Abstract: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… Show more
“…4 ), albeit it was beyond the capabilities of our study to confirm the increased secretion or activity of SOD3 enzyme in the extracellular milieu. This finding is also supported by previous studies that found oxidative stress induced by microplastic-mediated interference in mitochondrial function, suppression of cellular antioxidant systems, and increased generation of reactive oxygen species (Abidli et al 2021 ; An et al 2021 ; Chen et al 2021 ; Cortés et al 2020 ; Liu et al 2020 ; Wei et al 2021 ). Fig.…”
Section: Discussionsupporting
confidence: 86%
“…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 ).…”
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.
“…4 ), albeit it was beyond the capabilities of our study to confirm the increased secretion or activity of SOD3 enzyme in the extracellular milieu. This finding is also supported by previous studies that found oxidative stress induced by microplastic-mediated interference in mitochondrial function, suppression of cellular antioxidant systems, and increased generation of reactive oxygen species (Abidli et al 2021 ; An et al 2021 ; Chen et al 2021 ; Cortés et al 2020 ; Liu et al 2020 ; Wei et al 2021 ). Fig.…”
Section: Discussionsupporting
confidence: 86%
“…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 ).…”
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.
“…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].…”
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.
“…By assessing effects in the GIT and the liver of mice exposed to PS MP via drinking water, liver toxicity, gut microbiota dysbiosis, disruption of the intestinal barrier and metabolic dysregulation have been demonstrated [166,167]. Oral exposure of rats to PS MPs has also provided evidence of translocation to the heart, resulting in cardiovascular dysfunction and fibrosis [185]. Regarding lung exposure, intratracheal instillation of PS NPs into the lungs of Sprague-Dawley rats has highlighted an influx of immune cells in a size-dependent fashion, with the smallest particles causing the greatest effect [164].…”
Human exposure to nano- and microplastics (NMPs) has raised major societal concerns, yet no framework to assess the risks of NMPs for human health exists. A substantial proportion of plastic produced worldwide is not properly disposed and persists in the environment for decades while degrading. Plastic degradation generates a size continuum of fragments, including nano- and microplastic particles, with numerous associated environmental pollutants and plastic additives, and microbial communities colonising their surfaces. The ubiquitous presence of NMPs, their availability for uptake by organisms and their potential to act as vectors for toxicants and pathogens render risk assessment a priority on the political agenda at the global level. We provide a new, fully integrated risk assessment framework tailored to the specificities of NMPs, enabling an assessment of current and future human health risks from NMPs. The framework consists of four novel paradigms to the traditional risk assessment methodology. These paradigms deal with techniques in NMP analysis, gaps in empirical data, theoretical and modelling approaches and stakeholder engagement. Within the proposed framework, we propose how we can use research experiences gained so far to carry out the different steps of the assessment process, and we define priorities for further research.
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