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Exposure to micro‐ and nanoplastics (MNPs) is common because of their omnipresence in environment. Recent studies have revealed that MNPs may cause atherosclerosis, but the underlying mechanism remains unclear. To address this bottleneck, ApoE−/− mice are exposed to 2.5–250 mg kg−1 polystyrene nanoplastics (PS‐NPs, 50 nm) by oral gavage with a high‐fat diet for 19 weeks. It is found that PS‐NPs in blood and aorta of mouse exacerbate the artery stiffness and promote atherosclerotic plaque formation. PS‐NPs activate phagocytosis of M1‐macrophage in the aorta, manifesting as upregulation of macrophage receptor with collagenous structure (MARCO). Moreover, PS‐NPs disrupt lipid metabolism and increase long‐chain acyl carnitines (LCACs). LCAC accumulation is attributed to the PS‐NP‐inhibited hepatic carnitine palmitoyltransferase 2. PS‐NPs, as well as LCACs alone, aggravate lipid accumulation via upregulating MARCO in the oxidized low‐density lipoprotein‐activated foam cells. Finally, synergistic effects of PS‐NPs and LCACs on increasing total cholesterol in foam cells are found. Overall, this study indicates that LCACs aggravate PS‐NP‐induced atherosclerosis by upregulating MARCO. This study offers new insight into the mechanisms underlying MNP‐induced cardiovascular toxicity, and highlights the combined effects of MNPs with endogenous metabolites on the cardiovascular system, which warrant further study.

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miR‐221, an oncogenic microRNA, can promote cell proliferation and is highly expressed in various types of tumors. However, the role of exosomal miR‐221 in benzene‐caused carcinogenesis remains elusive. Our study was designed to investigate whether exosomes secreted by the hydroquinone (HQ; an active metabolite of benzene)‐transformed malignant cells can transmit miR‐221 to normal recipient cells and its possible effects on cell viability. Our investigation revealed that expression levels of miR‐221 were significantly increased in HQ‐transformed malignant cells relative to normal controls. Furthermore, exposure of control cells to exosomes that were derived from HQ‐transformed malignant cells increased miR‐221 levels and promoted their proliferation. Analyses of the biological potency of exosomes derived from HQ‐transformed malignant cells in which miR‐221 levels were decreased using an inhibitor, showed that both miR‐221 levels and proliferation of recipient cells were decreased, but still were higher than those of normal 16HBE cells. Our study indicates that exosomal miR‐221 derived from HQ‐transformed malignant human bronchial epithelial cells is involved in the proliferation of recipient cells.

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Accumulating evidence reveals that exosome plays an important role in cell-to-cell communication in both physiological and pathological processes by transferring bioactive molecules. However, the role of exosomal secretion in the adaption of its source cells to the stimuli of environmental chemicals remains elusive. In this study, we revealed that the exposure of hydroquinone (HQ; the main bioactive metabolite of benzene) to human bronchial epithelial cells (16HBE) resulted in decreased ability of cell proliferation and migration, and simultaneously DNA damage and micronuclei formation. Interestingly, when exosomal secretion of HQ treated 16HBE cells was inhibited with the inhibitor GW4869, cellular proliferation and migration were further significantly reduced; concurrently, their DNA damage and micronuclei formation were both further significantly aggravated. Herein, we conclude that exosomal secretion of 16HBE cells may be an important self-protective function against the toxic effects induced by HQ.

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