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Environmental Science and Pollution... Jul 2023Microplastics (MPs), with a diameter of less than 5 mm, include polymers such as polystyrene, polypropylene, and polyethylene. The MPs occur in different morphologies... (Review)
Review
Microplastics (MPs), with a diameter of less than 5 mm, include polymers such as polystyrene, polypropylene, and polyethylene. The MPs occur in different morphologies including fragments, beads, fibers, and films that are swallowed by fresh water and land-based animals and enter their food chain, where they produce hazardous effects such as uterine toxicity, infertility, and neurotoxicity. The aim of this review is to explore the effects of polystyrene MPs (PS-MPs) on the female reproductive system and understand the mechanisms by which they produce reproductive toxicity. Several studies suggested that the exposure to PS-MPs increased the probability of larger ovaries with fewer follicles, decreased the number of embryos produced, and decreased the number of pregnancies in female mice. It also changed sex hormone levels and caused oxidative stress, which could have an impact on fertility and reproduction. Exposure to PS-MPs caused the death of granulosa cells through apoptosis and pyroptosis via activation of the NLRP3/caspase pathway and disruption of the Wnt-signaling pathway. Activation of TL4/NOX2 caused the uterine fibrosis resulting in endometrium thinning. The PS-MPs had a negative impact on ovarian capacity, oocyte maturation, and oocyte quality. Furthermore, the PS-MPs disrupted the hypothalamus-pituitary-gonadal axis in marine animals, resulting in a decrease in hatching rate and offspring body size, causing trans-generational effects. It also reduced fecundity and produced germ-line apoptosis. The main focus of this review was to explore the different mechanisms and pathways through which PS-MPs adversely impact the female reproductive system.
Topics: Female; Animals; Mice; Microplastics; Polystyrenes; Plastics; Polyethylene; Ovary
PubMed: 37247153
DOI: 10.1007/s11356-023-27930-1 -
Particle and Fibre Toxicology Aug 2023Plastic pollution is greatly serious in the ocean and soil. Microplastics (MPs) degraded from plastic has threatened animals and humans health. The accumulation of MPs...
BACKGROUND
Plastic pollution is greatly serious in the ocean and soil. Microplastics (MPs) degraded from plastic has threatened animals and humans health. The accumulation of MPs in the tissues and blood in animals and humans has been found. There is therefore a need to assess the toxicological effects of MPs on the reproductive system.
RESULTS
In this study, we explored the effect of polystyrene microplastics (PS-MPs) on premature testicular aging in vitro and in vivo. In vitro, we found that testicular sertoli cells (TM4 cells) was prematurely senescent following PS-MPs treatment by the evaluation of a range of aging marker molecules (such as Sa-β-gal, p16 and 21). TM4 cells were then employed for in vitro model to study the potential molecular mechanism by which PS-MPs induce the premature senescence of TM4 cells. NF-κB is identified as a key molecule for PS-MPs-induced TM4 cellular senescence. Furthermore, through eliminating reactive oxygen species (ROS), the activation of nuclear factor kappa B (NF-κB) was blocked in PS-MPs-induced senescent TM4 cells, indicating that ROS triggers NF-κB activation. Next, we analyzed the causes of mitochondrial ROS (mtROS) accumulation induced by PS-MPs, and results showed that Ca overload induced the accumulation of mtROS. Further, PS-MPs exposure inhibits mitophagy, leading to the continuous accumulation of senescent cells. In vivo, 8-week-old C57 mice were used as models to assess the effect of PS-MPs on premature testicular aging. The results illustrated that PS-MPs exposure causes premature aging of testicular tissue by testing aging markers. Additionally, PS-MPs led to oxidative stress and inflammatory response in the testicular tissue.
CONCLUSION
In short, our experimental results revealed that PS-MPs-caused testicular premature aging is dependent on Ca/ROS/NF-κB signaling axis. The current study lays the foundation for further exploration of the effects of microplastics on testicular toxicology.
Topics: Humans; Male; Animals; Mice; Aging, Premature; Microplastics; Polystyrenes; Plastics; NF-kappa B; Reactive Oxygen Species
PubMed: 37641072
DOI: 10.1186/s12989-023-00546-6 -
Advanced Science (Weinheim,... Jul 2023Exposure to micro- and nanoplastics (MNPs) is common because of their omnipresence in environment. Recent studies have revealed that MNPs may cause atherosclerosis, but...
