Abstract
Acute or chronic exposures to pesticides have been linked to neurotoxicity and the potential development of neurodegenerative diseases (NDDs). This study aimed to consider the neurotoxicity of three widely utilized pesticides: malathion, chlorpyrifos, and paraquat within the hippocampus (HC), corpus striatum (CS), cerebellum [...] Read more.
Acute or chronic exposures to pesticides have been linked to neurotoxicity and the potential development of neurodegenerative diseases (NDDs). This study aimed to consider the neurotoxicity of three widely utilized pesticides: malathion, chlorpyrifos, and paraquat within the hippocampus (HC), corpus striatum (CS), cerebellum (CER), and cerebral cortex (CC). Neurotoxicity was evaluated at relatively low, medium, and high pesticide dosages. All pesticides inhibited acetylcholinesterase (AChE) and neuropathy target esterase (NTE) in each of the brain regions, but esterase inhibition was greatest in the HC and CS. Each of the pesticides also induced greater disruption to cellular bioenergetics within the HC and CS, and this was monitored via inhibition of mitochondrial complex enzymes I and II, reduced ATP levels, and increased lactate production. Similarly, the HC and CS were more vulnerable to redox stress, with greater inhibition of the antioxidant enzymes catalase and superoxide dismutase and increased lipid peroxidation. All pesticides induced the production of nuclear Nrf2 in a dose-dependent manner. Collectively, these results show that pesticides disrupt cellular bioenergetics and that the HC and CS are more susceptible to pesticide effects than the CER and CC. Full article
(This article belongs to the Special Issue The Neurotoxicity of Pesticides)
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