Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.

Propiconazole is fungicide widely used in agriculture, which may enter aquatic ecosystems and affect organisms. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant levels of propiconazole throughout the life cycle, from embryo to sexually mature adults, and the effects on growth, reproduction, and offspring viability were investigated. To investigate the mechanisms of propiconazole action, the sex steroid hormones and the expression of genes related to the hypothalamus-pituitary-gonad-liver (HPGL) axis and DNA methylation were examined. Growth decreased in the parental zebrafish (F0) after exposure to propiconazole for 120 days. In males, increases in the levels of 17β-estradiol and vitellogenin were observed. The alterations in sex steroid hormones were regulated by the expression of genes involved with the HPGL axis. The decreases in fecundity and fertilization of the F0 was induced by the global DNA methylation, and then may result in the abnormal development of the F1. Therefore, propiconazole disrupted the steroidogenic pathway and caused changes in global DNA methylation that induced reproductive toxicity.