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61,005 resultsShowing papers similar to Polystyrene microplastics (PS-MPs) disturb skeleto-muscular energy metabolism and tissue architecture following sub-acute exposure: A dose-responsive study
ClearInfluence of Polystyrene Microplastics on Mitochondrial Oxidative Damage in Renal and Muscular Tissues of the Freshwater Fish
Researchers exposed freshwater fish to environmentally relevant concentrations of polystyrene microplastics for up to 15 days and examined mitochondrial damage in kidney and muscle tissues. The exposure disrupted antioxidant defenses, increased oxidative stress, and altered metabolic enzyme activities in both tissue types. Histological examination revealed significant tissue damage including necrosis and degeneration, suggesting that microplastics can cause organ-level toxicity in fish through mitochondrial oxidative stress.
Dissection of the potential mechanism of polystyrene microplastic exposure on cardiomyocytes
Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
Probing Long-Term Impacts: Low-Dose Polystyrene Nanoplastics Exacerbate Mitochondrial Health and Evoke Secondary Glycolysis via Repeated and Single Dosing
This study exposed human intestinal cells to low doses of polystyrene nanoplastics over 12 days and found that repeated exposure caused cumulative damage to mitochondria, the energy-producing structures inside cells. Even concentrations considered environmentally realistic impaired cellular energy production and forced cells to switch to a less efficient backup energy system. This suggests that long-term, everyday nanoplastic exposure through food could gradually harm gut health in ways that might not be immediately noticeable.
Polystyrene microplastics-induced ROS overproduction disrupts the skeletal muscle regeneration by converting myoblasts into adipocytes
Researchers found that polystyrene microplastics impaired skeletal muscle repair in mice by triggering excess production of reactive oxygen species (ROS) inside muscle stem cells. This oxidative stress redirected muscle stem cells to become fat cells instead of new muscle fibers, resulting in increased fat deposits and reduced muscle fiber size. The study suggests that microplastic exposure could interfere with the body's natural ability to regenerate and maintain muscle tissue.
Microplastics induce insulin resistance by causing mitochondrial dysfunction associated with mROS in skeletal muscle in vitro
Researchers exposed human muscle cells to polystyrene micro and nanoplastics and found that the particles caused insulin resistance, meaning the cells could not properly absorb sugar from the blood. The plastics damaged the cells' mitochondria (the energy-producing structures) and triggered harmful oxidative stress, but a mitochondria-protecting antioxidant reversed the damage. This study suggests that microplastic exposure could contribute to metabolic problems like type 2 diabetes by impairing how muscles process sugar.
Polyethylene microplastics disrupt renal function, mitochondrial bioenergetics, redox homeostasis, and histoarchitecture in Wistar rats
Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
Determination of Biological and Molecular Attributes Related to Polystyrene Microplastic-Induced Reproductive Toxicity and Its Reversibility in Male Mice
Researchers exposed male mice to polystyrene microplastics through drinking water and found that the particles caused mitochondrial damage in testicular tissue, including reduced membrane potential and disrupted energy production. This mitochondrial dysfunction led to decreased sperm quality, likely driven by oxidative stress. Importantly, the study found that sperm quality recovered after one to two spermatogenic cycles without further exposure, suggesting that reproductive toxicity from microplastics may be reversible.
Polystyrene microplastics induced spermatogenesis disorder via disrupting mitochondrial function through the regulation of the Sirt1-Pgc1α signaling pathway in male mice
Researchers investigated how polystyrene microplastics of different sizes affect sperm development in male mice and found that exposure decreased sperm motility and caused structural abnormalities. The microplastics disrupted mitochondrial function in reproductive cells by interfering with a key energy regulation pathway. The study provides evidence that microplastic exposure may contribute to male reproductive health problems through mitochondrial damage.
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 mitochondrial damage in mouse GC-2 cells
Researchers exposed mouse reproductive cells to polystyrene microplastics and found that the particles caused significant mitochondrial damage, reducing energy production and disrupting normal cellular function. The study observed decreased mitochondrial membrane potential, lower ATP levels, and increased oxidative stress in the exposed cells. These findings help explain how microplastic exposure may impair sperm development by damaging the energy-producing structures within reproductive cells.
The Effect of Microplastics on the Bioenergetics of the Mussel Mytilus coruscus Assessed by Cellular Energy Allocation Approach
Researchers studied the effects of polystyrene microplastics on the energy budget of mussels using a cellular energy allocation approach. They found that higher concentrations of microplastics increased energy demands while depleting carbohydrate, lipid, and protein stores, with lipid and protein levels failing to fully recover even after the microplastics were removed.
Behavioral impairments and disrupted mitochondrial energy metabolism induced by polypropylene microplastics in zebrafish larvae
Zebrafish embryos exposed to polypropylene microplastics at environmentally relevant levels showed behavioral changes and disrupted energy production in their cells. The microplastics impaired the mitochondria -- the energy-producing structures inside cells -- in both intestinal and liver tissue, while also causing oxidative stress. These findings suggest that even at concentrations found in the environment, common polypropylene microplastics can interfere with basic cellular energy processes.
