Speakers - NWC 2024

Abstract

The continuous increase in plastic production and use, estimated at 33 billion tons by 2050, has created a severe environmental crisis, highlighting the need to understand the effects of plastic pollution, in particular its potential impact on human health. It was found that under the influence of physical forces, plastic waste disintegrates into nano- and microparticles (NPs and MPs). Particulate matter is known to exert toxic effects in biological systems due to its high reactivity. Therefore, although plastics are considered biochemically inactive and relatively non-toxic, their nanoparticulate form may pose a health risk. Polystyrene (PS) is one of the most widely used plastics. Therefore, polystyrene nanoparticles (PS-NPs) serve as model particles to understand cellular uptake and biological effects in in vitro studies. Evidence shows that exposure to PS-NPs increases oxidative stress markers, including reactive oxygen species (ROS). Still, the observed effects depend on particle size, concentration, and exposure time, indicating a complex relationship between NPs and cells. The toxic effects of nanoplastic, particularly neurotoxic effects, remain unclear and require detailed research. Therefore, this study aimed to investigate the impact of PS-NPs in primary astrocytes and neurons, particularly on oxidative stress. Cells were cultured in a complete growth medium with appropriate supplements, and then the cultures were exposed to PS-NPs in a concentration range of 1, 25, and 50 µg/mL at different time points (24, 48, 72 h). The size distribution and shape of the NPs were determined using transmission electron microscopy. The nanoparticles were spherical in shape and uniform in size, approximately 25 nm, and did not aggregate in the solution. The cytotoxic effect of PS-NPs was assessed using LDH assay, which revealed significant concentration- and time-dependent increases in enzyme release in both cell types. However, neurons were more susceptible than astrocytes. A significant increase in ROS levels was also observed in both cell types exposed to PS-NPs compared to the control group. If unbalanced with cellular antioxidant systems, ROS can lead to cell damage and death. Therefore, total antioxidant capacity (TAC) was measured, reflecting an overall level of antioxidants activated in response to exposure to PS-NPs. Moreover, the expression of selected antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), as well as the level of glutathione (GSH), which is the major non-enzymatic antioxidant involved in mitigating ROS-induced cell injury, were examined. The results indicate the damage to the antioxidant defense system, which, combined with increased ROS production, may result in oxidative stress.

In summary, after entering neural cells such as astrocytes and neurons, PS-NPs exhibit a cytotoxic effect, almost partially related to oxidative stress. Although oxidative stress appears to be the primary mechanism underlying the neurotoxicity of PS-NPs, other mechanisms are not excluded and require further investigation, particularly in the context of various physico-chemical characteristics of the NPs.

The National Science Center financed the study, grant no 2021/41/B/NZ7/02183