Microplastics and Health: Alarming New Research Reveals Widespread Biological Impact

  • Intestinal Impact: High-concentration polystyrene microplastics disrupt gut microbiota composition and induce intestinal inflammation through NK cell activation, leading to metabolic dysfunction even without leaky gut syndrome.
  • Liver Toxicity: Polyethylene microplastics promote hepatic fibrosis and metabolic disturbances by altering lipid metabolism pathways and activating hepatic stellate cells in both healthy and pathological conditions.
  • Gut Barrier Dysfunction: Polyethylene terephthalate microplastics cause significant intestinal damage with inflammatory cell infiltration, reduced mucus secretion, and compromised barrier integrity alongside microbiota dysbiosis.
  • Cardiovascular Effects: Polystyrene microplastics induce severe myocardial inflammation and cell death in aquatic organisms through TLR4/NF-κB pathway activation, suggesting potential cardiovascular risks.
  • Respiratory Toxicity: Polystyrene microplastic fragments specifically trigger pulmonary inflammation via TLR4-mediated pathways, while other plastic types show minimal respiratory effects.
  • Systemic Bioaccumulation: Size-dependent uptake patterns show smaller microplastics accumulate in multiple organs including liver, inducing oxidative stress and metabolic disruption across biological systems.
  1. Hasegawa, Y., et al. (2024). Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice. Frontiers in Immunology, 15:1407936. https://doi.org/10.3389/fimmu.2024.1407936
  2. Djouina, M., et al. (2023). Oral exposure to polyethylene microplastics induces inflammatory and metabolic changes and promotes fibrosis in mouse liver. Ecotoxicology and Environmental Safety, 264:115417. https://doi.org/10.1016/j.ecoenv.2023.115417
  3. Sun, X., et al. (2025). Polyethylene terephthalate microplastics affect gut microbiota distribution and intestinal damage in mice. Ecotoxicology and Environmental Safety, 294:118119. https://doi.org/10.1016/j.ecoenv.2025.118119
  4. Zhang, Q., et al. (2023). Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp. Fish and Shellfish Immunology, 135:108690. https://doi.org/10.1016/j.fsi.2023.108690
  5. Danso, I.K., et al. (2024). Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice. Toxicological Research, 40:313-323. https://doi.org/10.1007/s43188-023-00224-x
  6. Lu, Y., et al. (2016). Uptake and Accumulation of Polystyrene Microplastics in Zebrafish (Danio rerio) and Toxic Effects in Liver. Environmental Science & Technology, 50:4054-4060. https://doi.org/10.1021/acs.est.6b00183

Six groundbreaking research studies reveal the extensive biological impact of microplastics on mammalian health systems. The first study demonstrates that high concentrations of polystyrene microplastics alter intestinal environments and metabolic outcomes in mice, inducing inflammation and dysbiosis through NK cell activation. The second study shows that polyethylene microplastics cause inflammatory and metabolic changes while promoting liver fibrosis in mice through disrupted lipid metabolism and HSC activation. Research on polyethylene terephthalate microplastics reveals significant gut microbiota disruption and intestinal damage, with inflammatory responses and barrier dysfunction in exposed mice. A fourth study investigates polystyrene microplastics’ cardiotoxic effects in carp, showing myocardial inflammation and cell death via TLR4/NF-κB pathway activation. Pulmonary toxicity research demonstrates that polystyrene fragments specifically induce lung inflammation through TLR4-mediated NF-κB and NLRP3 inflammasome activation, while polypropylene and polyethylene show minimal effects. Finally, zebrafish studies reveal size-dependent uptake and accumulation of polystyrene microplastics, with liver toxicity manifesting as oxidative stress, inflammation, and disrupted lipid metabolism. Collectively, these studies establish clear dose-dependent relationships between microplastic exposure and systemic health impacts across multiple organ systems, highlighting urgent needs for environmental regulation and continued research into human health implications.

Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice

  • Metabolic Impact: High-concentration PS-MPs induced dyslipidemia and fatty liver disease without causing leaky gut syndrome, demonstrating alternative toxicity pathways beyond barrier disruption.
  • Immune Response: PS-MPs exposure significantly increased NK cell populations in intestinal tissues, triggering inflammation and contributing to metabolic dysfunction through immune-mediated mechanisms.
  • Microbiota Disruption: Exposure caused dose-dependent changes in gut microbiota composition with decreased diversity, reduced beneficial bacteria, and altered metabolic profiles affecting host health.
  • Gene Expression Changes: PS-MPs modulated intestinal gene expression related to inflammation, nutrient transport, and metabolic processes, indicating molecular-level disruption of normal physiological functions.
  • Dose-Dependent Effects: The severity of intestinal and metabolic disturbances increased with higher PS-MPs concentrations, establishing clear dose-response relationships for toxicity assessment.
  • Novel Pathway Discovery: The study identified NK cell-mediated intestinal inflammation as a new mechanism of microplastic toxicity, expanding understanding beyond traditional barrier function disruption.
  1. Hasegawa, Y., et al. (2024). Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice. Frontiers in Immunology, 15:1407936. https://doi.org/10.3389/fimmu.2024.1407936
  2. Deng, Y., et al. (2017). Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure. Scientific Reports, 7:46687. https://doi.org/10.1038/srep46687
  3. Lu, L., et al. (2018). Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice. Science of the Total Environment, 631-632:449-458. https://doi.org/10.1016/j.scitotenv.2018.03.051
  4. Yang, W., et al. (2020). Intestinal microbiota-derived short-chain fatty acids regulation of immune cell IL-22 production and gut immunity. Nature Communications, 11:4457. https://doi.org/10.1038/s41467-020-18262-6
  5. Zhao, L., et al. (2021). Prolonged oral ingestion of microplastics induced inflammation in the liver tissues of C57BL/6J mice. Ecotoxicology and Environmental Safety, 227:112882. https://doi.org/10.1016/j.ecoenv.2021.112882
  6. Stock, V., et al. (2019). Uptake and effects of orally ingested polystyrene microplastic particles in vitro and in vivo. Archives of Toxicology, 93:1817-1833. https://doi.org/10.1007/s00204-019-02478-7
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This comprehensive study investigated the effects of high-concentration polystyrene microplastics (PS-MPs) on intestinal health and metabolism in mice fed normal diets. Researchers exposed C57BL/6J mice to PS-MPs at concentrations of 1000 μg/L and 5000 μg/L for six weeks, focusing on intestinal permeability, gut microbiota changes, and metabolic outcomes. The study revealed that even without inducing leaky gut syndrome, high concentrations of PS-MPs significantly increased serum lipid levels and exacerbated fatty liver conditions. The research demonstrated dose-dependent intestinal disturbances characterized by increased natural killer (NK) cell populations, altered gut microbiota composition, and modulated expression of genes related to nutrient transport. Notably, the study showed decreased bacterial diversity with reduced Bacteroidetes and increased inflammation markers, even in the absence of traditional leaky gut symptoms. The findings highlight that PS-MPs can induce dyslipidemia and non-alcoholic fatty liver disease through intestinal inflammation mediated by NK cells, representing a novel pathway of microplastic toxicity that operates independently of compromised intestinal barrier function.

Oral exposure to polyethylene microplastics induces inflammatory and metabolic changes and promotes fibrosis in mouse liver

  • Lipid Metabolism Disruption: PE microplastics significantly altered hepatic lipid metabolism by upregulating genes involved in fatty acid uptake, synthesis, and β-oxidation, leading to increased liver cholesterol and triglycerides.
  • Inflammatory Response: Exposure induced chronic low-grade liver inflammation with increased inflammatory foci, elevated pro-inflammatory cytokines (TNF-α, IL-6), and enhanced hepatocyte proliferation rates.
  • Fibrogenesis Promotion: PE microplastics activated hepatic stellate cells and increased collagen deposition, demonstrating early fibrotic changes that could progress to serious liver pathology.
  • Exacerbation of Pathology: In CCl4-induced fibrosis models, PE exposure significantly worsened liver fibrogenesis, suggesting microplastics could accelerate pre-existing liver diseases.
  • Size-Independent Effects: Both 36 μm and 116 μm PE microbeads induced similar hepatotoxic responses, indicating that effects are not solely dependent on particle size.
  • Time-Dependent Progression: Hepatotoxic effects showed temporal progression with increasing severity from 6 to 9 weeks of exposure, suggesting cumulative damage potential.
  1. Djouina, M., et al. (2023). Oral exposure to polyethylene microplastics induces inflammatory and metabolic changes and promotes fibrosis in mouse liver. Ecotoxicology and Environmental Safety, 264:115417. https://doi.org/10.1016/j.ecoenv.2023.115417
  2. Lu, L., et al. (2018). Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice. Science of the Total Environment, 631-632:449-458. https://doi.org/10.1016/j.scitotenv.2018.03.051
  3. Yang, L., et al. (2022). Aged polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice. Environmental Science & Technology, 56:4968-4979. https://doi.org/10.1021/acs.est.1c07933
  4. Chen, X., et al. (2022). Chronic exposure to polyvinyl chloride microplastics induces liver injury and gut microbiota dysbiosis. Science of the Total Environment, 839:155984. https://doi.org/10.1016/j.scitotenv.2022.155984
  5. Cheng, W., et al. (2022). Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in liver organoids. Science of the Total Environment, 806:150328. https://doi.org/10.1016/j.scitotenv.2021.150328
  6. Shen, M., et al. (2022). Polyethylene microplastics promote liver fibrosis in mice via chronic inflammation. Environmental Science & Technology Letters, 9:482-488. https://doi.org/10.1021/acs.estlett.2c00137

