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Disruption of lipid metabolism under plastic siege: Unraveling the toxic mechanisms of microplastics and nanoplastics
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Researchers reviewed how microplastics and nanoplastics disrupt lipid metabolism across multiple animal species, finding they inhibit digestive enzymes, alter gut microbiota, dysregulate fat storage and breakdown, and activate inflammatory signaling pathways — causing both acute and chronic metabolic damage.
Excessive production and discharge of plastics into the environment results in the production, accumulation, and toxicity of microplastics (MPs) and nanoplastics (NPs) in marine and terrestrial animals. This review aimed at evaluating the toxic effects of MPs and NPs on lipid metabolism and the mechanism behind disruptive potential. It is demonstrated that the exposure to these MPs and NPs affects the metabolic enzymes involved in absorption, metabolism and storage of lipids. These effects are demonstrated as dysregulation of lipogenesis, fasting-induced lipolysis, and glycolipids production. In the gastrointestinal milieu, exposure to MPs incites the inhibition of digestive enzymes and modulation of the composition of intestinal microflora. MPs and NPs exhibit oxidative stress-induced metabolomic toxicity in different animal species, in conjunction with lipotoxicity, hepatotoxicity, and disrupted steroidogenesis. Moreover, MPs instigate disruptions in glycolipid metabolism via the activation of the mitogen-activated protein kinase and nuclear factor kappa B signaling pathways in addition to suppression of nucleotide synthesis. Exposure to MPs and NPs results in the acute and chronic disturbances of lipid metabolism.
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Microplastics and nanoplastics in human health: a comprehensive review of exposure pathways, cellular mechanisms, and toxicological implications
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Researchers reviewed human exposure pathways to microplastics and nanoplastics through seafood, salt, drinking water, inhalation, and skin contact, examining how these particles cross biological barriers to reach organs and trigger oxidative stress, inflammation, and endocrine disruption with poorly understood long-term consequences.
The effects of microplastics and nanoplastics on cardiovascular disease: mechanisms and perspectives
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This review synthesizes current evidence on how microplastics and nanoplastics (MNPs) may contribute to cardiovascular disease, examining their presence in blood, atherosclerotic plaques, thrombi, and heart tissue. Experimental studies point to oxidative stress, mitochondrial dysfunction, inflammation, and fibrotic remodeling as plausible mechanisms linking MNP exposure to heart disease, though causal relationships in humans remain unproven and standardized detection methods are still lacking.
Biochemical Effects of Microplastics on Human Health: A Comprehensive Review
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A comprehensive review documents how microplastics enter the human body through ingestion, inhalation, and skin contact, then reach the lungs, liver, kidneys, brain, and reproductive organs, triggering oxidative stress, inflammation, endocrine disruption, and genotoxicity. These biochemical pathways link microplastic exposure to serious chronic conditions including metabolic syndrome, neurodegenerative disease, reproductive dysfunction, and cancer.
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