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Exposure to Polyethylene Terephthalate Microplastic Induces Mouse Liver Fibrosis Through Oxidative Stress and p38
Rihao Ji1, Yanfang Yang1, Bohao Bian2
1School of Public Health, Baotou Medical College, Baotou, Inner Mongolia, China.
Abstract:
Microplastic (MP) pollution has garnered attention due to its potential impact on living organisms. Among these, polyethylene terephthalate microplastics (PET-MPs) are frequently detected in both environmental samples and human tissues. Despite this, the effects of PET-MPs on liver damage and fibrosis in mammals remain insufficiently understood. This study demonstrated that oral exposure to PET-MPs at doses of 1 mg/day (with a diameter of 1 μm) over 42 days resulted in inhibited weight gain and altered organ coefficients in male mice, suggesting possible liver damage. Using HE and Masson staining revealed pathological changes in the livers of exposed mice, such as hepatocyte swelling, inflammatory cell infiltration, and collagen deposition. Liver function tests confirmed elevated serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Further, the elevated levels of oxidative stress markers, along with the enhanced expression of proteins related to the p38 MAPK/p65 NF-κB signaling pathway as revealed by western blot analysis, both of which are strongly associated with liver damage and fibrosis. To further elucidate these mechanisms, experiments involving N-acetylcysteine (NAC) to counteract oxidative stress and SB203580 to inhibit p38 MAPK activation demonstrated that both interventions effectively mitigated liver fibrosis. Exposure to PET-MPs may trigger liver injury and fibrosis in mice. During this process, oxidative stress and the p38 MAPK/p65 NF-κB signaling pathway may play significant mediating roles.
Insights
Polyethylene terephthalate microplastics (PET-MPs) exposure in mice caused liver damage and fibrosis. Oxidative stress and the p38 MAPK/p65 NF-κB pathway mediate these harmful effects.
Area of Science:
- Environmental Science
- Toxicology
- Biomedical Research
Background:
- Microplastic (MP) pollution is a growing concern, with polyethylene terephthalate microplastics (PET-MPs) frequently found in the environment and human tissues.
- The impact of PET-MPs on mammalian liver health, particularly liver damage and fibrosis, is not well understood.
Purpose of the Study:
- To investigate the effects of oral PET-MP exposure on liver damage and fibrosis in male mice.
- To explore the underlying mechanisms, including oxidative stress and the p38 MAPK/p65 NF-κB signaling pathway.
Main Methods:
- Male mice were orally exposed to 1 μm PET-MPs (1 mg/day) for 42 days.
- Histopathological analysis (HE and Masson staining), liver function tests (ALT, AST), oxidative stress marker assessment, and western blot analysis were performed.
- Interventions with N-acetylcysteine (NAC) and SB203580 were used to examine the roles of oxidative stress and p38 MAPK.
Main Results:
- PET-MP exposure led to inhibited weight gain, altered organ coefficients, and pathological liver changes including hepatocyte swelling, inflammation, and collagen deposition.
- Elevated serum ALT and AST levels, increased oxidative stress markers, and enhanced p38 MAPK/p65 NF-κB signaling pathway protein expression were observed.
- NAC and SB203580 treatments effectively mitigated liver fibrosis, indicating the involvement of oxidative stress and the p38 MAPK/p65 NF-κB pathway.
Conclusions:
- Oral exposure to PET-MPs can induce liver injury and fibrosis in mice.
- Oxidative stress and the p38 MAPK/p65 NF-κB signaling pathway play significant roles in mediating PET-MP-induced liver damage and fibrosis.