This significant research examined the hepatotoxic effects of polyethylene (PE) microplastics, one of the most abundant polymers in environmental contamination. Female mice were exposed to 36 and 116 μm diameter PE microbeads at 100 μg/g food concentration for 6 and 9 weeks, with comprehensive analysis of liver function, inflammation, and fibrogenesis. The study revealed that PE exposure altered hepatic gene expression related to fatty acid metabolism, promoting increased uptake, synthesis, and β-oxidation of fatty acids. Biochemical analysis showed elevated liver cholesterol and triglyceride levels, indicating disrupted lipid homeostasis. The research demonstrated that PE microplastics induced low-grade liver inflammation characterized by increased inflammatory foci, elevated cytokine expression (TNF-α, IL-6), and enhanced cell proliferation. Importantly, the study identified hepatic stellate cell (HSC) activation and increased collagen deposition, indicating early fibrogenic changes. Using a CCl4-induced fibrosis model, researchers confirmed that PE exposure exacerbated liver fibrogenesis, suggesting that microplastic contamination could worsen pre-existing liver pathologies. The findings establish PE microplastics as hepatotoxic agents capable of promoting both metabolic dysfunction and fibrotic progression in mammalian liver tissue.

Polyethylene terephthalate microplastics affect gut microbiota distribution and intestinal damage in mice

  • Inflammatory Response: PET-MPs induced dose-dependent increases in pro-inflammatory cytokines (IL-2, TNF-α) while suppressing anti-inflammatory factors (IL-10) in both systemic circulation and local tissues.
  • Barrier Dysfunction: Exposure caused significant intestinal barrier compromise through reduced mucus secretion, damaged epithelial structures, and decreased expression of crucial tight junction proteins.
  • Microbiota Disruption: PET-MPs altered gut microbiota composition with temporal dynamics, showing initial dysbiosis followed by compensatory changes, indicating complex host-microbe interactions.
  • Systemic Effects: Beyond local intestinal damage, exposure elevated blood glucose and liver enzymes, suggesting systemic metabolic consequences through gut-liver axis disruption.
  • Dose-Response Relationship: Effects showed clear dose-dependent patterns with 250 mg/kg exposure causing the most severe inflammatory and structural changes.
  • Temporal Progression: The study revealed time-dependent changes in microbiota composition, with different patterns emerging at 14 and 28 days of exposure.
  1. Sun, X., et al. (2025). Polyethylene terephthalate microplastics affect gut microbiota distribution and intestinal damage in mice. Ecotoxicology and Environmental Safety, 294:118119. https://doi.org/10.1016/j.ecoenv.2025.118119
  2. Li, B., et al. (2020). Polyethylene microplastics affect the distribution of gut microbiota and inflammation development in mice. Chemosphere, 244:125492. https://doi.org/10.1016/j.chemosphere.2019.125492
  3. Chen, X., et al. (2022). Polyvinyl chloride microplastics induced gut barrier dysfunction, microbiota dysbiosis and metabolism disorder in adult mice. Ecotoxicology and Environmental Safety, 241:113809. https://doi.org/10.1016/j.ecoenv.2022.113809
  4. Jin, Y., et al. (2019). Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice. Science of the Total Environment, 649:308-317. https://doi.org/10.1016/j.scitotenv.2018.08.353
  5. Grogan, A.E., et al. (2021). Investigation of polyethylene terephthalate (PET) drinking bottles as marine reservoirs for fecal bacteria and phytoplankton. Marine Pollution Bulletin, 173:113052. https://doi.org/10.1016/j.marpolbul.2021.113052
  6. Harusato, A., et al. (2023). Impact of particulate microplastics generated from polyethylene terephthalate on gut pathology and immune microenvironments. iScience, 26:106474. https://doi.org/10.1016/j.isci.2023.106474

