Polyethylene, whose surface has been modified by UV irradiation, induces cytotoxicity: A comparison with microplastics found in beaches.

Microplastics, plastic particles 5 mm or less in size, are abundant in the environment; hence, the exposure of humans to microplastics is a great concern. Usually, the surface of microplastics found in the environment has undergone degradation by external factors such as ultraviolet rays and water waves. One of the characteristics of changes caused by surface degradation of microplastics is the introduction of oxygen-containing functional groups. Surface degradation alters the physicochemical properties of plastics, suggesting that the biological effects of environmentally degraded plastics may differ from those of pure plastics. However, the biological effects of plastics introduced with oxygen-containing functional groups through degradation are poorly elucidated owing to the lack of a plastic sample that imitates the degradation state of plastics found in the environment. In this study, we investigated the degradation state of microplastics collected from a beach. Next, we degraded a commercially available polyethylene (PE) particles via vacuum ultraviolet (VUV) irradiation and showed that chemical surface state of PE imitates that of microplastics in the environment. We evaluated the cytotoxic effects of degraded PE samples on immune and epithelial cell lines. We found that VUV irradiation was effective in degrading PE within a short period, and concentration-dependent cytotoxicity was induced by degraded PE in all cell lines. Our results indicate that the cytotoxic effect of PE on different cell types depends on the degree of microplastic degradation, which contributes to our understanding of the effects of PE microplastics on humans.

[Preparation of Degraded Microplastics That Imitate Surface Properties in the Environment].

Microplastics are small pieces of plastic that are less than 5 mm in length. These plastics have been detected in various environments, including the ocean, soil, and air. Their abundance have raised concerns regarding their potential effects on living organisms, including humans. The surface of microplastics degrades due to external factors such as ultraviolet rays and water waves in the environment. Therefore, assessing the biological impact of microplastics and considering their state of degradation is important. Among the physical properties of microplastics, we focused on the chemical degradation of microplastics. Specifically, we used vacuum ultraviolet (VUV) light to accelerate the degradation of polyethylene (PE) and prepared PE samples representing the degradation of PE to varying degrees. The surface properties of PE samples prepared using VUV were similar to those obtained from the environment. Cytotoxicity tests were then used to evaluate the effects of undegraded and degraded PE on cells. We found that the severity of cytotoxicity increased with the extent to which the PE would have been degraded, suggesting that the degree of degradation is strongly linked to the severity of the observed deleterious effects on living organisms. In conclusion, this finding contributes to our understanding of the effects of polyethylene microplastics on the human body.

Cell surface localization of importin α1/KPNA2 affects cancer cell proliferation by regulating FGF1 signalling.

Importin α1 is involved in nuclear import as a receptor for proteins with a classical nuclear localization signal (cNLS). Here, we report that importin α1 is localized to the cell surface in several cancer cell lines and detected in their cultured medium. We also found that exogenously added importin α1 is associated with the cell membrane via interaction with heparan sulfate. Furthermore, we revealed that the cell surface importin α1 recognizes cNLS-containing substrates. More particularly, importin α1 bound directly to FGF1 and FGF2, secreted cNLS-containing growth factors, and addition of exogenous importin α1 enhanced the activation of ERK1/2, downstream targets of FGF1 signalling, in FGF1-stimulated cancer cells. Additionally, anti-importin α1 antibody treatment suppressed the importin α1-FGF1 complex formation and ERK1/2 activation, resulting in decreased cell growth. This study provides novel evidence that functional importin α1 is located at the cell surface, where it accelerates the proliferation of cancer cells.