Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats

Li, Zekang; Zhu, Shuxiang; Liu, Qian; Wei, Jialin; Jin, Young–Joo; Wang, Xifeng; Zhang, Lianshuang

doi:10.1016/j.envpol.2020.115025

Cited by 146 publications

(59 citation statements)

References 59 publications

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“…In addition, MPs appeared near‐spherical shape under a SEM (Figure 1(C)). In all, these results showed that the diameter and dispersibility of MPs meet the requirement of this study, which is similar to the report by Li et al 27 …”

Section: Resultssupporting

confidence: 92%

The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats

Wei

Wang

Liu

et al. 2021

Environmental Toxicology

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110

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The extensive existing of microplastics (MPs) in the ecosystem have increased considerable attention concerning their potential adverse effects, the toxicities and the underlying mechanism of MPs are still scarce. To explore the effect of MPs on cardiac tissue in Wistar rats and unravel the mechanism of pyroptosis and oxidative stress in the process of cardiomyocytes injury, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 mm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Results revealed that MPs could damage cardiac structure and function with impaired mitochondria integrity, as well as increased levels of creatine kinase‐MB and cardiac troponinI (cTnI). Moreover, MPs administration triggered oxidative stress as indicated by increased levels of malondialdehyde and decreased activity of superoxide dismutase, glutathione peroxidase and catalase. Treatment with MPs resulted in apoptosis and pyroptosis as evidenced by increasing expressions of interleukin (IL)‐1β, IL‐18. Additionally, MPs were shown to induce the NOD‐like receptor protein 3 inflammasomes activation in cardiac tissue, enabling activation of Caspase‐1‐dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In summary, these results illustrated that pyroptosis played a vital role in polystyrene MPs‐induced cardiotoxicity, which might be helpful to understand the mechanism of cardiac dysfunction and induced by MPs.

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Section: Resultssupporting

confidence: 92%

The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats

Wei

Wang

Liu

et al. 2021

Environmental Toxicology

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110

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“…1 ). Previous research has shown the toxic effects of microplastics on cells and tissues, with effects such as DNA damage and mitochondrial dysfunction, and these underlying mechanisms, as well as activation of apoptotic pathways, may have contributed to the decreased cell viability observed here (Della Torre et al 2014 ; Estrela et al 2020 ; Li et al 2020d ; Wei et al 2021 ).…”

Section: Discussionmentioning

confidence: 65%

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

2021

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Microplastics are ubiquitous environmental pollutants that are a growing concern to many ecosystems, as well as human health. Many of the effects of microplastics on mammalian cells and tissues remain unknown. To address this, we treated L929 murine fibroblasts and Madin–Darby canine kidney (MDCK) epithelial cell lines with 1 μg/mL, 10 μg/mL, or 20 μg/mL of polyethylene (PE) or polystyrene (PS) microspheres in vitro for 6 and 24 h and measured the resulting changes in cell viability, metabolism, and transcriptional expression of inflammatory cytokines and antioxidant enzymes. We observed dose-dependent decreases in cell viability corresponding to increases in doses of both PE and PS. We conducted cell metabolism assays and observed dose-dependent increases in metabolism per cell with increasing doses of both PE and PS. Similarly, we also observed increased expression of the superoxide dismutase-3 gene ( SOD3 ), indicating oxidative stress caused by the microplastics treatments. We also observed increased expression of TNFα , but decreased expression of IFNβ , suggesting different mechanisms by which the microplastics regulate inflammatory responses in mammalian cells. Our results contribute new data to the growing understanding of the effects of microplastics on mammalian cells and indicate complex cellular stress responses to microplastics in the environment.

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“…The detrimental effects of MP/NP exposure in aquatic species include embryotoxicity in zebrafish and sea urchins [7,8], hepatotoxicity in zebrafish, goldfish and tadpoles [9][10][11], growth inhibition of microalgae and fish larvae [12][13][14], decreased life spans of shrimp and plankton upon long-term exposure [12,15], deterioration of intestinal tissues in sea bass [16], and alterations in feeding behavior, metabolism and innate immunity in fish [17][18][19]. In terrestrial animals such as rodents, ingestion of MP/NP altered intestinal barrier function [20,21], gut microbiome [21][22][23], metabolism [20,24], behavior [25,26], innate immunity [23], reproduction [27,28] and cardiovascular function [29,30].…”

Section: Introductionmentioning

confidence: 99%

Uptake and toxicity of polystyrene micro/nanoplastics in gastric cells: Effects of particle size and surface functionalization

2021

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Toxicity of micro or nanoplastics (MP/NP) in aquatic life is well-documented, however, information about the consequences of exposure to these particles in terrestrial species is scarce. This study was used to evaluate the uptake and/or toxicity of polystyrene MP/NP in human gastric cells, comparing doses, particle sizes (50, 100, 200, 500, 1000 or 5000 nm) and surface functionalization (aminated, carboxylated or non-functionalized). In general, the uptake of 50 nm particles was significantly higher than 1000 nm particles. Among the 50 nm particles, the aminated particles were more avidly taken up by the cells and were cytotoxic at a lower concentration (≥ 7.5 μg/mL) compared to same sized carboxylated or non-functionalized particles (≥ 50 μg/mL). High toxicity of 50 nm aminated particles corresponded well with significantly high rates of apoptosis-necrosis induced by these particles in 4 h (29.2% of total cells) compared to all other particles (≤ 16.8%). The trend of apoptosis-necrosis induction by aminated particles in 4 h was 50 > 5000 > 1000 > 500 > 200 > 100 nm. The 50 nm carboxylated or non-functionalized particles also induced higher levels of apoptosis-necrosis in the cells compared to 100, 1000 and 5000 nm particles with same surface functionalization but longer exposure (24 h) to 50 nm carboxylated or non-functionalized particles significantly (p<0.0001) increased apoptosis-necrosis in the cells. The study demonstrated that the toxicity of MP/NP to gastric cells was dependent on particle size, dose surface functionalization and exposure period.

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Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats

Cited by 146 publications

References 59 publications

The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats

The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase‐1 signaling pathway and oxidative stress in Wistar rats

Polystyrene and Polyethylene Microplastics Decrease Cell Viability and Dysregulate Inflammatory and Oxidative Stress Markers of MDCK and L929 Cells In Vitro

Uptake and toxicity of polystyrene micro/nanoplastics in gastric cells: Effects of particle size and surface functionalization

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