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20 resultsShowing papers similar to Endoplasmic reticulum stress exacerbates microplastics-induced toxicity in animal cells
ClearPolystyrene microplastic‐induced endoplasmic reticulum stress contributes to growth plate endochondral ossification disorder in young rat
Researchers found that polystyrene microplastics caused growth problems and bone damage in young rats by triggering stress in a part of the cell called the endoplasmic reticulum. This stress disrupted the normal process by which cartilage turns into bone in growing animals. The findings raise concerns that microplastic exposure during early development could interfere with normal bone growth in children.
Fluorescent visualization of endoplasmic reticulum stress induced by microplastic pollution via surge of intracellular reactive oxygen species
Researchers used peroxynitrite as a fluorescent probe to visualize how microplastics trigger endoplasmic reticulum (ER) stress inside cells, finding that MP invasion causes a surge in reactive oxygen species that activates ER stress pathways. The study clarified a key molecular mechanism linking microplastic internalization to cellular disease processes.
Microplastics induced endoplasmic reticulum stress to format an inflammation and cell death in hepatocytes of carp (Cyprinus carpio)
Researchers fed carp water containing polystyrene microplastics and found significant liver damage, including inflammation, disrupted cell recycling processes, and cell death. The microplastics triggered a stress response in the cell's protein-folding machinery (endoplasmic reticulum), which set off a chain reaction of inflammation and tissue damage. These findings in freshwater fish suggest that microplastics can cause serious organ damage through specific cellular stress pathways.
Endoplasmic reticulum stress-induced NLRP3 inflammasome activation as a novel mechanism of polystyrene microplastics (PS-MPs)-induced pulmonary inflammation in chickens
Researchers exposed chickens to polystyrene microplastics for 42 days and found significant lung damage, including tissue inflammation and cell stress responses. The microplastics triggered a chain reaction starting with stress in the endoplasmic reticulum (a cell structure involved in protein processing) that activated inflammatory pathways. While this study focused on poultry, similar inflammatory mechanisms could be relevant to understanding how microplastics affect lungs in other species, including humans.
Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death
This review examines how endoplasmic reticulum stress, a cellular response to accumulated misfolded proteins, can trigger various forms of cell death in acute kidney injury. While not directly about microplastics, these same stress pathways are activated when cells are exposed to nanoplastics, which have been shown to accumulate in kidney tissue. Understanding these mechanisms helps explain how microplastic exposure could contribute to kidney damage at the cellular level.
Molecular mechanisms underlying mitochondrial damage, endoplasmic reticulum stress, and oxidative stress induced by environmental pollutants
This review examines how environmental pollutants including microplastics, heavy metals, and pesticides damage cells by disrupting mitochondria, triggering endoplasmic reticulum stress, and generating harmful reactive oxygen species. Researchers describe the molecular signaling pathways through which these pollutants cause cell dysfunction and death. The study highlights the interconnected nature of these cellular stress responses and their relevance to understanding pollution-related health effects.
Endoplasmic reticulum stress-controlled autophagic pathway promotes polystyrene microplastics-induced myocardial dysplasia in birds
Researchers exposed chicks to different concentrations of polystyrene microplastics to study their effects on heart development. The study found that microplastics triggered endoplasmic reticulum stress and disrupted autophagy pathways in cardiac tissue, leading to myocardial dysplasia in exposed birds.
Microplastics caused embryonic growth retardation and placental dysfunction in pregnant mice by activating GRP78/IRE1α/JNK axis induced apoptosis and endoplasmic reticulum stress
When pregnant mice were fed polystyrene microplastics, their embryos showed growth delays and their placentas were damaged through a specific stress pathway involving the endoplasmic reticulum, the cell's protein-processing center. These findings suggest that microplastic exposure during pregnancy could interfere with fetal development by triggering cell death in placental tissue.
Male reproductive toxicity of polystyrene microplastics: Study on the endoplasmic reticulum stress signaling pathway
Researchers exposed mice to polystyrene microplastics for 35 days and found significant male reproductive toxicity, including decreased sperm counts and motility, increased sperm abnormalities, and reduced testosterone levels. The microplastics caused structural damage to the seminiferous tubules and triggered endoplasmic reticulum stress in testicular tissue. The study suggests that microplastic exposure may impair male reproductive health through stress-related signaling pathways in the testes.
