Dietary Transfer of Zinc Oxide Nanoparticles Induces Locomotive Defects Associated with GABAergic Motor Neuron Damage in Caenorhabditis elegans

Abstract

The widespread use of zinc oxide nanoparticles (ZnO-NPs) and their release into the environment have raised concerns about the potential toxicity caused by dietary transfer. However, the toxic effects and the mechanisms of dietary transfer of ZnO-NPs have rarely been investigated. We employed the bacteria-feeding nematode Caenorhabditis elegans as the model organism to investigate the neurotoxicity induced by exposure to ZnO-NPs via trophic transfer. Our results showed that ZnO-NPs accumulated in the intestine of C. elegans and also in Escherichia coli OP50 that they ingested. Additionally, impairment of locomotive behaviors, including decreased body bending and head thrashing frequencies, were observed in C. elegans that were fed E. coli pre-treated with ZnO-NPs, which might have occurred because of damage to the D-type GABAergic motor neurons. However, these toxic effects were not apparent in C. elegans that were fed E. coli pre-treated with zinc chloride (ZnCl2). Therefore, ZnO-NPs particulates, rather than released Zn ions, damage the D-type GABAergic motor neurons and adversely affect the locomotive behaviors of C. elegans via dietary transfer.

Toxicology of carbon nanomaterials in the Caenorhabditis elegans model: current status, characterization, and perspectives for testing harmonization

“…As its developmental physiology is sensitive to nutrient depletion (Kaplan et al, 2018), a decrease in nematode growth, reproduction, and fertility was observed. Other researchers noticed a possible dietary transfer of NMs to the food chain when C. elegans was fed with E. coli after its interaction with the tested NMs (Priyam et al, 2021;How and Huang, 2023).…”

Comprehensive Neurotoxicity of Lead Halide Perovskite Nanocrystals in Nematode Caenorhabditis elegans

“…[27] Thus, the neurotoxicity of many quan-tum dots (QDs) and nanoparticles (NPs) was performed using C. elegans. [28][29][30][31][32][33][34] Typically, in 2012, in the investigation of the neurotoxicity of Al 2 O 3 -NPs, Li et al [33] employed the model organism C. elegans to examine how the transmission of various neurotransmitters contributes to the development of neurotoxicity, as evidenced by changes in locomotion behavior. Their findings show that exposure to Al 2 O 3 -NPs affects the locomotion behavior of nematodes mainly by disrupting their glutamatergic, dopaminergic, and serotoninergic systems.…”

Nanoparticles in the Environment and Nanotoxicology

“…This Special Issue aims to provide recent novel research findings of nanoparticles on their determination, detection, and degradation in the environment as well as the toxicity of nanoparticles. This Special Issue provides ten outstanding papers comprising two review articles and eight research articles with a range of original contributions detailing various types of nanoparticles in terms of their toxicity [ 1 , 2 , 3 , 4 , 5 ], removal of antibiotics [ 2 , 6 ], and behavior in natural environments [ 3 , 7 , 8 ].…”

“…This Special Issue collected various research papers addressing the toxic effects of various types of nanoparticles using different tested organisms in various media. For example, How and Huang [ 1 ] utilized the soil nematode Caenorhabditis elegans to investigate neurotoxicity caused by zinc oxide nanoparticles (ZnO-NPs) exposure. They reported that ZnO-NPs particulates attribute to the neurotoxicity in C. elegan s via dietary transfer [ 1 ].…”

“…For example, How and Huang [ 1 ] utilized the soil nematode Caenorhabditis elegans to investigate neurotoxicity caused by zinc oxide nanoparticles (ZnO-NPs) exposure. They reported that ZnO-NPs particulates attribute to the neurotoxicity in C. elegan s via dietary transfer [ 1 ]. Le et al [ 4 ] synthesized nano-sized artificial black carbon (aBC), examining its toxicity on A549 human lung cells, and found that aBC with an increased content of the oxygen functional group displayed higher toxicity to A549 cells.…”