“…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%
“…Similar translocations of nanoplastics have been found to originate from the lungs via inhalation (Choi et al 2010 ). Animal models have found microplastic accumulation in mammalian male (Jin et al 2021 ) and female (An et al 2021 ; Hou et al 2021 ) gonadal tissues, possibly affecting fertility and reproductive capacity. Inside the body, in addition to their physical and mechanical interactions, microplastics can also leach chemical into tissues and circulation, including chemicals applied during manufacturing (e.g., bisphenols, phthalates, perfluoridated compounds, brominated flame retardants, UV stabilizers) (Cox et al 2019 ) and for aged plastics, substances absorbed and accumulated from the environment (e.g., organic pesticides, polyaromatic hydrocarbons, heavy metals, and pathogens) (Alimba and Faggio 2019 ; Cox et al 2019 ; Scopetani et al 2018 ; Torres 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%
“…Similar translocations of nanoplastics have been found to originate from the lungs via inhalation (Choi et al 2010 ). Animal models have found microplastic accumulation in mammalian male (Jin et al 2021 ) and female (An et al 2021 ; Hou et al 2021 ) gonadal tissues, possibly affecting fertility and reproductive capacity. Inside the body, in addition to their physical and mechanical interactions, microplastics can also leach chemical into tissues and circulation, including chemicals applied during manufacturing (e.g., bisphenols, phthalates, perfluoridated compounds, brominated flame retardants, UV stabilizers) (Cox et al 2019 ) and for aged plastics, substances absorbed and accumulated from the environment (e.g., organic pesticides, polyaromatic hydrocarbons, heavy metals, and pathogens) (Alimba and Faggio 2019 ; Cox et al 2019 ; Scopetani et al 2018 ; Torres 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.
“…In reproductive organs, polystyrene MP (5 μm) induce a significant reproductive toxicity including the decrease of sperm survival rate and testis weight, disorderly arrangement of spermatid cells in the testicular seminiferous tubules, and sperm denegation in the testis tubules of ICR mice [ 56 ]. Also, a similar reproductive toxicity such as apoptosis of granulosa cells and ovary fibrosis were observed in ovary of Wistar rats treated with polystyrene MP (0.5 μm) [ 57 ]. However, the present study has been focused the characterization of constipation phenotypes in ICR mice after treatment of polystyrene MP with 0.5 μm size without analyzing the toxicity and microbiota regulatory effects of MP.…”
Indirect evidence has determined the possibility that microplastics (MP) induce constipation, although direct scientific proof for constipation induction in animals remains unclear. To investigate whether oral administration of polystyrene (PS)-MP causes constipation, an alteration in the constipation parameters and mechanisms was analyzed in ICR mice, treated with 0.5 μm PS-MP for 2 weeks. Significant alterations in water consumption, stool weight, stool water contents, and stool morphology were detected in MP treated ICR mice, as compared to Vehicle treated group. Also, the gastrointestinal (GI) motility and intestinal length were decreased, while the histopathological structure and cytological structure of the mid colon were remarkably altered in treated mice. Mice exposed to MP also showed a significant decrease in the GI hormone concentration, muscarinic acetylcholine receptors (mAChRs) expression, and their downstream signaling pathway. Subsequent to MP treatment, concentrations of chloride ion and expressions of its channel (CFTR and CIC-2) were decreased, whereas expressions of aquaporin (AQP)3 and 8 for water transportation were downregulated by activation of the mitogen-activated protein kinase (MAPK)/nuclear factor (NF)-κB signaling pathway. These results are the first to suggest that oral administration of PS-MP induces chronic constipation through the dysregulation of GI motility, mucin secretion, and chloride ion and water transportation in the mid colon.
“…ROS generation is a common cause of nanoparticle-induced cell apoptosis [ 47 ]. ROS generation caused by PS micro- and nanoplastics has been reported in multiple organisms, such as zebrafish [ 10 ], rats [ 48 ] and mice [ 49 ], and ROS clearance alleviates the mucosal injury and damage in the intestine [ 50 ]. Via two proven effective antioxidants—lipoic acid and melatonin [ 51 ], the causality between PS micro- and nanoplastics exposure, ROS generation, epithelial cell apoptosis, and increased intestinal permeability has been confirmed in this study by clearing ROS during PS micro- and nanoplastic exposure.…”
Background
Micro- and nanoplastic pollution has become a global environmental problem. Nanoplastics in the environment are still hard to detect because of analysis technology limitations. It is believed that when microplastics are found in the environment, more undetected nanoplastics are around. The current “microplastic exposure” is in fact the mixture of micro- and nanoplastic exposures. Therefore, the biological interaction between organisms among different sizes of micro- and nanoplastics should not be neglected.
Results
We measured the biodistribution of three polystyrene (PS) particles (50 nm PS, PS50; 500 nm PS, PS500; 5000 nm PS, PS5000) under single and co-exposure conditions in mice. We explored the underlying mechanisms by investigating the effects on three major components of the intestinal barrier (the mucus layer, tight junctions and the epithelial cells) in four intestine segments (duodenum, jejunum, ileum and colon) of mice. We found that the amounts of both PS500 and PS5000 increased when they were co-exposed with PS50 for 24 h in the mice. These increased amounts were due primarily to the increased permeability in the mouse intestines. We also confirmed there was a combined toxicity of PS50 and PS500 in the mouse intestines. This manifested as the mixture of PS50 and PS500 causing more severe dysfunction of the intestinal barrier than that caused by PS50 or PS500 alone. We found that the combined toxicity of PS micro- and nanoplastics on intestinal barrier dysfunction was caused primarily by reactive oxygen species (ROS)-mediated epithelial cell apoptosis in the mice. These findings were further confirmed by an oxidants or antioxidants pretreatment study. In addition, the combined toxicity of PS micro- and nanoplastics was also found in the mice after a 28-day repeated dose exposure.
Conclusions
There is a combined toxicity of PS50 and PS500 in the mouse intestines, which was caused primarily by ROS-mediated epithelial cell apoptosis in the mice. Considering that most recent studies on PS micro- and nanoplastics have been conducted using a single particle size, the health risks of exposure to PS micro- and nanoplastics on organisms may be underestimated.
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