Recent consequences of micro-nanaoplastics (MNPLs) in subcellular/molecular environmental pollution toxicity on human and animals
This review examines the subcellular and molecular mechanisms by which micro- and nanoplastics cause toxicity in humans and animals, focusing on oxidative stress, inflammation, cell death pathways, and endocrine disruption at the cellular level.
The endoplasmic reticulum-mitochondrial crosstalk involved in nanoplastics and di(2-ethylhexyl) phthalate co-exposure induced the damage to mouse mammary epithelial cells
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.
Polystyrene microplastics induced nephrotoxicity associated with oxidative stress, inflammation, and endoplasmic reticulum stress in juvenile rats
This study found that polystyrene microplastics caused kidney damage in young rats through a combination of oxidative stress, inflammation, and a cellular stress response called endoplasmic reticulum stress. The microplastics also reduced body weight growth and affected multiple organs including the heart and ovaries. These findings suggest that microplastic exposure during development could be particularly harmful to kidney health in young, growing organisms.
Micro- and nanoplastics with diverse sizes and chemical structures compromise barrier integrity, cause extensive epithelial cell injury, and induce oxidative and endoplasmic reticulum stress
Researchers exposed human gut epithelial cells, peripheral blood cells, and nasal organoids to microplastics and nanoplastics of different sizes and polymer types, measuring barrier function, cell injury, and oxidative stress. All particle types compromised barrier integrity and caused cell injury, with smaller particles and higher exposures producing the most severe effects and triggering endoplasmic reticulum stress alongside oxidative damage.
Research progress on the cellular toxicity caused by microplastics and nanoplastics
This review summarizes current research on how microplastics and nanoplastics cause damage at the cellular level. Researchers identified four main ways these particles harm cells: triggering oxidative stress, damaging cell membranes and organelles, causing inflammation, and disrupting DNA. The findings highlight growing evidence that plastic particles small enough to enter cells can interfere with fundamental biological processes.
PET-Microplastics Trigger Endothelial Glycocalyx Loss via ER Stress and ROS Unleashing IL-1β-Driven SMC Switching and Early Aortic Structural Impairment
Researchers found that chronic oral exposure of rats to PET microplastics caused endothelial glycocalyx damage and aortic structural injury, with endoplasmic reticulum stress and reactive oxygen species triggering IL-1β-driven smooth muscle cell switching as the underlying mechanism.
Cellular and Systemic Effects of Micro- and Nanoplastics in Mammals—What We Know So Far
This review summarized known cellular and systemic effects of micro- and nanoplastics in mammals, finding that while ingestion is common, knowledge of health impacts remains limited, with oxidative stress and inflammation as the most reported biological responses.
Exploring toxicological pathways of microplastics and nanoplastics: Insights from animal and cellular models
This review examines what animal and cell studies have revealed about how microplastics and nanoplastics cause harm at the molecular level, including promoting inflammation, oxidative stress, and cell death. Most research has focused on reproductive toxicity and polystyrene particles, while effects on the gut, brain, and heart remain understudied. The authors note that many experiments use unrealistic concentrations and synthetic particles, making it difficult to apply the results to real-world human exposure.
Microplastics and Nanoplastics in Health Concerning Cellular Toxicity Mechanisms, Exposure Pathways, and Global Mitigation Strategies
This review synthesizes current knowledge on how micro- and nanoplastics cause cellular damage in the human body, covering mechanisms like oxidative stress, inflammation, DNA damage, and disruption of cell signaling pathways. Researchers note that exposure occurs through multiple routes including ingestion and inhalation, allowing particles to reach organs throughout the body. The study highlights significant gaps in understanding long-term and low-dose exposure effects that are most relevant to everyday human contact with these particles.
Micro- and nanoplastic induced cellular toxicity in mammals: A review
This review examines research on how micro- and nanoplastics cause cellular damage in mammalian systems, covering both laboratory and animal studies. Evidence indicates that these particles can trigger oxidative stress, inflammation, and DNA damage in cells, with smaller nanoplastics generally showing greater toxicity due to their ability to penetrate cell membranes more readily.
Nanoplastics induces oxidative stress and triggers lysosome-associated immune-defensive cell death in the earthworm Eisenia fetida
Researchers exposed earthworms to nanoplastics and found the tiny particles accumulated in their bodies, caused oxidative stress, and killed immune cells by rupturing their internal waste-processing structures (lysosomes). Positively charged nanoplastics were significantly more toxic than negatively charged ones. This study helps explain how nanoplastics damage living cells at a fundamental level, which is relevant to understanding their effects on any organism, including humans.