We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
The endoplasmic reticulum-mitochondrial crosstalk involved in nanoplastics and di(2-ethylhexyl) phthalate co-exposure induced the damage to mouse mammary epithelial cells
AI summary Read the abstract
Researchers found that nanoplastics combined with DEHP, a common plastic softener, caused severe damage to mouse mammary (breast) gland cells by disrupting communication between two key cell structures: the endoplasmic reticulum and mitochondria. The combined exposure was worse than either substance alone, triggering cell death, inflammation, and oxidative stress. This is concerning because people are typically exposed to both nanoplastics and plastic additives like DEHP simultaneously through food and consumer products.
With the extensive use of plastic products, significant amounts of microplastics, nanoplastic particles (NPs), and plasticizers such as Di(2-ethylhexyl) phthalate (DEHP) are continuously released into the environment. However, the toxic effects of NPs alone or in combination with DEHP on mammary glands remain unreported. This study investigates the impacts of NPs and DEHP on the structure and function of mouse mammary epithelial cells and elucidates the underlying molecular mechanisms. We found that co-exposure to NPs and DEHP induced severe pyroptosis, inflammation and oxidative stress in HC11 cells. Co-exposure also caused mitochondrial damage, as evidenced by changes in mitochondrial membrane potential, increase in mitochondrial ROS and inhibition of ATP production. Moreover, NPs and DEHP co-exposure increased the transcriptional levels of endoplasmic reticulum (ER) stress-related genes, activated the inflammation-related NLRP3 signaling pathway, and damaged the cell membrane integrity. Notably, Co-exposure enhanced the ER-mitochondria crosstalk in HC11 cells, as evidenced by the upregulated transcriptional levels of ER Ca channel proteins (Ip3r1, Grp75 and Vdac1), increased mitochondrial Ca levels, and expanded mitochondrial-ER contact areas. In summary, this study revealed that NPs and DEHP co-exposure had the potential to induce pyroptosis and inflammation by enhancing the ER-mitochondria crosstalk, ultimately resulting in injury to mammary glands. These findings would provide some new insights into the molecular mechanisms underlying the toxic effects of NPs and DEHP to mammary glands.
More Papers Like This
Co-exposure to polystyrene nanoplastics and di(2-ethylhexyl) phthalate: Effects and mechanistic insights into hepatic lipid metabolism in mice
AI summary Read the abstract
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.
Synergistic assault of DEHP and MPs: Unmasking the ER stress-triggered autophagic injury male fertility
AI summary Read the abstract
Researchers found that mice co-exposed to microplastics and the common plasticizer DEHP through drinking water experienced severe impairment of male reproductive function, including disrupted testicular structure, declining sperm quality, and hormonal dysregulation. The combined exposure activated endoplasmic reticulum stress and triggered excessive autophagy, contributing to reproductive damage beyond what either pollutant caused alone. The study highlights the significant risks of simultaneous exposure to microplastics and plastic additives for male fertility.
Di-(2-Ethylhexyl) Phthalate and Microplastics Induced Neuronal Apoptosis through the PI3K/AKT Pathway and Mitochondrial Dysfunction
AI summary Read the abstract
Researchers found that the plasticizer DEHP and microplastics caused neuronal cell death in mice brains through the PI3K/AKT signaling pathway and mitochondrial dysfunction. The study demonstrated that combined exposure to DEHP and microplastics produced greater toxic effects on brain neurons than either substance alone, leading to changes in mitochondrial function and increased cell death.
Nanoplastics drive toxicity under co-exposure with perfluorooctanesulfonic acid in human intestinal cells
AI summary Read the abstract
Researchers exposed human intestinal cells to nanoplastics, the industrial chemical PFOS, and their combination, and found that co-exposure caused more severe cellular disruption than either substance alone. Nanoplastics primarily damaged mitochondria while PFOS affected cell membranes and internal structures, and their combination triggered broader metabolic changes including disrupted amino acid and lipid metabolism. The study suggests that the interaction between nanoplastics and common environmental chemicals may pose compounding risks to gut health.
Di-(2-ethyl hexyl) phthalate induced oxidative stress promotes microplastics mediated apoptosis and necroptosis in mice skeletal muscle by inhibiting PI3K/AKT/mTOR pathway
AI summary Read the abstract
Researchers investigated how the plastic additive DEHP and polystyrene microplastics affect skeletal muscle in mice, finding that combined exposure caused more severe oxidative stress and cell death than either substance alone. The study suggests that co-exposure triggers apoptosis and necroptosis in muscle tissue by inhibiting a key cellular signaling pathway involved in cell survival.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.