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61,005 resultsShowing papers similar to Environmental microplastic accumulation exacerbates liver ischemia-reperfusion injury in rat: Protective effects of melatonin
ClearPrenatal melatonin reprograms liver injury in male pups caused by maternal exposure to a high-fat diet and microplastics
Researchers investigated whether prenatal melatonin could protect against liver injury in rat pups caused by maternal exposure to both a high-fat diet and microplastics. The study found that combined high-fat diet and microplastic exposure increased liver fat accumulation, inflammation, and oxidative stress in offspring, but melatonin treatment significantly reduced these effects, suggesting its potential as a protective agent against microplastic-related liver damage during early development.
Melatonin Alleviates Intestinal Barrier Damaging Effects Induced by Polyethylene Microplastics in Albino Rats
Researchers found that polyethylene microplastics damaged the intestinal barrier in rats by causing inflammation, reducing protective mucus, and disrupting the tight junctions between gut cells. The damage was more severe at higher doses and included changes in gut bacteria composition. The study also found that melatonin treatment helped protect against these intestinal effects, suggesting potential avenues for reducing microplastic-related gut damage.
Exploring Oxidative Stress and Metabolic Dysregulation in Lung Tissues of Offspring Rats Exposed to Prenatal Polystyrene Microplastics: Effects of Melatonin Treatment
Researchers found that rat pups exposed to polystyrene microplastics before birth showed significant oxidative stress and metabolic disruption in their lung tissues. The prenatal exposure altered nucleic acid metabolism and amino acid profiles in the lungs of newborn pups. Encouragingly, treatment with melatonin significantly improved lung function and reduced tissue damage in the affected offspring.
Melatonin Alleviates the Damage of Polystyrene Microplastics to Porcine Oocytes by Reducing Oxidative Stress and Mitochondrial Damage, and Regulating Autophagy and Apoptosis Levels
Researchers investigated whether the antioxidant melatonin could protect porcine oocytes from damage caused by polystyrene microplastics. The study found that microplastics at 30 micrograms per milliliter significantly impaired oocyte maturation, but melatonin treatment helped alleviate this damage by reducing oxidative stress, protecting mitochondrial function, and regulating autophagy and cell death pathways.
Melatonin mitigates polystyrene nanoplastics-induced impairment of oocyte maturation in mice
Researchers found that polystyrene nanoplastics impair egg cell maturation in mice by causing excessive oxidative stress, mitochondrial dysfunction, and disrupting the structural machinery needed for proper cell division. They then tested whether melatonin could counteract these effects and found that melatonin treatment significantly alleviated the damage by restoring mitochondrial function and reducing oxidative stress. The study suggests that melatonin may offer a protective strategy against nanoplastic-induced reproductive harm.
Microplastic-mediated new mechanism of liver damage: From the perspective of the gut-liver axis
This review describes how microplastics can damage the liver through the gut-liver axis: they first disrupt the gut's protective barrier and beneficial bacteria, allowing harmful substances to leak through the weakened intestinal wall into the bloodstream and travel to the liver. Once there, these substances cause inflammation, metabolic problems, and oxidative stress, offering a new explanation for how microplastic exposure could lead to liver disease.
Exposure to microplastics and liver oncogenesis: A comprehensive review on molecular mechanisms and pathogenic pathways
Researchers reviewed mechanisms by which microplastic exposure may promote liver cancer, identifying oxidative stress, mitochondrial dysfunction, inflammatory signaling, and epigenetic disruption as key pathways, while noting that microplastics can also carry heavy metals and organic pollutants that synergistically amplify hepatotoxic and carcinogenic risk.
Potential toxicity of microplastics on vertebrate liver: A systematic review and meta–analysis
This meta-analysis of 118 studies found that microplastics damage vertebrate livers by inducing oxidative stress and intracellular toxicity, altering biotransformation processes, and disrupting lipid metabolism. Organisms at earlier life stages, exposed to smaller particles, and for longer durations showed the greatest liver damage, with catalase, GST, reactive oxygen species, and alkaline phosphatase levels progressively increasing with microplastic concentration.
