Nanoplastics are associated with several risks to the ecology and toxicity to humans. Nanoplastics are synthetic polymers with dimensions ranging from 1 nm to 1 μm. They are directly released to the environment or secondarily derived from plastic disintegration in the environment. Nanoplastics are widely detected in environmental samples and the food chain; therefore, their potentially toxic effects have been widely explored. In the present review, an overview of another two potential sources of nanoplastics, exposure routes to illustrate hazard identification of nanoplastics, cell internalization, and effects on intracellular target organelles are presented. In addition, challenges on the study of nanoplastics and future research areas are summarized. This paper also summarizes some approaches to eliminate or minimize the levels of nanoplastics to ensure environmental safety and improve human health.

Perfluorooctanoic acid (PFOA), a perfluoroalkyl compound, is linked to congenital heart diseases, though its underlying mechanisms remain unclear. We hypothesized that PFOA induces cardiac defects through the inhibition of the Keap1/Nrf2 pathway, leading to oxidative damage in cardiomyocytes. In this study, zebrafish embryos exposed to PFOA showed significant cardiac malformations and dysfunction, characterized by excessive reactive oxygen species (ROS), malondialdehyde (MDA) production, decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. Additionally, we observed dysregulation in the expression of key cardiac development genes (vmhc, gata4, nkx2.5, and sox9b). PFOA also reduced the expression of keap1, nrf2, and ho-1. After overexpression of Nrf2, levels of ROS and MDA decreased, while levels of SOD, CAT, and GSH-Px increased. Additionally, cardiomyocyte apoptosis and cardiac malformations were alleviated. These findings have suggested that PFOA induces oxidative stress through Keap1/Nrf2 pathway inhibition, ultimately leading to cardiac defects.

The purpose of this meta-analysis was to evaluate the relationship between serum 25-hydroxyvitamin D[25(OH)D] levels and gastric cancer. PubMed, Embase, Cochrane Library, Web of Science, The China Academic Journals full-text database, Wanfang Database of Chinese Academic Journals, VIP Chinese Science and Technology Periodicals database, and Chinese Biomedical Literature database were systematically searched. Case-control studies on the correlation between serum 25-hydroxyvitamin D levels and gastric cancer were retrieved, and the data extracted were analyzed. The results of 9 case-control studies containing 671 patients showed that serum 25(OH)D levels in the gastric cancer group were lower than those in the control group (weighted mean difference (WMD) = −8.90, 95% confidence interval (CI): −11.5, −6.32, p < 0.01); the risk of vitamin D deficiency in the gastric cancer group was higher than that in the control group (Odds ratio = 3.09, 95% CI: 1.96, 4.87, p < 0.01). The serum 25(OH)D levels in patients with well and moderately differentiated gastric cancer were higher than those in patients with poorly differentiated gastric cancer (WMD = −3.58, 95% CI: −6.41, −0.74, p = 0.01). Thus, low levels of vitamin D may increase the risk of gastric cancer. Systematic review registration: PROSPERO CRD42022327942.