Abstract:As
one of the most widely used materials, plastic polymer fragments
can abrasively degrade into microplastic (MP) and smaller nanoplastic
(NP) particles. The present study aimed to investigate the influence
of particle size on neurodevelopmental toxicity induced by polystyrene
nanoplastics (PS-NPs) in Caenorhabditis elegans and to explore the underlying potential mechanism. C. elegans were exposed to different concentrations
of PS-NPs with various sizes (25, 50, and 100 nm) for 72 h. Our results
showed that al… 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.…”
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.…”
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.
“…MNPs can induce neurodevelopmental toxicity depending on particle size, which is mediated by mitochondrial damage and dopamine reduction. Data from the mutant test demonstrated that improved expression of sel-12 and hop-1 is involved in the regulation of MNP-induced oxidative stress, mitochondrial damage, and neurodevelopmental toxicity in Caenorhabditis elegans [ 74 ].…”
Section: Toxicities Of Micro- and Nanoplastics On Mitochondriamentioning
Mitochondria are highly dynamic cellular organelles that perform crucial functions such as respiration, energy production, metabolism, and cell fate decisions. Mitochondrial damage and dysfunction critically lead to the pathogenesis of various diseases including cancer, diabetes, and neurodegenerative and cardiovascular disorders. Mitochondrial damage in response to environmental contaminant exposure and its association with the pathogenesis of diseases has also been reported. Recently, persistent pollutants, such as micro- and nanoplastics, have become growing global environmental threats with potential health risks. In this review, we discuss the impact of micro- and nanoplastics on mitochondria and review current knowledge in this field.
“…In C. elegans the expression of the dopaminergic neuron reporter dat-1pr::GFP shows decreased fluorescence upon exposure to polystyrene nanoplastics (PS-NP). This was also associated with decreased mitochondria function and increased oxidative stress ( Liu et al, 2020c ), suggesting dopaminergic specific toxicity upon PS-MP exposure. The exposure to UV-aged PS-MPs caused more severe dopaminergic defects than virgin MPs, probably due to the leaching of toxic materials ( Chen et al, 2021a ).…”
Section: The Effects Of Microplastics and Nanoplastics On Reproductiv...mentioning
Biologically active environmental pollutants have significant impact on ecosystems, wildlife, and human health. Microplastic (MP) and nanoplastic (NP) particles are pollutants that are present in the terrestrial and aquatic ecosystems at virtually every level of the food chain. Moreover, recently, airborne microplastic particles have been shown to reach and potentially damage respiratory systems. Microplastics and nanoplastics have been shown to cause increased oxidative stress, inflammation, altered metabolism leading to cellular damage, which ultimately affects tissue and organismal homeostasis in numerous animal species and human cells. However, the full impact of these plastic particles on living organisms is not completely understood. The ability of MPs/NPs to carry contaminants, toxic chemicals, pesticides, and bioactive compounds, such as endocrine disrupting chemicals, present an additional risk to animal and human health. This review will discusses the current knowledge on pathways by which microplastic and nanoplastic particles impact reproduction and reproductive behaviors from the level of the whole organism down to plastics-induced cellular defects, while also identifying gaps in current knowledge regarding mechanisms of action. Furthermore, we suggest that the nematode Caenorhabditis elegans provides an advantageous high-throughput model system for determining the effect of plastic particles on animal reproduction, using reproductive behavioral end points and cellular readouts.
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