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Protocol for Microplastics Sampling on the Sea Surface and Sample Analysis
Published on: December 16, 2016
The cardiovascular toxicity of polystyrene microplastics in rats: based on untargeted metabolomics analysis
Zikai Song1, Haidi Wu1, Xiaoqi Fang2
1Department of Cardiology, The First Hospital of Jilin University, Changchun, China.
Background:
Polystyrene microplastics (PS-MPs) exhibit multi-target, multi-dimensional, chronic, and low toxicity to the cardiovascular system. They enter the bloodstream through the gastrointestinal tract and respiratory system, altering blood parameters and conditions, inducing thrombotic diseases, and damaging myocardial tissue through the promotion of oxidative stress and inflammatory responses in myocardial cells. However, many of the links and mechanisms remain unclear.
Methods:
In this study, 48 wistar rats were randomly divided into four groups and exposed to different concentrations of PS-MPs: control group (0 mg/kg/d), low dose group (0.5 mg/kg/d), middle dose group (5 mg/kg/d) and high dose group (50 mg/kg/d), with 12 rats in each group. After 90 consecutive days of intragastric administration of PS-MPs, biochemical markers in myocardium, aorta and blood were detected, and HE staining was performed to observe the toxic effects of PS-mps on cardiovascular system. Furthermore, non-targeted metabolomics methods were used to analyze the effect of PS-MPs exposure on the metabolism of cardiovascular system in rats, and to explore its potential molecular mechanism.
Results:
The results revealed no pathological changes in the heart and aorta following PS-MPs exposure. However, the myocardial enzyme levels in the high dose PS-MPs group of rats showed a significant increase. Moreover, exposure to polystyrene microplastics caused a disorder in lipid metabolism in rats, and led to an increase in indicators of inflammation and oxidative stress in myocardial and aortic tissues, but resulted in a decrease in the level of IL-6. Untargeted metabolomics results showed that metabolites with antioxidant and anti-inflammatory effects, including equol and 4-hydroxybenzoic acid, were significantly upregulated.
Conclusion:
These results suggest that long-term exposure to high concentrations of PS-MPs may lead to abnormal lipid metabolism and cardiovascular system damage. The mechanism may be related to oxidative stress and inflammatory response. Exogenous antioxidants and changes in own metabolites may have a protective effect on the injury. Therefore, understanding the toxicological mechanism of PS-MPs not only helps to elucidate its pathogenesis, but also provides new ideas for the treatment of chronic diseases.
Insights
Polystyrene microplastics (PS-MPs) exposure in rats disrupted lipid metabolism and increased oxidative stress, potentially damaging the cardiovascular system. Upregulated antioxidant metabolites may offer protection against PS-MP toxicity.
Area of Science:
- Environmental Toxicology
- Cardiovascular Science
- Metabolomics
Background:
- Polystyrene microplastics (PS-MPs) pose chronic, low-level toxicity risks to the cardiovascular system.
- PS-MPs can enter circulation via the gastrointestinal and respiratory tracts, impacting blood parameters and potentially causing thrombotic diseases.
- Mechanisms underlying PS-MP cardiovascular toxicity, including oxidative stress and inflammation in myocardial cells, require further elucidation.
Purpose of the Study:
- To investigate the cardiovascular effects of chronic PS-MP exposure in rats.
- To explore the molecular mechanisms of PS-MP toxicity using metabolomics.
- To assess the impact of PS-MPs on lipid metabolism, oxidative stress, and inflammation in cardiovascular tissues.
Main Methods:
- Wistar rats (n=48) were exposed to varying concentrations of PS-MPs (0, 0.5, 5, 50 mg/kg/d) for 90 days.
- Biochemical markers, HE staining, and non-targeted metabolomics were employed to analyze myocardial, aortic, and blood samples.
- Assessment focused on pathological changes, enzyme levels, lipid metabolism, inflammation, and oxidative stress indicators.
Main Results:
- High-dose PS-MP exposure significantly increased myocardial enzyme levels without causing gross pathological changes in the heart or aorta.
- PS-MP exposure disordered lipid metabolism and increased inflammation and oxidative stress markers in myocardial and aortic tissues.
- Metabolomics revealed significant upregulation of antioxidant and anti-inflammatory metabolites, such as equol and 4-hydroxybenzoic acid.
Conclusions:
- Long-term, high-concentration PS-MP exposure may induce cardiovascular damage via abnormal lipid metabolism, oxidative stress, and inflammation.
- Endogenous metabolites with antioxidant properties and exogenous antioxidants might mitigate PS-MP-induced cardiovascular injury.
- Understanding PS-MP toxicological mechanisms offers insights into chronic disease pathogenesis and potential therapeutic strategies.
