The role of Sod-2 in different types of neuronal damage and behavioral changes induced by polystyrene nanoplastics in Caenorhabditis elegans.

Polystyrene nanoplastics (PS-NPs) have been demonstrated to accumulate in organisms especially from soil and exhibit neurotoxicity. However, the specific mechanisms by which PS-NPs caused neurotoxic effects remain largely unexplored. In this study, we employed PS-NPs with a diameter of 50 nm as the toxicant and used estimated exposure concentrations which are similar to those found in Chinese agricultural soil (i.e., 0, 1, 5 and 10 μg/mL). We found that PS-NPs induced significant neurotoxicity and behavioral damage in nematodes. Taking advantage of neuronal-specific reporter nematodes, we unveiled the order of neuronal damage induced by PS-NPs being DAergic neurons, followed by Achergic neurons and GABAergic neurons. Additionally, PS-NPs significantly reduced the neurotransmitter levels corresponding to these three types of neurons, with the order of reduction being Ach followed by DA and GABA. Moreover, we demonstrated that PS-NPs led to an increase in ROS production, the activation of gst-4 and a decrease in Sod-2 protein content. Furthermore, we unveiled that Sod-2 could suppress the generation of ROS induced by PS-NPs. Then we proved that the pretreatment with mitochondrial ROS scavenger Mitoquinone (Mito Q) was able to alleviate PS-NPs-induced neurotoxic effects and behavioral damage by scavenging ROS and subsequently regulating Sod-2 protein expression. In summary, we have demonstrated for the first time that ROS-mediated reduction of Sod-2 protein plays a crucial role in PS-NPs-induced neurotoxicity and behavioral damage. Furthermore, Mito Q shows potential therapeutic value in alleviating the toxic effects of PS-NPs, providing new insights for the prevention and treatment of PS-NPs-induced neurotoxicity.