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DEHP disrupts lipid Metabolism via autophagy hyperactivation and mitochondrial dysfunction
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Researchers exposed mice and cultured cells to DEHP plasticizer over the long term and found it triggers degradation of the DNA methyltransferase DNMT1 via autophagy, causing promoter demethylation that excessively activates autophagosome formation, ultimately impairing mitochondrial function and driving lipid accumulation in the liver.
Di(2-ethylhexyl) phthalate (DEHP) is a widely used industrial plasticizer, raising global concerns due to its potential endocrine-disrupting effects and environmental persistence. Human exposure to DEHP primarily occurs through the ingestion of contaminated food and water, inhalation of airborne particles, and dermal contact with products containing DEHP. Understanding the toxicological mechanisms of DEHP is essential for evaluating its health risks and developing effective strategies to mitigate its adverse effects. In this study, we conducted long-term exposure experiments to DEHP using both an animal model and in vitro system to investigate the complex interplay among DNA methylation, hyperactivation of macroautophagy/autophagy, mitochondrial dysfunction, and lipid accumulation induced by DEHP. The results revealed that DEHP exposure induced the degradation of DNMT1 (DNA methyltransferase 1) by enhancing its interaction with the autophagy-related protein SQSTM1 (sequestosome 1). DNMT1 degradation resulted in decreased methylation of the promoter regions of genes associated with autophagosome formation, subsequently increasing their expression. The resulting demethylation excessively activated autophagy, contributing to mitochondrial dysfunction and lipid accumulation in the liver. This study uncovered a previously unrecognized interplay among hyperactivation of autophagy, mitochondrial dysfunction, and lipid accumulation in the context of DEHP exposure. These findings enhanced our understanding of DEHP’s toxicity and underscored concerns about the long-term health effects of environmental pollutants, particularly regarding metabolic diseases.
More Papers Like This
DEHP disrupts lipid Metabolism via autophagy hyperactivation and mitochondrial dysfunction
AI summary Read the abstract
Researchers found that long-term DEHP exposure degrades the DNA methylation enzyme DNMT1 through autophagy, causing a cascade of excessive autophagosome formation, mitochondrial dysfunction, and abnormal lipid accumulation in the liver — revealing a novel epigenetic mechanism linking plasticizer exposure to metabolic disease.
DEHP disrupts lipid Metabolism via autophagy hyperactivation and mitochondrial dysfunction
AI summary Read the abstract
Researchers exposed mice and cell cultures to the plasticizer DEHP and found it degrades the DNA methylation enzyme DNMT1 via autophagy, triggering a cascade that hyperactivates cellular recycling pathways, disrupts mitochondria, and causes fat accumulation in the liver — revealing a novel mechanism linking plasticizer exposure to metabolic disease.
DEHP disrupts lipid metabolism via autophagy hyperactivation and mitochondrial dysfunction
AI summary Read the abstract
DEHP, a chemical used to make plastics soft and flexible, is found in many everyday products and can leach into food, water, and air. This study found that long-term DEHP exposure disrupts liver cells' internal cleanup process (called autophagy) by damaging a key regulatory protein, which throws off the liver's ability to manage fat and can lead to fat buildup similar to what's seen in fatty liver disease. Since DEHP exposure is nearly unavoidable in modern life, these findings add to growing evidence that everyday plastic chemicals may quietly contribute to metabolic health problems over time.
Co-exposure to polystyrene nanoplastics and di(2-ethylhexyl) phthalate: Effects and mechanistic insights into hepatic lipid metabolism in mice
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In mice, exposure to tiny plastic particles (nanoplastics) combined with a plastic chemical called DEHP caused more liver fat buildup and liver damage than either alone. Tests in liver cells showed this involved a specific stress pathway, and blocking that pathway reduced the fat buildup caused by the combined exposure.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
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This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
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