This research investigated the biological effects of polyethylene terephthalate microplastics (PET-MPs), a prevalent environmental contaminant, on intestinal health and gut microbiome composition. Male C57BL/6 mice were exposed to 10 μm PET-MPs at concentrations of 10, 50, and 250 mg/kg body weight for 28 days, with comprehensive analysis of inflammatory responses, intestinal barrier function, and microbiota changes. The study revealed dose-dependent increases in inflammatory cytokines (IL-2, TNF-α) and decreased anti-inflammatory markers (IL-10) in both serum and colon tissues. Histopathological examination showed inflammatory cell infiltration, structural damage to colonic crypts, and reduced mucus secretion, indicating compromised intestinal barrier integrity. Molecular analysis demonstrated significantly decreased expression of mucus-related genes (Muc2, Muc3) and tight junction proteins (Occludin, Claudin-1), confirming barrier dysfunction. Gut microbiota analysis revealed altered diversity and composition, with temporal changes showing initial increases in Firmicutes/Bacteroidetes ratio at 14 days, followed by reversed patterns at 28 days. The research also identified elevated blood glucose and liver enzyme levels, suggesting systemic metabolic effects. These findings establish PET-MPs as potent disruptors of intestinal homeostasis with implications for systemic health through gut-liver axis dysfunction.

Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp

  • Cardiotoxic Mechanisms: PS-MPs induced severe myocardial damage through TLR4/NF-κB pathway activation, leading to inflammation, cell death, and structural tissue disruption in carp hearts.
  • Inflammatory Response: Exposure significantly increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) while suppressing anti-inflammatory IL-10, creating a sustained inflammatory environment.
  • Cell Death Pathways: PS-MPs activated both apoptotic and necroptotic cell death mechanisms, with apoptosis predominating through altered Bcl-2/Bax ratios and caspase activation.
  • Molecular Targeting: The study identified TLR4 as the specific receptor mediating PS-MPs recognition and subsequent inflammatory cascades in cardiac tissue.
  • Dose-Dependent Effects: Both in vivo and in vitro experiments demonstrated clear dose-response relationships for inflammatory markers and cell death indicators.
  • Structural Damage: Histopathological analysis revealed extensive myocardial fiber disruption, enlarged intercellular spaces, and inflammatory cell infiltration following PS-MPs exposure.
  1. Zhang, Q., et al. (2023). Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp. Fish and Shellfish Immunology, 135:108690. https://doi.org/10.1016/j.fsi.2023.108690
  2. Zhang, Y., et al. (2022). Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes. Science of the Total Environment, 840:156727. https://doi.org/10.1016/j.scitotenv.2022.156727
  3. Zhao, L., et al. (2021). Prolonged oral ingestion of microplastics induced inflammation in the liver tissues of C57BL/6J mice through polarization of macrophages and increased infiltration of natural killer cells. Ecotoxicology and Environmental Safety, 227:112882. https://doi.org/10.1016/j.ecoenv.2021.112882
  4. Qiao, R., et al. (2019). Microplastics induce intestinal inflammation, oxidative stress, and disorders of metabolome and microbiome in zebrafish. Science of the Total Environment, 662:246-253. https://doi.org/10.1016/j.scitotenv.2018.12.041
  5. Deng, Y., et al. (2017). Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure. Scientific Reports, 7:46687. https://doi.org/10.1038/srep46687
  6. Carbery, M., et al. (2018). Trophic transfer of microplastics and mixed contaminants in the marine food web and implications for human health. Environment International, 115:400-409. https://doi.org/10.1016/j.envint.2018.03.007

