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61,005 resultsShowing papers similar to Microplasticsand Nanoplastics Cause Thyroid Dysfunctionin Adolescent Mice through the Intestinal Microbiota-Mediated Hypothalamus-Pituitary-ThyroidAxis
ClearMicroplastics and Nanoplastics Cause Thyroid Dysfunction in Adolescent Mice through the Intestinal Microbiota-Mediated Hypothalamus-Pituitary-Thyroid Axis
Adolescent mice exposed to PP and PET micro/nanoplastics in diet showed reduced thyroid hormone levels, and fecal microbiota transplantation experiments confirmed that gut microbiota mediated thyroid dysfunction via the intestinal-hypothalamus-pituitary-thyroid axis.
Small particles, big impact: A narrative review of microplastics and their effects on thyroid function
This narrative review synthesized evidence linking microplastic and nanoplastic exposure to thyroid dysfunction, examining mechanisms including endocrine disruption, oxidative stress, and immune dysregulation. The authors identified thyroid-disrupting effects in both animal models and human epidemiological data, with children and pregnant women as particularly vulnerable populations.
Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.
Thyroid and parathyroid function disorders induced by short-term exposure of microplastics and nanoplastics: Exploration of toxic mechanisms and early warning biomarkers
Mice exposed to micro- and nanoplastics through both breathing and eating showed disrupted thyroid and parathyroid gland function in just a short exposure period. Microplastics ingested through food were more harmful to the thyroid, while inhaled nanoplastics caused the most damage to the parathyroid, which helps regulate calcium levels in the body. These findings suggest that everyday microplastic exposure could interfere with important hormone systems that affect metabolism and bone health.
Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.
A long-term mouse study examined how chronic exposure to polystyrene microspheres interacts with a high-fat diet to affect obesity-related outcomes, finding that microplastics worsened metabolic disruption and fat accumulation compared to diet alone. The results raise concern that microplastic exposure may be an environmental factor contributing to the global obesity epidemic.
Gut Check: Microbiota and Obesity in Mice Exposed to Polystyrene Microspheres
Researchers found that gut microbiota appeared to play a mediating role in the obesity outcomes observed in mice fed manufactured polystyrene microspheres, suggesting that microplastic-induced alterations to the gut microbiome may be a mechanism linking microplastic exposure to metabolic dysfunction and weight gain.
Perturbation of gut microbiota plays an important role in micro/nanoplastics-induced gut barrier dysfunction
Researchers investigated how micro- and nanoplastics disrupt gut barrier function in mice, finding that different surface chemistries caused varying levels of damage. The study suggests that these plastic particles harm the gut by altering the gut microbiome, which then leads to inflammation and weakening of the intestinal barrier that normally keeps harmful substances out of the body.
Adolescent exposure to micro/nanoplastics induces cognitive impairments in mice with neuronal morphological damage and multi-omic alterations
Adolescent mice exposed to polystyrene nanoplastics showed significant memory and learning problems, along with neuron loss and reduced new brain cell growth in the hippocampus. The nanoplastics also disrupted gut bacteria and brain chemistry, with strong links found between gut microbiome changes and brain metabolic disruption, suggesting that plastic exposure during youth may impair brain development through the gut-brain connection.
Long-term exposure to polystyrene microplastics promotes HFD-induced obesity in mice through exacerbating microbiota dysbiosis
Researchers found that long-term polystyrene microplastic exposure worsened high-fat-diet-induced obesity in mice by exacerbating gut microbiota dysbiosis, suggesting microplastic ingestion may amplify metabolic disease risk through disruption of the gut microbiome.
Microplastic-induced gut microbiota and serum metabolic disruption in Sprague-Dawley rats
Researchers exposed rats to a mixture of common microplastic types at concentrations reflecting real-world human exposure and found significant disruptions to gut bacteria and blood metabolites. The microplastic mixture altered the balance of beneficial and harmful gut microbes and changed metabolic pathways related to amino acids and lipids. The study suggests that everyday microplastic exposure from food and water may affect mammalian gut health and metabolism.
Polystyrene Microplastics‐Induced Thyroid Dysfunction in Mice: A Study of Gene Expression, Oxidative Stress, and Histopathological Changes
In a mouse study, polystyrene microplastics caused thyroid dysfunction by altering gene expression, increasing oxidative stress, and damaging thyroid tissue. The findings show that microplastic exposure can disrupt the endocrine system, specifically the thyroid gland which controls metabolism and development. As environmental microplastic contamination increases, this research raises concerns about potential thyroid-related health problems in both animals and humans.
Micro/nanoplastics induce thyroid follicular cell pyroptosis to trigger thyrotoxicity by activating NF-κB signaling
Researchers found that micro- and nanoplastics induce pyroptosis (inflammatory cell death) in thyroid follicular cells through activation of NF-kB signaling, triggering thyroid toxicity in mice. The study demonstrated that both 5-micrometer microplastics and 50-nanometer nanoplastics administered orally for up to 8 weeks caused thyroid dysfunction, revealing a specific mechanism by which plastic particles may disrupt thyroid function.
