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

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 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 and also in OP50 that they ingested. Additionally, impairment of locomotive behaviors, including decreased body bending and head thrashing frequencies, were observed in that were fed 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 that were fed pre-treated with zinc chloride (ZnCl). Therefore, ZnO-NPs particulates, rather than released Zn ions, damage the D-type GABAergic motor neurons and adversely affect the locomotive behaviors of via dietary transfer.