Melatonin counteracts polyethylene microplastics induced adreno-cortical damage in male albino rats
Researchers found that polyethylene microplastics damaged the adrenal glands of male rats, disrupting cortisol production and reducing genes needed for hormone synthesis. This is the first study to specifically examine microplastic effects on the adrenal glands, which are critical for the body's stress response. The study also showed that melatonin, a natural hormone, provided significant protection against this damage, suggesting a possible way to counteract microplastic-related endocrine disruption.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
Melatonin attenuates polystyrene microplastics induced motor neurodevelopmental defect in zebrafish (Danio rerio) by activating nrf2 - isl2a Axis
Researchers found that melatonin protected zebrafish embryos from polystyrene microplastic-induced motor neuron developmental defects by activating the Nrf2-Isl2a signaling pathway, reducing oxidative stress and restoring normal motor neuron axon development.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study
Researchers tested UV-aged polypropylene microplastics from everyday plastic cup lids on mice and lab-grown liver tissue, finding that more heavily aged particles caused greater liver damage. The aged microplastics disrupted energy production in liver cells and caused a harmful buildup of antioxidant molecules, suggesting that the weathered microplastics people encounter in daily life may be more toxic than pristine ones.
Kidney and Liver Disorders Due to Microplastic Exposure: Chronic in Vivo Study in Male White Rats
Male white rats were chronically exposed to microplastics (particles 5 mm or smaller) to assess kidney and liver toxicity, with exposure resulting from environmental weathering and ultraviolet irradiation of plastic materials. The study found measurable histopathological and biochemical damage in both organs, confirming that long-term microplastic exposure causes organ-level injury in mammals.
Emerging threat of environmental microplastics: A comprehensive analysis of hepatic metabolic dysregulation and hepatocellular damage (Review)
This review summarizes existing research on how microplastics damage the liver, which is a key organ for filtering toxins from the body. Studies show that microplastics can cause liver tissue damage, trigger cell death, and disrupt fat metabolism, with smaller particles and longer exposure causing worse effects. The findings highlight the liver as a particularly vulnerable organ because it accumulates microplastics that enter the body through food and water.
Toxicological effects of microplastics in renal ischemia–reperfusion injury
Researchers studied how microplastic exposure affects kidney injury and recovery in a mouse model of reduced blood flow to the kidneys. They found that microplastics worsened kidney damage by triggering inflammatory responses and disrupting cellular repair processes. The study suggests that microplastic accumulation in the body may increase vulnerability to kidney complications.
Melatonin alleviates oxidative stress damage in mouse testes induced by bisphenol A
Researchers investigated whether melatonin could alleviate oxidative stress damage caused by bisphenol A (BPA) exposure in mouse testicular tissue. The study found that melatonin treatment reduced BPA-induced oxidative damage and improved sperm quality indicators, suggesting a potential protective role against the reproductive effects of this common plastic-associated chemical.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
Polystyrene microplastic particles induced hepatotoxic injury via pyroptosis, oxidative stress, and fibrotic changes in adult male albino rats; the therapeutic role of silymarin
Researchers examined the liver toxicity of polystyrene microplastic particles in adult male rats and evaluated whether silymarin, a liver-protective compound, could mitigate the damage. The study found that exposure to 1 and 5 micrometer microplastics induced liver injury through pyroptosis, oxidative stress, and fibrotic changes, and that silymarin treatment showed potential therapeutic effects against these microplastic-induced injuries.
Melatonin and probiotics ameliorate nanoplastics-induced hematopoietic injury by modulating the gut microbiota-metabolism
Researchers found that melatonin and probiotics can ameliorate nanoplastic-induced hematopoietic injury in mice by modulating gut microbiota and metabolism, offering potential prevention strategies against plastic particle toxicity to bone marrow stem cells.
Impact of microplastics exposure on liver health: A comprehensive meta-analysis
This meta-analysis of 70 studies across mice, fish, crabs, and shrimp found that microplastic exposure significantly increases liver enzymes (ALT, AST), oxidative stress marker MDA, and pro-inflammatory cytokines (IL-6, TNF-alpha), while reducing protective antioxidant enzymes (SOD, CAT, GSH, GPx). The findings demonstrate that microplastics disrupt liver function through oxidative stress and inflammation across multiple animal species.
Integrated transcriptomics and metabolomics to explore the varied hepatic toxicity induced by aged- and pristine-microplastics: in vivo and human-originated liver organoids-based in vitro study
Using human liver organoids (miniature lab-grown livers), researchers found that sun-aged microplastics caused more damage to liver cells than fresh microplastics, even at concentrations matching what is found inside human bodies. The aged particles specifically disrupted energy production in mitochondria and altered an amino acid metabolism pathway linked to cardiovascular disease. This is significant because most microplastics in the environment have been weathered by sunlight, meaning the real health risk may be greater than studies using pristine plastics suggest.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
Palliative effect of taurine against hepatic injury induced by polystyrene microplastics through antioxidant and metabolic pathway modulation in mice
Researchers found that polystyrene microplastics caused liver damage in an animal model through oxidative stress and lipid metabolic disruption, and that taurine supplementation exerted a protective effect by modulating oxidative and metabolic pathways. The results support taurine as a potential therapeutic agent for microplastic-induced hepatotoxicity.