Nanoplastics (NPs) are a matter of widespread concern, as they are easily absorbed by a wide variety of organisms and accumulate in biological tissues. While there is evidence that nanoplastics are toxic to various organisms, few studies have investigated the mechanisms underlying the toxicities of NPs with different surface functionalizations to macrophage cells. In this study, mouse mononuclear macrophage (RAW264.7) cells were exposed to polystyrene nanoplastics (PS-NPs) with three different surface functionalizations, namely pristine polystyrene (PS), carboxyl-functionalized polystyrene (PS-COOH), and amino-functionalized polystyrene (PS-NH2), to evaluate the cellular endocytosis, lactate dehydrogenase (LDH) release, cell viability, reactive oxygen species (ROS), mitochondrial membrane potential, apoptosis, and related gene expression. Results showed that all three PS-NPs were endocytosed into cells. However, in the concentration range of 0-100 μg/mL, PS had no effect on cell viability or apoptosis, but it slightly increased cellular ROS and decreased mitochondrial membrane potential. PS-NH2 exhibited the highest cytotoxicity. PS-COOH and PS-NH2 induced ROS production, altered the mitochondrial membrane potential, and caused cell apoptosis regulated by the mitochondrial apoptosis pathway. Results also showed that cell membrane damage induced by PS-NH2 is one of the primary mechanisms of its cytotoxicity to RAW264.7 cells. The results of this study clarify the toxicities of PS-NPs with different surface functionalizations to macrophages, thereby improving the identification of immune system risks related to nanoplastics.
Keywords: Apoptosis; Cell membrane damage; Cytotoxicity; Nanoplastics; RAW264.7 cells; Reactive oxygen species.
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