Exposure to micro- and nanoplastics (MNPs) is common because of their omnipresence in environment. Recent studies have revealed that MNPs may cause atherosclerosis, but the underlying mechanism remains unclear. To address this bottleneck, ApoE mice are exposed to 2.5-250 mg kg polystyrene nanoplastics (PS-NPs, 50 nm) by oral gavage with a high-fat diet for 19 weeks. It is found that PS-NPs in blood and aorta of mouse exacerbate the artery stiffness and promote atherosclerotic plaque formation. PS-NPs activate phagocytosis of M1-macrophage in the aorta, manifesting as upregulation of macrophage receptor with collagenous structure (MARCO). Moreover, PS-NPs disrupt lipid metabolism and increase long-chain acyl carnitines (LCACs). LCAC accumulation is attributed to the PS-NP-inhibited hepatic carnitine palmitoyltransferase 2. PS-NPs, as well as LCACs alone, aggravate lipid accumulation via upregulating MARCO in the oxidized low-density lipoprotein-activated foam cells. Finally, synergistic effects of PS-NPs and LCACs on increasing total cholesterol in foam cells are found. Overall, this study indicates that LCACs aggravate PS-NP-induced atherosclerosis by upregulating MARCO. This study offers new insight into the mechanisms underlying MNP-induced cardiovascular toxicity, and highlights the combined effects of MNPs with endogenous metabolites on the cardiovascular system, which warrant further study.
Topics: Animals; Mice; Microplastics; Polystyrenes; Atherosclerosis; Plaque, Atherosclerotic; Aorta
PubMed: 37144527
DOI: 10.1002/advs.202205876 -
Environment International Sep 2023Microplastic particles (MP) are prevalent in both industrial production and the natural environment, posing a significant concern for human health. Daily diet, air...
Microplastic particles (MP) are prevalent in both industrial production and the natural environment, posing a significant concern for human health. Daily diet, air inhalation, and skin contact are major routines of MP intake in human. The main injury target systems of MPs include the digestive system, respiratory system, and cardiovascular system. However, the study on MPs' adverse effects on the heart is less than other target organs. Previous in vivo studies have demonstrated that MPs can induce heart injuries, including abnormal heart rate, apoptosis of cardiomyocytes, mitochondrial membrane potential change, and fibrin overexpression. To address animal welfare concerns and overcome inter-species variations, this study employed a human pluripotent stem cell-derived in vitro three-dimensional cardiac organoid (CO) model to investigate the adverse effects of MPs on the human heart. The distinct cavities of COs allowed for the observation of MPs' aggregation and spatial distribution following polystyrene-MP (PS) exposure in a dynamic exposure system. After exposure to various concentrations of PS (0.025, 0.25 and 2.5 µg/mL, with the lowest concentration equivalent to human internal exposure levels), the COs exhibited increased oxidative stress, inflammatory response, apoptosis, and collagen accumulation. These findings were consistent with in vivo observations, in terms of increases in the interventricular septal thickness. The expression of hypertrophic-related genes of COs (MYH7B/ANP/BNP/COL1A1) changed noticeably and the cardiac-specific markers MYL2/MYL4/CX43 were also markedly elevated. Our findings revealed the PS could induced cardiac hypertrophy in vivo and in vitro, indicating that MP may be an under-recognized risk factor for cardiovascular system.
Topics: Humans; Animals; Mice; Cardiotoxicity; Plastics; Microplastics; Polystyrenes; Drug-Related Side Effects and Adverse Reactions; Myocytes, Cardiac; Organoids
PubMed: 37669592
DOI: 10.1016/j.envint.2023.108171 -
Environmental Pollution (Barking, Essex... Sep 2023Nanoplastics (NPs) are defined as a group of emerging pollutants. However, the adverse effect of NPs and/or heavy metals on mammals is still largely unclear. Therefore,...
Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney.
Nanoplastics (NPs) are defined as a group of emerging pollutants. However, the adverse effect of NPs and/or heavy metals on mammals is still largely unclear. Therefore, we performed a 35-day chronic toxicity experiment with mice to observe the impacts of exposure to Cadmium (Cd) and/or polystyrene nanoplastics (PSNPs). This study revealed that combined exposure to Cd and PSNPs added to the mice's growth toxicity and kidney damage. Moreover, Cd and PSNPs co-exposure obviously increased the MDA level and expressions of 4-HNE and 8-OHDG while decreasing the activity of antioxidase in kidneys via inhibiting the Nrf2 pathway and its downstream genes and proteins expression. More importantly, the results suggested for the first time that Cd and PSNPs co-exposure synergistically increased iron concentration in kidneys, and induced ferroptosis through regulating expression levels of SLC7A11, GPX4, PTGS2, HMGB1, FTH1 and FTL. Simultaneously, Cd and PSNPs co-exposure further increased the expression levels of Pink, Parkin, ATG5, Beclin1, and LC3 while significantly reducing the P62 expression level. In brief, this study found that combined exposure to Cd and PSNPs synergistically caused oxidative stress, ferroptosis and excessive mitophagy ultimately aggravating kidney damage in mice, which provided new insight into the combined toxic effect between heavy metals and PSNPs on mammals.
