RESUMEN
Polystyrene nanoplastics are a novel class of pollutants. They are easily absorbed by living organisms, and their potential toxicity has raised concerns. However, the impact of polystyrene nanoplastics on auditory organs remains unknown. Here, our results showed that polystyrene nanoplastics entered the cochlea of mice, HEI-OC1 cells, and lateral line hair cells of zebrafish, causing cellular injury and increasing apoptosis. Additionally, we found that exposure to polystyrene nanoplastics resulted in a significant elevation in the auditory brainstem response thresholds, a loss of auditory sensory hair cells, stereocilia degeneration and a decrease in expression of Claudin-5 and Occludin proteins at the blood-lymphatic barrier in mice. We also observed a significant decrease in the acoustic alarm response of zebrafish after exposure to polystyrene nanoplastics. Mechanistic analysis revealed that polystyrene nanoplastics induced up-regulation of the Nrf2/HO-1 pathway, increased levels of malondialdehyde, and decreased superoxide dismutase and catalase levels in cochlea and HEI-OC1 cells. Furthermore, we observed that the expression of ferroptosis-related indicators GPX4 and SLC7A11 decreased as well as increased expression of ACLS4 in cochlea and HEI-OC1 cells. This study also revealed that polystyrene nanoplastics exposure led to increased expression of the inflammatory factors TNF-α, IL-1ß and COX2 in cochlea and HEI-OC1 cells. Further research found that the cell apoptosis, ferroptosis and inflammatory reactions induced by polystyrene nanoplastics in HEI-OC1 cells was reversed through the pretreatment with N-acetylcysteine, a reactive oxygen species inhibitor. Overall, our study first discovered and systematically revealed the ototoxicity of polystyrene nanoplastics and its underlying mechanism.
RESUMEN
Despite the phenolic acids' health benefits, their interactions with proteins are still unclear. In this study, the interactions of Bovine Serum Albumin (BSA) with chlorogenic acid (CHA), caffeic acid (CA), and their Al3+, Cu2+ complexes were studied by using circular dichroism (CD) spectroscopy, fluorescence spectroscopy, and UV/Vis spectroscopy. It was found that esterification of carboxyl group of CA with quinic acid increased the binding affinities for BSA. After chelating with Cu2+ and Al3+, both CHA and CA exhibited high binding affinities for BSA. CHA could form CHA-Cu2 and CHA-Al2 complex with Cu2+ and Al3+. The result of CD spectroscopy demonstrated that the binding of CHA and Al3+ with BSA contributed to the folding of BSA secondary structure. In addition, with the presence of CHA, binding with Al3+ could also induce changes in BSA conformation. The binding sites of both CHA and CA were closed to Trp213.