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Potential Effects of Orally Ingesting Polyethylene Terephthalate Microplastics on the Mouse Heart
Tao Lu1, Desheng Li1, Xiaoqing Yuan1
1The Key Laboratory of Traditional Chinese Medicine Prescription Effect and Clinical Evaluation of State Administration of Traditional Chinese Medicine, School of Pharmacy, Binzhou Medical University, YanTai, 264003, ShanDong, People's Republic of China.
Abstract:
Polyethylene terephthalate microplastics (PET MPs) are widespread in natural environment, and can enter organisms and accumulate in the body, but its toxicity has not been well studied. Therefore, in order to investigate the toxic effects of PET microplastics on mammals, this study investigated the toxic effects of PET MPs on ICR mice and H9C2 cells by different treatment groups. The results indicated the cardiac tissue of mice in the PET-H (50 µg/mL) group showed significant capillary congestion, myocardial fiber breakage, and even significant fibrosis compared to the PET-C (control) group (P < 0.01). Results of the TUNEL assay demonstrated significant apoptosis in myocardial tissue in the PET-H and PET-M (5 µg/mL) groups (P < 0.01). Meanwhile, Western blotting showed increased expression of the apoptosis-related protein Bax and decreased expression of PARP, caspase-3, and Bcl-2 proteins in both myocardial tissues and H9C2 cells. In addition, flow cytometry confirmed that PET MPs decreased the mitochondrial membrane potential and apoptosis in H9C2 cells; however, this trend was reversed by N-acetylcysteamine application. Moreover, PET MP treatment induced the accumulation of reactive oxygen species (ROS) in H9C2 cells, while the MDA level in the myocardial tissue was elevated, and the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were decreased (P < 0.01), indicating a change in the redox environment. In conclusion, PET MPs promoted cardiomyocyte apoptosis by inducing oxidative stress and activating mitochondria-mediated apoptotic processes, ultimately leading to myocardial fibrosis. This study provides ideas for the prevention of PET MP toxicity and promotes thinking about enhancing plastic pollution control.
Insights
Polyethylene terephthalate microplastics (PET MPs) cause cardiac damage and apoptosis in mice by inducing oxidative stress. N-acetylcysteamine partially reversed these toxic effects in H9C2 cells, highlighting potential therapeutic avenues.
Area of Science:
- Environmental Toxicology
- Cardiovascular Research
- Cellular Biology
Background:
- Polyethylene terephthalate microplastics (PET MPs) are ubiquitous environmental contaminants.
- The toxicological impact of PET MPs on mammalian cardiovascular systems remains poorly understood.
- Understanding PET MP toxicity is crucial for public health and environmental safety.
Purpose of the Study:
- To investigate the cardiotoxic effects of PET microplastics in a mammalian model (ICR mice) and cellular model (H9C2 cells).
- To elucidate the underlying mechanisms of PET MP-induced cardiac damage, focusing on apoptosis and oxidative stress.
- To explore potential protective strategies against PET MP toxicity.
Main Methods:
- Administration of varying concentrations of PET MPs to ICR mice and H9C2 cells.
- Histopathological examination of cardiac tissues to assess structural damage.
- TUNEL assay for apoptosis detection, Western blotting for apoptosis-related proteins (Bax, PARP, caspase-3, Bcl-2), and flow cytometry for mitochondrial membrane potential and reactive oxygen species (ROS) assessment.
- Measurement of malondialdehyde (MDA) levels and antioxidant enzyme activities (CAT, SOD, GSH-Px).
Main Results:
- PET MPs induced significant capillary congestion, myocardial fiber breakage, and fibrosis in mouse cardiac tissue.
- Significant cardiomyocyte apoptosis was observed in PET MP-exposed groups, confirmed by TUNEL assay and altered expression of apoptosis-related proteins.
- PET MPs disrupted mitochondrial function, increased ROS production, and altered the redox environment, evidenced by elevated MDA and decreased antioxidant enzyme activities.
- N-acetylcysteamine partially mitigated PET MP-induced mitochondrial dysfunction and apoptosis in H9C2 cells.
Conclusions:
- PET microplastics promote cardiomyocyte apoptosis via oxidative stress and mitochondria-mediated pathways, leading to myocardial fibrosis.
- The findings highlight the cardiotoxic potential of PET MPs and underscore the need for enhanced plastic pollution control.
- This research provides insights into PET MP toxicity mechanisms and suggests potential interventions.
