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Chronic environmental exposure to polystyrene microplastics increases the risk of nonalcoholic fatty liver disease
Yujie Shi1, Runyang Hong1, Zhencheng Fan1
1Yangzhou University Medical College, Yangzhou University, Yangzhou, Jiangsu Province 225009, China.
Abstract:
Microplastics (MPs), as the crucial environmental pollutants, can be easily transported into the human body and accumulate in the liver. However, current studies mainly focus on acute exposure to MPs, investigations on long-term interactions with MPs alone remain limited. Thereby, we examined noxious properties of MPs and selected the most common polystyrene (PS) MPs as the research object, including unmodified PS MPs (PS-MPs) and positive-charged PS MPs (PS-NH2) at 10 mg/L employing oral drinking water methods in mice for six consecutive months in vivo. In vitro, we treated the human hepatocyte cells with MPs at 25 microg/mL to explore involved mechanisms. The results revealed that six-month MPs exposure led to nonalcoholic fatty liver disease (NAFLD) including impaired liver functions, extensive lipid depositions accompanied by abnormal levels of metabolic genes and PS-NH2 MPs exerted a stronger effect than PS-MPs. Concurrently, mice treated with MPs revealed the accumulation of senescent hepatocytes, leading to increased secretions of senescent phenotypes in the liver. We also discovered that MPs initiated the HO-1/Nrf2 axis consequently inducing ferroptosis in vivo and in vitro, as shown by massive iron deposition, extensive lipid peroxidation along with significant protein expressions in ferroptosis-related markers. Additionally, targeting the HO-1/Nrf2 pathway to further alleviate ferroptosis with corresponding inhibitors could efficiently alleviate cell senescence. Therefore, our study reveals new evidence of the relationship between chronic exposure to MPs and NAFLD and furthers the understanding of how plastic pollution affects human health.
Insights
Chronic exposure to microplastics (MPs) causes nonalcoholic fatty liver disease (NAFLD) in mice. Positively charged MPs showed stronger effects, inducing liver cell senescence and ferroptosis via the HO-1/Nrf2 pathway.
Area of Science:
- Environmental Science
- Toxicology
- Hepatology
Background:
- Microplastics (MPs) are pervasive environmental pollutants with potential human health impacts.
- Limited research exists on the long-term effects of microplastic exposure, particularly on liver health.
- Polystyrene (PS) microplastics, including unmodified and positively charged variants, are common and warrant investigation.
Purpose of the Study:
- To investigate the chronic in vivo effects of polystyrene microplastics on liver health in mice.
- To elucidate the in vitro mechanisms underlying microplastic-induced liver damage.
- To explore the role of cellular senescence and ferroptosis in microplastic-induced nonalcoholic fatty liver disease (NAFLD).
Main Methods:
- Mice were exposed orally to unmodified PS MPs and positively charged PS-NH2 MPs (10 mg/L) for six months.
- Human hepatocyte cells were treated with MPs (25 µg/mL) in vitro to study cellular mechanisms.
- Analysis included liver function tests, lipid deposition assessment, gene expression profiling, and evaluation of senescence and ferroptosis markers.
Main Results:
- Six-month MP exposure induced NAFLD, characterized by impaired liver function and extensive lipid accumulation.
- Positively charged PS-NH2 MPs demonstrated a more pronounced effect than unmodified PS MPs.
- MP exposure led to hepatocyte senescence and ferroptosis, mediated by the HO-1/Nrf2 pathway, evidenced by iron deposition and lipid peroxidation.
Conclusions:
- Chronic microplastic exposure is linked to the development of nonalcoholic fatty liver disease.
- The HO-1/Nrf2 pathway plays a critical role in mediating microplastic-induced ferroptosis and subsequent cell senescence.
- Targeting the HO-1/Nrf2 pathway offers a potential therapeutic strategy to mitigate microplastic-induced liver damage.
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