The potential toxicity of polystyrene nanoplastics to human trophoblasts in vitro

Hu, Jianing; Zhu, Yueyue; Zhang, Jinwen; Xu, Yichi; Wu, Jiayi; Zeng, Weihong; Lin, Yi; Liu, Xiao-Rui

doi:10.1016/j.envpol.2022.119924

Cited by 31 publications

(8 citation statements)

References 44 publications

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“…Dysfunctions of trophoblast cells, such as migration/invasion, during early pregnancy might induce miscarriage . It was also found that exposure to PS-MPs (0.5 μm) repressed the migration of human umbilical vein endothelial cells, and exposure to PS-NPs (100 nm) weakened the capacities of migration/invasion in HTR-8/Svneo cells . However, the mechanism underlying the migration and invasion suppressed by PS-NPs in trophoblast cells was largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage

Wan,

Wang,

Chen

et al. 2024

ACS Nano

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Nanoplastics (NPs), as emerging pollutants, have attracted global attention. Nevertheless, the adverse effects of NPs on female reproductive health, especially unexplained miscarriage, are poorly understood. Defects of trophoblast cell migration and invasion are associated with miscarriage. Migrasomes were identified as cellular organelles with largely unidentified functions. Whether NPs might affect migration, invasion, and migrasome formation and induce miscarriage has been completely unexplored. In this study, we selected polystyrene nanoplastics (PS-NPs, 50 nm) as a model of plastic particles and treated human trophoblast cells and pregnant mice with PS-NPs at doses near the actual environmental exposure doses of plastic particles in humans. We found that exposure to PS-NPs induced a pregnant mouse miscarriage. PS-NPs suppressed ROCK1-mediated migration/invasion and migrasome formation. SOX2 was identified as the transcription factor of ROCK1. PS-NPs activated autophagy and promoted the autophagy degradation of SOX2, thus suppressing SOX2-mediated ROCK1 transcription. Supplementing with murine SOX2 or ROCK1 could efficiently rescue migration/invasion and migrasome formation and alleviate miscarriage. Analysis of the protein levels of SOX2, ROCK1, TSPAN4, NDST1, P62, and LC-3BII/I in PS-NP-exposed trophoblast cells, villous tissues of unexplained miscarriage patients, and placental tissues of PS-NP-exposed mice gave consistent results. Collectively, this study revealed the reproductive toxicity of nanoplastics and their potential regulatory mechanism, indicating that NP exposure is a risk factor for female reproductive health.

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Section: Discussionmentioning

confidence: 99%

Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage

Wan,

Wang,

Chen

et al. 2024

ACS Nano

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“…Although this review did not identify any studies with male participants, the first reports of microplastics detected in human testes and semen were published within 5 months of our last search date, in June 2023. 46 Given the growing body of evidence from cell culture and animal studies on the potential reproductive toxicity of micro-and nanoplastics, [24][25][26][27][28][29] we propose that establishing the effects of these pollutants on human fertility and pregnancy outcomes is a public health imperative. Evidence of potential harmful consequences could inform guidance and interventions to reduce plastic exposure preconception, during pregnancy and postpartum, as well as advocating for the reduction of unnecessary single-use plastics in healthcare settings.…”

Section: Discussionmentioning

confidence: 99%

“…[16][17][18][19][20][21] The first reports of microplastics detected in human placenta and meconium were published in 2021 22,23 and in recent years there has been an expansion in studies examining potential detrimental reproductive effects of these particles on a cellular level and in animal models. [24][25][26][27][28][29] Recent insights into the presence of microplastics in human tissues and evidence of their potential reproductive toxicity are summarised in Figure 1.…”

