Abstract
BACKGROUND: Nanoplastics (NPs), as emerging foodborne contaminants, can accumulate in the heart and induce toxic effects. However, whether NPs exert differential cardiac impacts depending on dietary habits remains unclear. METHODS: In this study, mice subjected to different dietary patterns (Normal diet, ND; High-fat diet, HFD; High-fructose diet, HFrD) were orally administered 80 nm polystyrene nanoplastics (PS-NPs) at a dose of 10 mg/(kg·day) for 1, 4, and 8 weeks. The fluorescence tracing, histopathological analysis, quantification of inflammatory and fibrotic markers, and transcriptomic sequencing were used to evaluate the distribution and hazardous effect of PS-NPs. RESULTS: By the 8th week, significant fluorescence labeled PS-NPs accumulation was detected in the hearts of mice on HFD group and HFrD group. Histopathological and immunofluorescence analyses revealed that both HFD and HFrD groups exacerbated cardiac collagen deposition and inflammatory infiltration in PS-NP-exposed mice. Transcriptomic analysis further indicated that under HFD, PS-NP exposure primarily activated MAPK signaling pathway-mediated inflammation, thereby promoting fibrosis. In contrast, under HFrD, PS-NP80 amplified cardiac injury via the TNF signaling pathway. CONCLUSIONS: These findings demonstrate that dietary habits can aggravate the cardiac toxicity induced by foodborne nanoplastics, highlighting the importance of considering dietary patterns in the risk assessment of food contaminants.