Topics: Animals; Mice; Cadmium; Microplastics; Polystyrenes; Ferroptosis; Mitophagy; Oxidative Stress; Kidney; Mammals
PubMed: 37270049
DOI: 10.1016/j.envpol.2023.121947 -
ACS Nano Aug 2023Dietary pollution by polystyrene microplastics (MPs) can cause hepatic injuries and microbial dysbiosis. Epigallocatechin-3-gallate (EGCG), the major polyphenol in green...
Dietary pollution by polystyrene microplastics (MPs) can cause hepatic injuries and microbial dysbiosis. Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, exerts beneficial effects on the liver by modulating the gut microbiota. However, the role of microbiota in MPs-induced hepatic injuries and the protective effect of EGCG have not been clarified. Here, 5 μm MPs were orally administered to mice to induce hepatic injuries. Subsequently, antibiotic cocktail (ABX) and fecal microbial transplant (FMT) experiments were performed to investigate the underlying microbial mechanisms. Additionally, EGCG was orally administered to mice to explore its protection against MPs-induced hepatic injuries. Our results showed that MPs activated systemic and hepatic inflammation, promoted fibrosis, and altered the liver metabolome; meanwhile, MPs damaged the gut homeostasis by disturbing the gut microbiome, promoting colonic inflammation, and impairing the intestinal barrier. Notably, MPs reduced the abundance of the probiotics Akkermansia, Mucispirillum, and Faecalibaculum while increasing the pathogenic Tuzzerella. Interestingly, the elimination of gut microbiota mitigated MPs-induced colonic inflammation and intestinal barrier impairment. Moreover, ABX ameliorated MPs-induced systemic and hepatic inflammation but not fibrosis. Correspondingly, microbiota from MPs-administered mice induced colonic, systemic, and hepatic inflammation, while their profibrosis effect on the liver was not observed. Finally, EGCG elevated the abundance of probiotics and effectively repressed MPs-induced colonic inflammation. MPs-induced systemic and hepatic inflammation, fibrosis, and remodeling of the liver metabolome were also attenuated by EGCG. These findings illustrated that gut microbiota contributed to MPs-induced colonic and hepatic injuries, while EGCG could serve as a potential prevention strategy for these adverse consequences.
Topics: Animals; Mice; Gastrointestinal Microbiome; Microplastics; Plastics; Polystyrenes; Inflammation
PubMed: 37486121
DOI: 10.1021/acsnano.3c04449 -
Journal of Hazardous Materials Jan 2024Particle size is one of the most important factors in determining the biological toxicity of microplastics (MPs). In this study, we attempted to examine the systemic...
Particle size is one of the most important factors in determining the biological toxicity of microplastics (MPs). In this study, we attempted to examine the systemic toxicity of polystyrene MPs of different sizes (0.5 µm MP1 and 5 µm MP2) in C57BL/6 J mice. After the mice were given oral gavage of MPs for 8 consecutive weeks, histopathology and molecular biology assays, 16 S rRNA sequencing of the gut microbiota, and untargeted metabolomics were performed. The results showed that MPs were distributed in the organs in a size-dependent manner, with smaller particles demonstrating greater biodistribution. Further analysis indicated that exposure to MPs caused multi-organ damage through distinct toxicity pathways. Specifically, exposure to 0.5 µm MP1 led to excessive accumulation and induced more serious inflammation and mechanical damage in the spleen, kidney, heart, lung, and liver. However, 5 µm MP2 led to more severe intestinal barrier dysfunction, as well as gut dysbiosis and metabolic disorder in association with neuroinflammation. These results are helpful in expanding our knowledge of the toxicity of MPs of different sizes in mammalian models.
Topics: Animals; Mice; Polystyrenes; Microplastics; Plastics; Gastrointestinal Microbiome; Tissue Distribution; Mice, Inbred C57BL; Mammals
PubMed: 37717443
DOI: 10.1016/j.jhazmat.2023.132503 -
Journal of Hazardous Materials Sep 2023The adsorption of toxic substances on polystyrene microplastics (PSMPs) can modify their biological toxicity and exacerbate the threat to human health. The effects of...