Micro/nanoplastics induce thyroid follicular cell pyroptosis to trigger thyrotoxicity by activating NF-κB signaling
Researchers found that micro- and nanoplastics induce pyroptosis (inflammatory cell death) in thyroid follicular cells through activation of NF-kB signaling, triggering thyroid toxicity in mice. The study demonstrated that both 5-micrometer microplastics and 50-nanometer nanoplastics administered orally for up to 8 weeks caused thyroid dysfunction, revealing a specific mechanism by which plastic particles may disrupt thyroid function.
Adolescent exposure to polystyrene nanoplastics induces male reproductive damage via the microbiome-gut-testis axis
Researchers exposed adolescent rats to polystyrene nanoplastics for five weeks and observed dose-dependent damage to testicular tissue, disrupted spermatogenesis, and compromised blood-testis barrier integrity. The study revealed a novel microbiome-gut-testis axis mechanism, where nanoplastics altered gut bacteria composition, which in turn contributed to reproductive toxicity in developing males.
Nano and microplastics: unveiling their profound impact on endocrine health
This review summarizes existing research showing that micro- and nanoplastics can disrupt the endocrine (hormone) system, altering reproductive hormones, thyroid function, and gene expression in lab and animal studies. Exposure to these particles triggered inflammation markers and oxidative stress in hormone-producing organs, suggesting that widespread plastic pollution may be contributing to rising rates of hormonal and reproductive health problems.
Placental microplastics contamination and its impact on thyroid function in newborns
Researchers analyzed placental tissue from over 1,200 mother-child pairs and found microplastics present in the samples, then examined whether these levels were associated with thyroid hormone profiles in the newborns. The study found associations between placental microplastic contamination and variations in newborn thyroid function, which is critical for early growth and development. These findings suggest that prenatal microplastic exposure warrants further investigation as a potential factor in infant health.
Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice
Researchers fed mice two sizes of polystyrene microplastics for five weeks and observed significant disruption of gut bacteria and changes in liver fat metabolism. The microplastics decreased mucus production in the gut and shifted the balance of key bacterial populations at multiple taxonomic levels. The study suggests that microplastic ingestion can trigger gut microbiota imbalance in mammals, which may in turn affect metabolic health.
Distinctive metabolic disturbances associated with redox homeostasis, nervous and hormonal functions during gut microbial enrichment upon polystyrene microplastic exposure
Researchers tracked gut microbial enrichment, virome shifts, and metabolomic changes in organisms exposed to polystyrene microplastics, finding Eubacteriales-dominated dysbiosis accompanied by colitis. Microplastic exposure activated polyamine synthesis pathways, altered serotonin and thyroxine metabolism, and increased cholesterol-derived hormone synthesis, revealing complex hormonal and neurochemical disruption.
Polyethylene Microplastic Exposure Disrupts Sex and Gut Hormones via Gut Microbial and Metabolic Pathways.
Researchers exposed female mice to polyethylene microplastics for four weeks and found significantly reduced levels of GLP-1, PYY, AMH, and testosterone, linked to reduced Akkermansia gut bacteria and disrupted metabolites, identifying a gut microbiome-mediated pathway through which microplastics disrupt sex and metabolic hormones.
The ant that may well destroy a whole dam: a systematic review of the health implication of nanoplastics/microplastics through gut microbiota
This systematic review summarizes existing research on how nanoplastics and microplastics disrupt gut bacteria in various organisms. The findings show that plastic particle exposure consistently alters gut microbiome composition, which in turn affects the host's immune function, metabolism, and overall health. These gut bacteria changes may be a key pathway through which microplastics harm human health.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
Researchers orally exposed adult male mice to polyethylene microplastics under both normal and high-fat diets, assessing effects on the gastrointestinal tract. The study found that diet influences microplastic-induced gut changes, with greater effects observed in animals fed a western-style high-fat diet.
Microbiome: A forgotten target of environmental micro(nano)plastics?
This review examines how micro- and nanoplastics affect the microbiome of various organisms, an area that has received less attention than other toxicological endpoints. Researchers found that most studies focused on polystyrene particles and that exposure consistently disrupted microbiome composition, triggered immune responses, and altered enzyme activity across organisms including crustaceans, fish, and mammals. The study highlights the microbiome as an important but often overlooked target of microplastic pollution.
Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
In a mouse study, oral exposure to polystyrene microplastics of two sizes altered the gut bacteria community and caused metabolic changes in both the intestines and the brain. The disrupted gut bacteria appeared to drive changes in bile acid, energy, and other metabolic pathways. These findings support the idea that microplastics in food and water could affect brain health indirectly by first disrupting the gut microbiome and its chemical signals.
Combined exposure to microplastics and tetracycline leads to impaired skeletal development in young mice by the microbiota gut bone axis
Young mice co-exposed to microplastics and tetracycline antibiotic for 8 weeks showed significantly worse bone development than those exposed to either alone, driven by gut microbiota dysbiosis and disruption of the gut-bone axis.