Changes in life-history traits, antioxidant defense, energy metabolism and molecular outcomes in the cladoceran Daphnia pulex after exposure to polystyrene microplastics
Researchers exposed the freshwater zooplankton Daphnia pulex to polystyrene microplastics and observed dose-dependent effects on survival, antioxidant capacity, and energy metabolism. The study found that microplastics accumulated in the digestive tract, caused lipid oxidative damage, disrupted sugar and fat metabolism, and activated DNA repair mechanisms while inhibiting lipid metabolism pathways.
The Effect of Polystyrene Microplastic Exposure in the Rearing Water on Muscle Morphology of Mutiara Catfish (Clarias gariepinus Burchell, 1822)
Catfish (Clarias gariepinus) were exposed to polystyrene microplastics at 0, 1, 10, and 100 mg/L for 28 days and muscle tissue was examined histologically. Microplastics accumulated in muscle tissue in a dose-dependent manner, and myofiber diameter and area decreased significantly at higher concentrations, indicating microplastic-induced muscle damage.
Impact of polystyrene microplastic exposure at low doses on male fertility: an experimental study in rats
Researchers exposed adult male rats to varying doses of polystyrene microplastics and found dose-dependent declines in semen quality along with disrupted reproductive hormone levels. Higher doses caused increased oxidative stress, mitochondrial damage, and inflammatory responses in testicular tissue. The study suggests that even relatively low doses of microplastic exposure may have adverse effects on male reproductive health in animal models.
Polystyrene microplastics disrupt adrenal steroid synthesis in male mice via mitochondrial dysfunction
Researchers found that polystyrene microplastics disrupted steroid hormone production in the adrenal glands of male mice by causing mitochondrial dysfunction and oxidative stress. Chronic exposure led to reduced corticosterone levels and increased cell death in adrenal tissue. The study suggests that microplastics may interfere with the body's stress response and hormonal balance through damage to the energy-producing structures within cells.
Effects of Polystyrene Microplastics on Bone-related Protein Expression, Mineralization Capacity, and Mitochondrial Function in Osteoblast-like Cells (mg-63)
Osteoblast-like cells (MG-63) were exposed to polystyrene microplastics at 5–50 µg/mL, and bone-related protein expression, mineralisation capacity, and mitochondrial function were assessed. PS-MPs were internalised and reduced mineralisation and osteocalcin levels while impairing mitochondrial bioenergetics, suggesting microplastics may negatively affect bone cell function.
Adverse effects polystyrene microplastics exert on zebrafish heart – Molecular to individual level
Researchers fed zebrafish microplastic-enriched food for 21 days and found significant damage to heart function, including reduced contraction strength and frequency, along with decreased swimming ability. At the cellular level, the fish showed increased oxidative stress, DNA damage, and disrupted energy metabolism in heart tissue. The study provides evidence that microplastic exposure can affect cardiovascular health in fish from the molecular level up to whole-organism fitness.
Assessment of the Accumulation and Potential Toxicity of Polystyrene Microplastics in Rats
This study assessed polystyrene microplastic accumulation in aquatic organisms and evaluated associated toxicity endpoints including oxidative stress, histological changes, and behavioral effects. Microplastics accumulated in multiple tissues and caused dose-dependent physiological harm.
Dose-dependent alteration in hepatic and cerebral glucose metabolism following exposure to polystyrene microplastic in Wistar rats
Researchers exposed Wistar rats to polystyrene microplastics and observed dose-dependent changes in glucose metabolism in both the liver and brain. The study suggests that microplastic exposure may disrupt normal metabolic processes, with higher doses leading to more pronounced alterations in hepatic and cerebral glucose handling.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
Researchers exposed mice to tiny polystyrene particles for 16 weeks and found the plastics accumulated in their livers, disrupting fat metabolism and energy production. The microplastics altered lipid profiles and interfered with key enzymes involved in cellular energy cycles. The study suggests that long-term microplastic exposure may contribute to liver damage through metabolic disruption.
Polystyrene nanoplastics target electron transport chain complexes in brain mitochondria
Researchers investigated the effects of polystyrene nanoplastics on mitochondrial function in rat brain tissue. They found that nanoplastic exposure significantly impaired the electron transport chain, specifically disrupting electron flow between respiratory complexes I-III and II-III in both synaptic and non-synaptic mitochondria. The findings reveal a potential mechanism by which nanoplastics could contribute to brain energy metabolism deficits and neurotoxicity.
Chronic exposure to polystyrene microplastics at environmentally relevant concentration induced growth retardation in Macrobrachium rosenbergii via multi-pathway toxicity: Oxidative stress, microbial dysbiosis, and biodistribution
Researchers exposed juvenile freshwater prawns to environmentally relevant concentrations of polystyrene microplastics for 42 days and found significant growth inhibition, with a 15.6% reduction in body length and 29.6% decrease in body weight. The microplastics accumulated in gills, stomachs, intestines, and hemolymph, causing persistent mitochondrial damage, oxidative stress, and gut microbiota imbalance that did not fully recover even after the exposure ended.
Testicular mitochondrial redox imbalance and impaired oxidative phosphorylation underlie microplastic-induced testicular dysfunction in Wistar rats
Researchers investigated how polyethylene microplastics affect male reproductive function in rats by examining testicular mitochondrial health. The study found that microplastic exposure disrupted mitochondrial redox balance and impaired oxidative phosphorylation in testicular tissue, providing mechanistic evidence for how microplastics may contribute to male reproductive toxicity.