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Impact of a pristine versus gastric acid-treated low-density polyethylene in a human epithelial colorectal adenocarcinoma (Caco-2) cell line
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When plastic particles from common food packaging pass through stomach acid, they change chemically in ways that make them more reactive—and these "digested" plastics caused more disruption to cell energy production (mitochondria) than untreated plastic particles, even without entering the cells directly. This suggests that what happens to microplastics during digestion, not just the plastics themselves, may be an overlooked factor in how they could affect our gut health.
An increasing number of studies report the presence and accumulation of micro- and nanoplastics (MNPs) in the human body. After ingestion, MNPs undergo weathering by gastric and intestinal fluids that modify their physicochemical properties. Although these changes can influence biological responses, their impact remains understudied, forming the foundation of this research. We investigated how a simplified chemical weathering model of simulated gastric fluid exposure alters the physicochemical properties of environmentally relevant microplastics and how these changes influence their subsequent effects on a human epithelial colorectal adenocarcinoma (Caco-2) cell line. We focused on Low-Density Polyethylene (LDPE) due to its widespread use in agriculture and food packaging, as well as its status as one of the most widely produced plastic polymers. Particle properties changed after artificial stomach acid (ASA) treatment, including metal leaching, surface modifications, stronger redox-inducing potential, and increased floatability. These changes in the particles' characteristics were reflected in the observed effects, with ASA-treated particles producing more pronounced alterations in mitochondrial network features, including increased mitochondrial fusion and a larger mitochondrial footprint. No internalization was observed in any of the cases, with membrane integrity (5-CFDA,AM) disrupted after exposure to pristine and ASA-treated particles, regardless of the underlying mechanistic pathways. In summary, our findings show that ASA-treated microplastics differ in redox-inducing potential, which can influence cellular metabolism regardless of cellular uptake. This suggests that indirect changes after ASA treatment may represent an underestimated part of microplastic toxicity after ingestion.
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The influence of digestive tract protein on cytotoxicity of polyvinyl chloride microplastics
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This study examined how human digestive enzymes change the properties of PVC microplastics as they pass through a simulated digestive tract. After digestion, the microplastics became more water-friendly and mobile in the body, and they caused greater damage to intestinal cells, including reduced cell survival, increased oxidative stress, and disrupted energy metabolism. These findings suggest that the digestion process itself may make microplastics more harmful to the human gut than previously assumed.
Influence of artificial digestion on characteristics and intestinal cellular effects of micro-, submicro- and nanoplastics
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Researchers simulated human digestion to study how micro-, submicro-, and nanoplastics change as they pass through the stomach and intestines. They found that the digestive process altered the surface properties and size distribution of the plastic particles, potentially affecting how they interact with intestinal cells. The study suggests that the body's digestive environment may transform plastic particles in ways that influence their biological impact.
Polystyrene microplastic exposure disrupts mitochondrial pathways and nuclear processes in primary intestinal epithelial cells
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Scientists exposed gut cells to tiny plastic particles (microplastics) and found they threw off normal cell function, ramping up energy production while slowing down processes needed for cell repair and division. This happened more with fresh plastic than plastic that had been through digestion, suggesting how plastics break down in our gut may change how harmful they are. More research is needed to know what this means for long term gut health.
Mitochondrial Complex I hyperactivation drives PET microplastic-induced intestinal bioenergetic collapse
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Researchers found that PET microplastics derived from commercial bottles, after passing through simulated digestion, caused a cascade of metabolic damage in intestinal cells. The digested particles triggered hyperactivation of mitochondrial Complex I, leading to excessive free radical production, ATP shutdown, and oxidative stress. The study suggests that the digestive transformation of everyday PET plastics alters their surface properties in ways that make them more biologically harmful to gut cells.
In vitro digestion of microplastics in human digestive system: Insights into particle morphological changes and chemical leaching
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Researchers simulated human digestion on four common types of microplastics and found that stomach acid and digestive enzymes changed the particles' shape, surface texture, and caused them to release chemical additives. The study shows that microplastics are not inert once swallowed -- they are actively transformed in the gut, which could increase their ability to interact with intestinal tissues and release potentially harmful chemicals.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.