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61,005 resultsShowing papers similar to ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells
ClearAcute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
Researchers discovered that very small polystyrene nanoparticles (20 nanometers) cause liver damage in mice by accumulating inside immune cells called macrophages, disrupting their energy-producing structures (mitochondria), and triggering a form of cell death that then spreads damage to liver cells. This study reveals a specific mechanism by which nanoplastic exposure could harm the liver, an organ critical for filtering toxins from the body.
Polystyrene microplastics trigger hepatocyte apoptosis and abnormal glycolytic flux via ROS-driven calcium overload
This study investigated how polystyrene microplastics damage liver cells and found they trigger a chain reaction involving excess reactive oxygen species (ROS) that leads to calcium overload inside cells. The calcium buildup disrupts normal energy metabolism and ultimately causes liver cell death. The findings reveal a specific molecular pathway connecting microplastic-driven oxidative stress to liver toxicity.
Impact of environmental microplastic exposure on HepG2 cells: unraveling proliferation, mitochondrial dynamics and autophagy activation
Lab experiments on human liver cells found that exposure to common microplastics (polyethylene and PET) increased cell growth but also triggered oxidative stress, damaged mitochondria (the cell's energy centers), and activated autophagy -- a process where cells try to clean up internal damage. These findings suggest that microplastics may disrupt normal liver cell function in ways that could have long-term health consequences.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells
Researchers discovered that polystyrene nanoplastics damage human liver cells by causing oxidative stress and mitochondrial damage, but the cells activate a protective pathway called Nrf2 to fight back. When the Nrf2 defense was blocked, the damage from nanoplastics became significantly worse, confirming its protective role. This study helps explain how the liver tries to defend itself against nanoplastic toxicity, and suggests that people with weaker antioxidant defenses may be more vulnerable to liver damage from plastic exposure.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
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.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
The effect of polystyrene nanoplastics on arsenic-induced apoptosis in HepG2 cells
Researchers studied the combined effects of polystyrene nanoplastics and arsenic on human liver cells in the laboratory. They found that nanoplastics, particularly those around 50 nanometers in size, significantly enhanced arsenic-induced cell death by disrupting mitochondrial function. The study identifies key genes involved in this interaction, suggesting that microplastic exposure may worsen the toxic effects of heavy metals on liver cells.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
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.
Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size
Researchers exposed mouse liver cells to polystyrene microplastics of different sizes and found that smaller particles caused more oxidative stress and damage than larger ones. The microplastics disrupted protective antioxidant systems and increased harmful reactive oxygen species inside the cells. This suggests that the smallest microplastic particles may pose the greatest risk to liver health because they can enter cells more easily and cause more internal damage.
Cytotoxic and dysmetabolic impact of polystyrene nanoplastics, a new potential atherosclerotic cardiovascular risk factor, on a steatosis model of HepG2 cells
Researchers exposed cell cultures to polystyrene nanoplastics and found significant cytotoxic effects and metabolic disruption including mitochondrial dysfunction and altered glucose metabolism, suggesting nanoplastics may act as a novel class of metabolic disruptors.
Polystyrene Nanoplastics Induce Pyroptosis in HepG2 Cells via the YAP1-cGAS-STING Signaling Axis.
Scientists found that tiny plastic particles from polystyrene (commonly used in disposable cups and food containers) can trigger a harmful type of cell death in liver cells. When these microscopic plastic pieces enter liver cells, they activate a specific pathway that causes the cells to essentially self-destruct, which could potentially damage the liver over time. This research helps explain how the plastic pollution we're exposed to daily might be harming our bodies, particularly our liver health.
New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
Chickens exposed to polystyrene microplastics in their drinking water developed significant spleen damage, with higher doses causing worse effects. The microplastics disrupted mitochondrial function in spleen cells, triggering both apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), along with harmful oxidative stress. These findings are relevant to human health because the spleen plays an important role in immune function, and similar damage pathways could potentially occur in people exposed to microplastics.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
Researchers demonstrated that polystyrene nanoplastics can cross the blood-brain barrier and accumulate in mouse brains, leading to cognitive impairment and loss of connections between brain cells. The damage was driven by excessive splitting of mitochondria, the energy-producing structures within cells, which triggered runaway cellular cleanup processes. Importantly, a drug that blocks this mitochondrial splitting reversed the cognitive damage, suggesting a potential therapeutic approach to nanoplastic-related brain injury.
Impact of Micro- and Nanoplastics on Mitochondria
This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
Cellular Distribution of Polystyrene Nanoplastics from Food Chain and Their Effects on Mitochondrial Quality in H9C2 Cells
Researchers investigated the cellular distribution of polystyrene nanoplastics entering via the food chain and examined their effects on mitochondrial quality in H9C2 cardiac cells, assessing how nanoplastic accumulation disrupts mitochondrial function.
Polystyrene Microplastics Induce Injury to the Vascular Endothelial Through NLRP3 ‐Mediated Pyroptosis
Researchers found that polystyrene microplastics caused blood vessel damage in rats by triggering a type of inflammatory cell death called pyroptosis through the NLRP3 pathway. The microplastics activated this destructive immune response in the cells lining blood vessels, leading to inflammation and tissue injury. This study provides a specific mechanism by which microplastic exposure could contribute to cardiovascular disease in humans.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
The Mitochondrial Battleground: A Review of Microplastic-Induced Oxidative Stress and Inflammatory Pathways in Human Health
This review synthesizes research on how microplastics damage mitochondria through oxidative stress and inflammation across aquatic, terrestrial, and mammalian systems. Researchers found that microplastics generate reactive oxygen species that disrupt mitochondrial function, with smaller and aged particles causing greater toxicity, while inflammatory signaling creates a feedback loop that worsens cellular damage.
Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis
In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.