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Large polystyrene microplastics results in hepatic lipotoxicity in mice
Hexia Chen1, Yongfeng Deng1, Qing Wang2
1School of Environment and Guangdong Key Laboratory of Environmental Pollution and Health, Jinan University, Guangzhou 510632, China.
Abstract:
Like small microplastics (MPs), recent studies reveal that large MPs could cause health risks in mice, even if they are not enriched in tissues. However, potential hepatoxicity following large MPs exposure and the underlying mechanisms have not been thoroughly investigated. In the present study, we explored the disruption of hepatic lipid metabolism and potential underlying toxic mechanisms in mice caused by long-term exposure to large polystyrene MPs (40-100 μm) based on a multi-omic approach. After 21 weeks of feeding foods containing MPs (50 and 500 mg/kg food), lipidomic revealed that environmentally relevant and higher doses MP exposures resulted in significant changes in a total of 20 lipid classes. Ceramide (Cer) and dihydroceramide (dhCer) were significantly reduced, while cholesteryl ester (CE), lysoalkylphosphatidylcholine (LPCO), lysophosphatidylethanolamine (LPE) and total glyceride (TG) were all elevated by MPs. The transcriptomic and other physiological data suggested that the potential toxic mechanisms may be related to disorders of fatty acid and cholesterol synthesis and metabolism disorders, and transporting of TG. Our findings demonstrate the hepatic lipotoxicity following exposure to environmentally relevant and higher doses of large MPs, calling for future research and management of the environmental risks of MPs with relatively large particle sizes.
Insights
Large microplastics (MPs) exposure causes liver damage in mice by disrupting lipid metabolism. This study highlights potential health risks from large MPs, even at environmentally relevant doses.
Area of Science:
- Environmental Health
- Toxicology
- Metabolomics
Background:
- Recent studies suggest large microplastics (MPs) pose health risks, similar to smaller MPs.
- The specific hepatotoxicity and underlying mechanisms of large MPs exposure remain under-investigated.
Purpose of the Study:
- To investigate the disruption of hepatic lipid metabolism caused by long-term exposure to large polystyrene MPs (40-100 μm) in mice.
- To explore the potential toxic mechanisms underlying large MPs-induced liver damage using a multi-omic approach.
Main Methods:
- Mice were fed diets containing large polystyrene MPs (50 and 500 mg/kg food) for 21 weeks.
- A multi-omic approach, including lipidomics and transcriptomics, was employed to analyze liver tissue.
- Physiological data were collected to assess overall health impacts.
Main Results:
- Exposure to environmentally relevant and higher doses of large MPs significantly altered 20 lipid classes.
- Key changes included reduced levels of ceramide (Cer) and dihydroceramide (dhCer), and increased levels of cholesteryl ester (CE), lysoalkylphosphatidylcholine (LPCO), lysophosphatidylethanolamine (LPE), and total glyceride (TG).
- Transcriptomic and physiological data indicated disorders in fatty acid and cholesterol synthesis, metabolism, and TG transport.
Conclusions:
- Long-term exposure to large MPs induces hepatic lipotoxicity in mice.
- The findings suggest that large MPs can disrupt lipid metabolism, leading to potential liver damage.
- This research underscores the need for further investigation and management of environmental risks associated with large MPs.
