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The role of Sod-2 in different types of neuronal damage and behavioral changes induced by polystyrene nanoplastics in Caenorhabditis elegans
Summary
Researchers used the roundworm C. elegans to study how polystyrene nanoplastics damage the nervous system at concentrations found in agricultural soils. They found that the nanoplastics caused nerve damage in a specific order, first affecting dopamine neurons, then acetylcholine neurons, and finally GABA neurons, through a process involving oxidative stress and reduced antioxidant protein levels. The study identifies a specific cellular pathway through which nanoplastics cause neurotoxic effects, and shows that a mitochondrial antioxidant could help alleviate the damage.
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.
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