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confidence: 99%

Exposure to microplastics and human reproductive outcomes: A systematic review

Hunt,

Davies,

Fraser

et al. 2024

BJOG

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BackgroundMicroplastics, produced through degradation of environmental plastic pollution, have been detected in human tissues including placenta and fetal meconium. Cell culture and animal studies have demonstrated potential reproductive toxicity of these particles; however, their association with adverse fertility or pregnancy outcomes in humans is not known.ObjectivesTo synthesise evidence for the presence of microplastics in human reproductive tissue and their associations with environmental exposures and reproductive outcomes.Search StrategyMEDLINE, Embase, Emcare, CINAHL, ClinicalTrials.gov and ICTRP were searched from inception to 03/02/2023.Selection CriteriaStudies of human participants, assessing presence of microplastics in reproductive tissues, environmental exposures to microplastics, and fertility‐ or pregnancy‐related outcomes.Data Collection and AnalysisTwo independent reviewers selected studies and extracted data on study characteristics, microplastics detected, environmental exposures and reproductive outcomes. Narrative synthesis was performed due to methodological heterogeneity.Main ResultsOf 1094 citations, seven studies were included, covering 96 participants. Microplastics composed of 16 different polymer types were detected in both placental and meconium samples. Two studies reported associations between lifestyle factors (daily water intake, use of scrub cleanser or toothpaste, bottled water and takeaway food) and placental microplastics. One study reported associations between meconium microplastics and reduced microbiota diversity. One reported placental microplastic levels correlated with reduced birthweights and 1‐minute Apgar scores.ConclusionsThere is a need for high‐quality observational studies to assess the effects of microplastics on human reproductive health.

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“…In vitro human placenta models with NP concentrations of 10 and 100 μg/ml, internalization of MP particles by placental cells was solely observed, and acute cytotoxicity of PE-MPs or damages to DNA was not detected (Hesler et al, 2019). Studies conducted by Dusza et al (Hu, Zhu, et al, 2022). In all, current in vitro studies suggested a potential link between MP exposure and gynecological aberrant such as early pregnancy loss, although the toxic effects of MPs on human embryos remain obscure and further studies are needed to provide additional insights.…”

Section: Placental Toxicity Of Mps and Nps On Human Placental (In Vitro)mentioning

confidence: 95%

“…Meanwhile, other toxic effects of MPs should be assessed. However, in human trophoblast cell culture experiments with PS‐NP concentrations of 0, 10, 50, and 100 μg/ml have shown that MPs may end in numerous toxic endpoints in embryonic cells, including reduced cell vitality and cell cycle arrest, reduced trophoblast migration and invasion ability by a dose‐dependent manner, increased production of cytoplasmic ROS and pro‐inflammatory cytokines, and affected gene expression patterns in trophoblast cell lines (Hu, Zhu, et al, 2022). In all, current in vitro studies suggested a potential link between MP exposure and gynecological aberrant such as early pregnancy loss, although the toxic effects of MPs on human embryos remain obscure and further studies are needed to provide additional insights.…”

Section: Human‐derived Germ Cell/organoid Toxicity Of Mps and Npsmentioning

confidence: 99%

The reproductive and transgenerational toxicity of microplastics and nanoplastics: A threat to mammalian fertility in both sexes

Yin

2023

J of Applied Toxicology

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Microplastics (MPs) and nanoplastics (NPs) are extensively distributed in the environment. However, a comprehensive review and in‐depth discussion on the effects of MPs and NPs to reproductive capacity and transgenerational toxicity on mammals, especially on humans, is lacked. It is suggested that microplastics and nanoplastics could accumulate in mammalian reproductive organs and exert toxic effects on the reproductive system for both sexes. For males, the damage of microplastics consists of abnormal testicular and sperm structure, decreased sperm vitality, and endocrine disruption, which were caused by oxidative stress, inflammation, apoptosis of testicular cells, autophagy, abnormal cytoskeleton, and abnormal hypothalamic‐pituitary‐testicular axis. For females, the damage of microplastics includes abnormal ovary and uterus structure and endocrine disruption, which were caused by oxidative stress, inflammation, granulosa cell apoptosis, hypothalamic‐pituitary‐ovary axis abnormalities, and tissue fibrosis. For transgenerational toxicity, premature mortality existed in the rodent offspring after maternal exposure to microplastics. Among the surviving offspring, metabolic disorders, reproductive dysfunction, immune, neurodevelopmental, and cognitive disorders were detected, and these events directly correlated with transgenerational translocation of MPs and NPs. Studies on human‐derived cells or organoids demonstrated that transgenerational toxicity studies for both sexes are yet in the phase of exploring suitable experimental models, and more detailed research on the threat of MPs and NPs to human fertility is still urgently needed. Further studies will help assess the MPs and NPs threat to public fertility and reproductive health risks.

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The potential toxicity of polystyrene nanoplastics to human trophoblasts in vitro

Cited by 31 publications

References 44 publications

Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage

Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage

Exposure to microplastics and human reproductive outcomes: A systematic review

The reproductive and transgenerational toxicity of microplastics and nanoplastics: A threat to mammalian fertility in both sexes

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