We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
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
Summary
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.
Microplastics (MP) have distributed ubiquitously and emerged as a significant health risk to human beings. The adverse effect induced by aged MP at concentrations being equivalent to human internal exposure level, has raised special concern, however, is still unclear. In this study, human embryonic stem cells-derived liver organoids (LOs), a novel three-dimensional in vitro model, were exposed to 75 ng/mL self-made polypropylene (PP) and aged PP (aPP), following UV-photoaging for 0- and 500-h respectively, were subject to transcriptomic and metabolomic analysis individually and jointly, to explore the potential adverse effect of PP and aPP on human liver. The mean size of PP and aPP were 7.60 and 6.91 μm, with rough and irregular surface, and varied carbonyl index (CI) (0.08 and 0.25 respectively), indicating there were distinguished physicochemical properties. Transcriptomic analysis suggested the NADH dehydrogenase at mitochondrial complex and ATP synthesis maybe more sensitive to aPP, rather than PP. Metabolomic analysis enriched KEGG pathways including cysteine (Cys) and methionine metabolism significantly. Collectively, the homocysteine (Hcy) metabolism, were anchored upon integrated analysis. To validate, the changes in NADH dehydrogenase-encoding genes, activities of complexs, mitochondrial membrane potential, Hcy and Cys contents, as well, the cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), were detected both in vitro and in vivo. Finally, increased serum Cys and decreased hepatic Cys were confirmed, without inflammation in the liver. The peripheral Hcy may serve as a potential biomarker for indicating the MP-induced systematic adverse health outcomes, due to the disturbance in the Hcy metabolism in the liver.
Sign in to start a discussion.
More Papers Like This
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.
Comparative Analysis of Metabolic Dysfunctions Associated with Pristine and Aged Polyethylene Microplastic Exposure via the Liver-Gut Axis in Mice
Mice fed both new and weathered polyethylene microplastics developed disrupted fat metabolism, liver oxidative stress, and shifts in gut bacteria, with weathered (aged) particles causing more severe effects. This study suggests that the microplastics people encounter in the real world, which have been degraded by sunlight and time, may be more harmful than the pristine particles typically used in lab studies.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
The iron matters: Aged microplastics disrupted the iron homeostasis in the liver organoids
Researchers compared the effects of fresh versus aged polystyrene microplastics on lab-grown human liver tissue and found that aged particles caused significantly more damage. The aged microplastics disrupted iron balance in liver cells, leading to a form of cell death called ferroptosis, and triggered inflammatory responses. The study suggests that weathered microplastics encountered in everyday life may pose greater risks to liver health than the pristine particles typically used in laboratory studies.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
Researchers fed mice low doses of pristine and aged polyethylene microplastics for several weeks and analyzed changes in blood metabolites, liver proteins, and gut bacteria. Both forms caused lipid metabolism disruptions and reduced beneficial gut bacteria, with aged microplastics showing greater toxicity linked to changes in fatty acid processing enzymes.