This groundbreaking study examined the cardiotoxic effects of polystyrene microplastics (PS-MPs) in aquatic organisms, specifically investigating the molecular mechanisms underlying myocardial damage in carp (Cyprinus carpio). Researchers exposed carp to 1000 ng/L PS-MPs (1-10 μm) for 21 days and isolated primary cardiomyocytes for in vitro analysis at concentrations of 100 and 200 μg/mL. The study revealed severe myocardial structural damage characterized by fiber breaks, enlarged cell gaps, and extensive inflammatory cell infiltration. Mechanistic investigation identified TLR4 as the primary pattern recognition receptor activated by PS-MPs, leading to downstream NF-κB pathway activation and NLRP3 inflammasome stimulation. The research demonstrated that PS-MPs exposure significantly increased expression of inflammatory cytokines (TNF-α, IL-1β, IL-6) while suppressing anti-inflammatory IL-10. Cell death analysis revealed that PS-MPs induced both apoptosis and necrosis, with apoptosis predominating through Bcl-2 downregulation and Bax upregulation, ultimately activating caspase cascades. The study also showed activation of necroptotic pathways through RIPK3 and MLKL upregulation. This research provides the first comprehensive evidence of PS-MPs cardiotoxicity in aquatic vertebrates, establishing important precedents for understanding cardiovascular risks in exposed organisms.

Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice

  • Polymer-Specific Toxicity: PS microplastics induced severe pulmonary inflammation while PP and PE showed minimal effects, establishing clear differential toxicity patterns among common plastic polymers.
  • TLR-Mediated Mechanisms: PS activated TLR4-dependent inflammatory pathways leading to NF-κB and NLRP3 inflammasome activation, while PP activated TLR2 without downstream inflammatory signaling.
  • Surface Charge Correlation: Microplastic toxicity correlated with surface charge properties, with PS showing the highest negative zeta potential (-38.93 mV) and greatest inflammatory potential.
  • Inflammatory Response: PS exposure significantly increased inflammatory cell infiltration, cytokine production (IL-1β, IL-6), and chemokine expression in bronchoalveolar lavage fluid.
  • Histopathological Changes: PS-exposed mice showed inflammatory cell infiltration and macrophage accumulation in perivascular and peribronchial regions of lung tissue.
  • NLRP3 Inflammasome Activation: PS specifically triggered NLRP3 inflammasome assembly and activation, leading to enhanced IL-1β processing and sustained inflammatory responses.
  1. Danso, I.K., et al. (2024). Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice. Toxicological Research, 40:313-323. https://doi.org/10.1007/s43188-023-00224-x
  2. Li, X., et al. (2022). Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice. Ecotoxicology and Environmental Safety, 232:113238. https://doi.org/10.1016/j.ecoenv.2022.113238
  3. Cao, J., et al. (2023). Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice. Environmental Pollution, 320:121068. https://doi.org/10.1016/j.envpol.2023.121068
  4. Woo, J.W., et al. (2023). Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage. Particle and Fibre Toxicology, 20:2. https://doi.org/10.1186/s12989-022-00512-8
  5. Jin, Y.J., et al. (2023). Characterisation of changes in global genes expression in the lung of ICR mice in response to the inflammation and fibrosis induced by polystyrene nanoplastics inhalation. Toxicological Research, 39:575-599. https://doi.org/10.1007/s43188-023-00188-y
  6. Jenner, L.C., et al. (2022). Detection of microplastics in human lung tissue using μFTIR spectroscopy. Science of the Total Environment, 831:154907. https://doi.org/10.1016/j.scitotenv.2022.154907

This comparative study investigated the differential pulmonary toxicity of three common microplastic polymer types: polypropylene (PP), polystyrene (PS), and polyethylene (PE) fragments in C57BL/6 mice. Researchers administered 5 mg/kg of each microplastic type daily via intratracheal instillation for 14 days, with comprehensive analysis of inflammatory responses, molecular mechanisms, and histopathological changes. The study revealed polymer-specific toxicity patterns, with PS microplastic fragments inducing the most severe pulmonary inflammation characterized by significantly increased inflammatory cell infiltration, elevated cytokine levels (IL-1β, IL-6), and enhanced chemokine expression (MCP-1, MIP-1α, MIP-2, KC). Mechanistic investigation identified TLR4 as the primary mediator of PS-induced inflammation, while PP specifically activated TLR2 without downstream inflammatory signaling. The research demonstrated that PS exposure activated NF-κB phosphorylation and NLRP3 inflammasome components (NLRP3, ASC, Caspase-1), leading to sustained inflammatory responses. Interestingly, PE microplastics showed minimal inflammatory effects despite similar exposure conditions. The study also revealed that surface charge properties (zeta potential) correlated with toxicity, with PS showing the highest negative charge (-38.93 mV) and greatest inflammatory potential. These findings establish important precedents for understanding respiratory risks from different microplastic types.

