Evaluation of Pesticide Toxicities with Differing Mechanisms UsingCaenorhabditis elegans

Abstract

The aim of this study was to (1) determine whether model organism Caenorhabditis elegans was sensitive to pesticides at the maximum concentration limits regulated by national agency standards, and (2) examine the multi-biological toxicities occurring as a result of exposure to pesticides. Five pesticides, namely, chlorpyrifos, imibacloprid, buprofezin, cyhalothrin, and glyphosate, with four different mechanisms of action were selected for the investigation. In accordance with national agency requirements, 4 exposed groups were used for each tested pesticide with the concentration scales ranging from 1.0 x 10(-3) to 1 mg/L. L4 larvae were exposed for 24 and 72 h, respectively. Endpoints of locomotion, propagation, and development were selected for the assay as parameters of toxicity. After exposure for 24 h, both the body bend frequency and head thrash frequency of nematodes exposed to chlorpyrifos, imibacloprid, and cyhalothrin decreased in a concentration-dependent manner, and there were significant differences between exposed groups at maximum concentration level (MCL) compared to control. The generation time of nematodes exposed to buprofezin 24 h significantly increased in a concentration-dependent manner in the highest exposed group. When exposed for 72 h, the body bend frequency and head thrash frequency of nematodes exposed to cyhalothrin markedly decreased at MCL. The generation time and brood size of nematodes exposed to buprofezin were reduced in a concentration-dependent manner. The behavior of nematodes was sensitive to pesticides with neurotoxic properties, while pesticides affecting insect growth modified the reproductive system. The effects of pesticides on nematodes exposed for 24 h appeared more sensitive than with exposure for 72 h. Caenorhabditis elegans may thus be used for assessing the adverse effects of pesticide residues in aquatic environment.

The nematode Caenorhabditis elegans as an integrated toxicological tool to assess water quality and pollution

“…This aspect reinforces the concept that there must be other substances or chemicals in the water samples that were not detected a priori but even so exert weighty toxicological effects. Several reports showed that C. elegans was sensitive to different substances such as pesticides, heavy metals and toxins (Höss et al, 2013;Jiang et al, 2016;Lewis et al, 2013;Negga et al, 2011;Ruan et al, 2009;Yunhui et al, 2009). So it is possible that C. elegans toxicity could be explained by pollutants derived from the anthropogenic activities developed in the area (like agriculture, livestock and recreations).…”

“…The use of advanced analytical technologies such as high-performance liquid chromatography, gas chromatography-mass spectrometry and atomic absorption makes it possible to detect a wider range of pollutants (Ju et al, 2010;Ruan et al, 2009). Still, all those technologies fail to identify all of the pollutants and their interactions, which are critical to assess the aquatic ecological status.…”

Assessment of food toxicology

“…More than 50% of human genes have functional orthologs in C. elegans and all 959 somatic cells of the worms have been characterized with respect to lineage [46,150,151]. As for D. melanogaster, a variety of molecular tools provide the availability of a large number of transgenic strains suited for a differential toxicity screening by high-throughput genomic studies [46, Page 21 of 43 A c c e p t e d M a n u s c r i p t [150][151][152]. Since C. elegans is capable of rudimentary learning and many neurotransmitters are well conserved it is also well suited for neurotoxicity testing [151,153,154].…”

Caenorhabditis elegans: An Emerging Model System for Pesticide Neurotoxicity

“…Since then, C. elegans has been valuable in generating data in neurotoxicity studies involving OPs [126,127]. Importantly, studies have shown that the toxicity rank and mechanism of action in C. elegans are comparable to those observed in more traditional mammalian models [128].…”