Compound effect and mechanism of oxidative damage induced by nanoplastics and benzo [a] pyrene

Nanoplastics and polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in soil environments. In order to objectively evaluate the toxic interaction between polystyrene nanoplastics (PS NPs) and benzo [a] pyrene (BaP), oxidative damage at the level of earthworm cells and biomacromolecules was investigated by experiments combined with molecular dynamics simulation. Studies on cells reveal that PS NPs and BaP had synergistic toxicity when it came to causing oxidative stress. Cellular reactive oxygen species (ROS) levels under combined pollutant exposure were 24% and 19% higher, respectively than when PS NPs and BaP were exposed alone (compared to the blank group). In addition, BaP and PS NPs inhibited the ability of CAT to decompose H2O2 by affecting the structure of the proximal amino acid Tyr 357 in the active center of CAT, which exacerbated oxidative stress to a certain extent. Therefore, the synergistic toxic effect of BaP and PS NPs is due to the mutual complement of the two to the induction of protein structural looseness, and the strengthening of the stability of the conjugate (CAT-BaP-PS) under the weak interaction. This work provides a new perspective and approach on how to talk about the toxicity of combined pollutants.

Automated summary

Through combined experimental and simulation studies, it was found that polystyrene nanoplastics (PS NPs) and benzo[a]pyrene (BaP) exhibit synergistic toxicity in inducing oxidative stress. The cellular reactive oxygen species (ROS) levels were higher under co-exposure of PS NPs and BaP compared to individual exposure. Furthermore, BaP and PS NPs inhibited the decomposition of H2O2 by affecting the structure of the enzyme CAT, exacerbating oxidative stress. This study provides a new perspective and approach for understanding the toxicity of combined pollutants.