Uptake and Accumulation of Polystyrene Microplastics in Zebrafish (Danio rerio) and Toxic Effects in Liver

  • Size-Dependent Uptake: Microplastic accumulation showed clear size-dependent patterns with 5 μm particles reaching liver tissue while 20 μm particles remained in gills and gut.
  • Rapid Bioaccumulation: PS-MPs achieved steady-state tissue concentrations within 48 hours, demonstrating efficient uptake and retention in multiple organ systems.
  • Hepatotoxic Effects: Both 70 nm and 5 μm PS-MPs induced liver inflammation, lipid accumulation, and cellular damage in exposed zebrafish.
  • Metabolic Disruption: Exposure significantly altered hepatic metabolomic profiles, disrupting lipid metabolism, energy production, and amino acid homeostasis.
  • Oxidative Stress Response: PS-MPs induced dose-dependent increases in antioxidant enzyme activities (SOD, CAT), indicating cellular oxidative damage.
  • Unexpected Size Effects: Larger 5 μm particles induced greater oxidative stress than smaller 70 nm particles, challenging conventional size-toxicity assumptions.
  1. Lu, Y., et al. (2016). Uptake and Accumulation of Polystyrene Microplastics in Zebrafish (Danio rerio) and Toxic Effects in Liver. Environmental Science & Technology, 50:4054-4060. https://doi.org/10.1021/acs.est.6b00183
  2. Mattsson, K., et al. (2015). Altered behavior, physiology and metabolism in fish exposed to polystyrene nanoparticles. Environmental Science & Technology, 49:553-561. https://doi.org/10.1021/acs.est.5b04532
  3. Browne, M.A., et al. (2008). Ingested microscopic plastic translocates to the circulatory system of the mussel, Mytilus edulis (L.). Environmental Science & Technology, 42:5026-5031. https://doi.org/10.1021/es800249a
  4. Della Torre, C., et al. (2014). Accumulation and embryotoxicity of polystyrene nanoparticles at early stage of development of sea urchin embryos Paracentrotus lividus. Environmental Science & Technology, 48:12302-12311. https://doi.org/10.1021/es503297u
  5. Cedervall, T., et al. (2012). Food Chain Transport of Nanoparticles Affects Behaviour and Fat Metabolism in Fish. PLoS One, 7:e32254. https://doi.org/10.1371/journal.pone.0032254
  6. Wright, S.L., et al. (2013). The physical impacts of microplastics on marine organisms: A review. Environmental Pollution, 178:483-492. https://doi.org/10.1016/j.envpol.2013.02.031

This pioneering study established foundational understanding of microplastic bioaccumulation and toxicity using zebrafish as a model organism. Researchers investigated the uptake patterns of fluorescently-labeled polystyrene microplastics (PS-MPs) of different sizes (70 nm, 5 μm, 20 μm) and their subsequent toxic effects in liver tissue. The accumulation experiment revealed size-dependent distribution patterns, with 5 μm particles accumulating in gills, liver, and gut, while larger 20 μm particles were restricted to gills and gut tissues. Quantitative analysis showed rapid accumulation within 48 hours, reaching steady-state concentrations with highest levels in liver and gut compared to gills. Toxicity assessment using 70 nm and 5 μm PS-MPs at concentrations of 20-2000 μg/L for 3 weeks demonstrated significant hepatotoxic effects including inflammation, lipid accumulation, and oxidative stress. Metabolomic analysis revealed disrupted lipid and energy metabolism with altered fatty acid profiles, decreased branched-chain amino acids, and disturbed ATP/ADP/AMP ratios. The study also showed increased activities of antioxidant enzymes (SOD, CAT), indicating oxidative stress responses. Interestingly, larger 5 μm particles induced greater oxidative stress than smaller 70 nm particles, suggesting complex size-toxicity relationships. This research established important methodological approaches for microplastic research and provided early evidence of systemic metabolic disruption.