The adsorption of toxic substances on polystyrene microplastics (PSMPs) can modify their biological toxicity and exacerbate the threat to human health. The effects of benzo [a] pyrene (B (a) P)-loaded aged PSMPs on colonic barrier integrity remains unclear. Here, we showed that binding environmentally relevant concentrations of B (a) P alteredl̥ the physicochemical features and markedly enhanced the toxicity of PSMPs. Compared to pristine PSMP, PSMP@B (a) P promoted colonic barrier degradation, body weight loss, colon length shortening, oxidative stress (OS), autophagy, inflammation, and bacterial translocation. Microplastic (MP) exposure induced injury to the colon barrier, including tight junction (TJ) and mucosal barriers, via overactivation of the Notch signalling pathway under increased OS in mice and intestinal organoids. Notably, PSMP@B (a) P exposure exacerbated damage to TJ and the mucosal barrier via the overproduction of reactive oxygen species (ROS), which could be related to the release of B (a) P from PSMP@B (a) P induced by the acidic environment of autophagosomes, which in turn exert synergistic toxic effects with PSMPs. Our study elucidates some of the potential molecular mechanisms by which B (a) P enhances PSMP-related intestinal toxicity, which provides a potential therapeutic approach for diseases caused by PSMP@B (a)P and PSMP pollution.
Topics: Humans; Animals; Mice; Aged; Microplastics; Polystyrenes; Plastics; Benzo(a)pyrene; Colon; Oxidative Stress
PubMed: 37320903
DOI: 10.1016/j.jhazmat.2023.131820 -
The Science of the Total Environment Dec 2023Polystyrene microplastics (PSMPs) are some of the most common microplastic components, and the resulting pollution has become a global problem. Extensive studies have...
Polystyrene microplastics (PSMPs) are some of the most common microplastic components, and the resulting pollution has become a global problem. Extensive studies have been conducted on the toxic effects of PSMPs on the heart, lungs, liver, kidneys, nerves, intestines and other tissues. However, the impact of PSMPs on vascular toxicity is poorly understood at present. The aim of this study was to reveal the vascular toxicity of microplastics (MPs). Patients were assigned to a calcification group (25 patients) or a non-calcification group (22 patients) based on the presence or absence of calcification in the thoracic aorta wall. We detected 7 polymer types in human feces. Patients with vascular calcification (VC) had higher levels of total MPs, polypropylene (PP) and polystyrene (PS) in feces than patients without VC. The thoracic aortic calcification score was significantly positively correlated with the total MP abundance (Spearman r = 0.8109, p < 0.0001), PP (Spearman r = 0.7211, p = 0.0160) and PS (Spearman r = 0.6523, p = 0.0471) in feces. We then explored the effects of PSMP exposure on normal and vitamin D3 + nicotine (VDN)-treated rats. PSMP exposure induced mild VC in normal rats and aggravated VC in VDN-treated rats. PSMP exposure disturbed the gut microbiota, causing Proteobacteria and Escherichia_Shigella to be the dominant phylum and genus, respectively. It also induced intestinal inflammatory responses in normal rats, aggravated intestinal inflammation in VDN-treated rats, impaired the intestinal mucosal barrier, and increased intestinal permeability. This study provides a theoretical basis for the risk assessment of MP-induced cardiovascular disease.
Topics: Rats; Humans; Animals; Microplastics; Plastics; Polystyrenes; Vascular Calcification; Kidney; Cholecalciferol
PubMed: 37734602
DOI: 10.1016/j.scitotenv.2023.167215 -
Ecotoxicology and Environmental Safety Nov 2023As the concerned emerging pollutants, several lines of evidence have indicated that nanoplastics (NPs) lead to reproductive toxicity. However, the biological mechanism... (Review)
Review
As the concerned emerging pollutants, several lines of evidence have indicated that nanoplastics (NPs) lead to reproductive toxicity. However, the biological mechanism underlying NPs disturbed spermatogenesis remains largely unknown. Therefore, we aimed to reveal the potential mechanism of impaired spermatogenesis caused by long-term NPs exposure from the perspective of integrated metabolome and microbiome analysis. After 12 weeks of gavage of polystyrene nanoplastics (PS-NPs) and animo-modified polystyrene nanoplastics (Amino-NPs), a well-designed two-exposure stages experimental condition. We found that NPs exposure induced apparent abnormal spermatogenesis, which appeared more severe in the Amino-NPs group. Mechanistically, 14 floras associated with glucose and lipid metabolism were significantly altered, as evidenced by 16 S rRNA sequencing. Testicular metabolome revealed that the Top 50 changed metabolites were also enriched in lipid metabolism. Subsequently, the combined gut microbiome and metabolome analysis uncovered the strong correlations between Klebsiella, Blautia, Parabacteroides, and lipid metabolites (e.g., PC, LysoPC and GPCho). We speculate that the dysbiosis of gut microbiota-related disturbed lipid metabolism may be responsible for long-term NPs-induced damaged spermatogenesis, which provides new insights into NPs-induced dysregulated spermatogenesis.
Topics: Male; Humans; Gastrointestinal Microbiome; Microplastics; Polystyrenes; Spermatogenesis; Metabolome
PubMed: 37890247
DOI: 10.1016/j.ecoenv.2023.115626