Dose-effect of polystyrene microplastics on digestive toxicity in chickens (Gallus gallus): Multi-omics reveals critical role of gut-liver axis

Yin, Kai; Wang, Dongxu; Zhang, Yue; Lu, Hongmin; Wang, Yu; Xing, Mingwei

doi:10.1016/j.jare.2022.10.015

Cited by 49 publications

(8 citation statements)

References 77 publications

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“…Inflammatory factors and chemokines play an important role in macrophage function and inflammation. − To investigate whether 1,4 NQ-BC contributes to inflammation, we detected the gene expression levels of 14 inflammatory factors and chemokines in RAW264.7 cells. Previous studies have shown that TNF, IL6, IL12a, IL13, CCL5, CXCL2, CXCL9, CXCL10, and CXCL11 are cytokines with proinflammatory effects, while IL10 has anti-inflammatory effects. − In this experiment, after 1,4 NQ-BC exposure, the mRNA expression levels of TNF, IL6, IL12a, IL13, CCL5, CXCL2, CXCL9, CXCL10, and CXCL11 increased, while the expression level of IL10 decreased, as shown in Figure S1A,B. These above results indicated that 1,4 NQ-BC exposure would cause inflammation.…”

Section: Discussionsupporting

confidence: 76%

1,4-Naphthoquinone-Coated Black Carbon, a Kind of Atmospheric Fine Particulate Matter, Affects Macrophage Fate: New Insights into Crosstalk between Necroptosis and Macrophage Extracellular Traps

Cui

Xiao

Yuan

et al. 2023

Environ. Sci. Technol.

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1,4-Naphthoquinone-coated BC (1,4 NQ-BC) is an important component of PM2.5 and a representative secondary particle. However, there is no research on the crosstalk mechanism between necroptosis and macrophage extracellular traps (METs) after 1,4 NQ-BC exposure. In this study, we treated RAW264.7 cells with 50, 100, and 200 mg/L 1,4 NQ-BC for 24 h, with 10 μM necrostatin-1 for 24 h, and with 2.5 μM phorbol 12-myristate 13-acetate (PMA) for 3 h. Our experiment revealed that under normal physiological conditions, when macrophages receive external stimuli (such as pathogens; in this experiment, PMA), they will form METs and capture and kill pathogens, thus exerting innate immune function. However, exposure to 1,4 NQ-BC can cause necroptosis in macrophages, accompanied by increased levels of reactive oxygen species (ROS) and cytosolic calcium ions, as well as the expression disorder of inflammatory factors and chemokines, prevent the formation of METs, lead to loss of the function of capturing and killing pathogens, and weaken the innate immune function. Notably, inhibition of necroptosis restored the formation of METs, indicating that necroptosis inhibited the formation of METs. Our study was the first to explore the crosstalk mechanism between necroptosis and METs. This experiment will enrich the mechanism of macrophage injury caused by 1,4 NQ-BC exposure.

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Section: Discussionsupporting

confidence: 76%

1,4-Naphthoquinone-Coated Black Carbon, a Kind of Atmospheric Fine Particulate Matter, Affects Macrophage Fate: New Insights into Crosstalk between Necroptosis and Macrophage Extracellular Traps

Cui

Xiao

Yuan

et al. 2023

Environ. Sci. Technol.

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“…Then, the cells were re‐suspended with binding buffer and adjusted concentration to 5 × 10 5 cells/mL. Adding 5 μL Annexin V‐FITC respectively and before testing using flow cytometry (Becton Dickinson, FACSCalibur) appended 5 μL propidium iodide within 1 h 35 …”

Section: Methodsmentioning

confidence: 99%

Di(2‐ethylhexyl) phthalate and microplastics cause necroptosis and apoptosis in hepatocytes of mice by inducing oxidative stress

Chen

Zhang

et al. 2023

Environmental Toxicology

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Di(2‐ethylhexyl) phthalate (DEHP) is a plasticizer and an endocrine disruptor. Microplastics (MPs) are pathogenic small plastic particles and abundant in the aqueous environment. The problem of residual hazards of plastic products is worthy of study, especially the joint exposure of a variety of plastic‐related products to the toxic effect. We used 200 mg/kg DEHP and 10 mg/L MPs to establish exposure model in vivo and 2 mM DEHP and 200 μg/L MPs to establish AML12 cell exposure model in vitro. In vivo study results showed that compared with the control group (NC) group, DEHP and MPs significantly increased the contents of malondialdehyde and hydrogen peroxide, and significantly decreased the contents of glutathione and the activity of superoxide dismutase, total antioxidant capacity, catalase and glutathione peroxidase. The level of oxidative stress was further aggravated after combined exposure. The reactive oxygen species level of AML12 exposed to DEHP and MPs in vitro was significantly higher than NC group, and the combined exposure was significantly higher than the single exposure. The in vivo and in vitro also confirmed that DEHP and MPs could significantly increase the mRNA and protein levels of apoptosis markers and necroptosis markers and there was an additive effect. After N‐acetylcysteine treatment in vitro, the above‐mentioned oxidative stress level and cell damage decreased significantly. This study provided a reference for advocating the reduction of the mixed use of plastic products, and provided a basis for preventing the harm of plastic products residues.

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“…Mice showed significance for experiencing oxidative stress and building up resistance to it after one week of exposure to microplastics. The exposure to microplastics in mice disrupted the gut–liver axis based on information on intestinal microbiota and differently expressed metabolites [ 126 ]. In another investigation, a dose of 1 mg/L of 5 m PS-MPs was exposed to chickens.…”

Section: Alteration In Gut–liver Axis Due To Nanoplastic Toxicitymentioning

confidence: 99%

“…The findings showed that liver injury was caused by disruption of the intestinal flora through the intestinal liver axis, and that pathogenic bacteria and their byproducts were implicated in liver damage through translocation of the gut–liver axis. According to metabolomics and transcriptome data, apoptosis and abnormal lipid metabolism were the primary contributors to the liver damage produced by PS-MPs [ 126 ].…”

Section: Alteration In Gut–liver Axis Due To Nanoplastic Toxicitymentioning

confidence: 99%

Nanoplastics Toxicity Specific to Liver in Inducing Metabolic Dysfunction—A Comprehensive Review

Haldar

Yhome

Muralidaran

et al. 2023

Genes

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Plastic pollution in the world is widespread and growing. The environment is swamped with nanoplastics (<100 nm), and the health consequences of these less visible pollutants are unknown. Furthermore, there is evidence that microplastics can release nanoplastics by digestive disintegration, implying that macroplastic exposure can cause direct and indirect disease via nanoplastics. The existence and impact of nanoplastics in numerous tissues from invertebrates to larger vertebrates that consume significant amounts of plastics were investigated, and histopathological techniques were utilized to determine physiological reactions and inflammation from the plastics. Nanoplastics enters an organism through the respiratory and gastro-intestinal tract where they accumulate into the liver through blood circulation via absorption, or epidermal infiltration. It is stated that macroplastics can cause damage directly at the site of exposure, whereas nanoplastics can influence the liver, causing subsequent damage to other organs. Multi-organ dysfunction is brought on by liver changes, and nanoplastics can readily enter the gut-liver axis and disturb the gut microflora. By exploring the literature and summarizing the research that has been published to date, this review article reveals the deleterious effect and mechanisms of nanoplastics on the pathophysiological functions of the hepatic system.

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Dose-effect of polystyrene microplastics on digestive toxicity in chickens (Gallus gallus): Multi-omics reveals critical role of gut-liver axis

Cited by 49 publications

References 77 publications

1,4-Naphthoquinone-Coated Black Carbon, a Kind of Atmospheric Fine Particulate Matter, Affects Macrophage Fate: New Insights into Crosstalk between Necroptosis and Macrophage Extracellular Traps

1,4-Naphthoquinone-Coated Black Carbon, a Kind of Atmospheric Fine Particulate Matter, Affects Macrophage Fate: New Insights into Crosstalk between Necroptosis and Macrophage Extracellular Traps

Di(2‐ethylhexyl) phthalate and microplastics cause necroptosis and apoptosis in hepatocytes of mice by inducing oxidative stress

Nanoplastics Toxicity Specific to Liver in Inducing Metabolic Dysfunction—A Comprehensive Review

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