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61,005 resultsShowing papers similar to Anthocyanin-rich polyphenols from Hibiscus syriacus activate autophagy to reverse polystyrene microplastic-induced osteogenic dysfunction
ClearEffects 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.
Polystyrene microplastics disrupt osteogenic differentiation via lysosome-mediated mitochondrial dysfunction: Protective role of mTOR signaling
Researchers identified a mechanistic pathway by which polystyrene microplastics impair bone formation in zebrafish and mouse preosteoblasts: PS-MPs accumulate in lysosomes, trigger mitochondrial dysfunction, and suppress osteogenic differentiation. Activation of the mTOR signaling pathway was found to partially protect against this bone toxicity.
Polystyrene microplastics induces senescence of osteocytes by activating the cyclooxygenase-2 signaling pathway
Researchers found that polystyrene microplastics can be taken up by osteocytes, the most abundant cells in bone tissue, and cause them to undergo premature aging through a process called senescence. The microplastics triggered oxidative stress and activated a specific inflammatory signaling pathway involving cyclooxygenase-2. The study suggests that microplastic exposure could potentially impair bone health by disrupting the normal function of the cells responsible for maintaining bone tissue.
Micro-algal astaxanthin ameliorates polystyrene microplastics-triggered necroptosis and inflammation by mediating mitochondrial Ca2+ homeostasis in carp’s head kidney lymphocytes (Cyprinus carpio L.)
Researchers investigated whether astaxanthin, a natural pigment from microalgae, could protect carp immune cells from damage caused by polystyrene microplastics. They found that astaxanthin reduced inflammation and cell death triggered by microplastics by helping maintain calcium balance within the cells' mitochondria. The study suggests that natural antioxidant compounds may help mitigate some of the harmful immune effects of microplastic exposure in fish.
Polystyrene microplastics arrest skeletal growth in puberty through accelerating osteoblast senescence
Researchers found that polystyrene microplastics accumulated in the bones of mice during puberty, leading to reduced body and bone length and impaired bone structure. The microplastics accelerated premature aging (senescence) of bone-building cells called osteoblasts, suppressing their ability to form new bone. The study suggests that microplastic exposure during critical growth periods may pose a risk to skeletal development.
Anthocyanins as protectors of gut microbiota: mitigating the adverse effects of microplastic-induced disruption
This review examines how anthocyanins, bioactive compounds found in berries and other pigmented plants, may protect gut microbiota from disruption caused by microplastic exposure. Researchers synthesized evidence suggesting that anthocyanins counteract microplastic-induced oxidative stress and inflammation in the gut. The findings indicate that dietary anthocyanins could serve as a protective factor against the adverse effects of microplastics on digestive health.
Chronic exposure to polystyrene microplastics triggers osteoporosis by breaking the balance of osteoblast and osteoclast differentiation
Mice that drank water containing polystyrene microplastics for six months developed significant bone loss resembling osteoporosis, with weakened bone structure and reduced bone formation. The microplastics triggered inflammation in bone stem cells and disrupted the balance between bone-building and bone-breaking processes, suggesting that long-term microplastic exposure could contribute to bone disease.
Exogenous Hydrogen Sulfide Mitigates Oxidative Stress and Mitochondrial Damages Induced by Polystyrene Microplastics in Osteoblastic Cells of Mice
Researchers found that polystyrene microplastics induced oxidative stress, mitochondrial damage, and altered gene expression in mouse bone-forming cells, while exogenous hydrogen sulfide treatment mitigated these toxic effects by modulating key signaling pathways.
Canidin-3-glucoside prevents nano-plastics induced toxicity via activating autophagy and promoting discharge
Researchers showed that cyanidin-3-glucoside (C3G), a natural anthocyanin, reduced polystyrene nanoplastic toxicity in Caco-2 cells and C. elegans by activating autophagy and promoting cellular discharge of internalized particles, suggesting a dietary protective mechanism.
Aged nanoplastics reprogram the ER stress-autophagy crosstalk: A mechanistic gateway to skeletal malformations in zebrafish
Researchers exposed zebrafish embryos to both new and UV-aged nanoplastics and found that the aged particles caused significantly worse skeletal deformities, higher mortality, and lower hatching rates. The aged nanoplastics disrupted cellular stress responses and a self-cleaning process called autophagy in developing bone and cartilage cells. The study suggests that weathered nanoplastics in the environment may pose greater developmental risks than freshly produced particles.
Effect of polystyrene nanoplastics and their degraded forms on stem cell fate
Researchers studied how polystyrene nanoplastics and their degraded forms affect human bone marrow-derived stem cells. They found that both intact and degraded nanoplastics showed reactive oxygen species scavenging activity, enhanced mitochondrial fusion, and promoted cell proliferation and fat cell differentiation. However, the degraded nanoplastics showed higher long-term cytotoxicity, suggesting that as nanoplastics break down in the environment, their biological effects on human cells may change.
Investigating the protective effects of epigallocatechin-gallate against polystyrene microplastics-induced biochemical and hematological alterations in rats
This study investigated whether epigallocatechin-gallate (EGCG) -- a green tea antioxidant -- could protect rats from biochemical and hematological damage caused by polystyrene microplastic ingestion. EGCG supplementation partially mitigated oxidative stress and inflammatory markers elevated by polystyrene microplastic exposure, suggesting a potential dietary protective strategy.
Evaluation of Possible Ameliorative Role of Robinetin to Counteract Polystyrene Microplastics Instigated Renal Toxicity in Rats
Researchers tested whether robinetin, a plant-derived compound, could protect rat kidneys from damage caused by polystyrene microplastic exposure. They found that microplastics caused significant kidney harm through oxidative stress, inflammation, and cell death, but robinetin supplementation substantially reversed these effects. The study suggests that natural antioxidant compounds may offer a protective strategy against microplastic-related organ damage.
Polystyrene nanoplastics mediate skeletal toxicity through oxidative stress and the BMP pathway in zebrafish (Danio rerio)
Exposing zebrafish embryos to polystyrene nanoplastics caused skeletal deformities, reduced body length, and disrupted bone development pathways. The nanoplastics triggered oxidative stress and cell death in developing bone tissue, with longer exposure periods causing worse outcomes. While this study was conducted in fish, the bone development pathways affected are similar to those in humans, raising questions about whether nanoplastic exposure could affect skeletal development.
Autophagic response of intestinal epithelial cells exposed to polystyrene nanoplastics
Researchers found that polystyrene nanoplastics accumulate in the cytoplasm of intestinal epithelial cells, impairing autophagic flux and triggering an autophagic stress response confirmed in both cell and animal models.
Polystyrene nanoplastics induce ovarian granulosa cell senescence via autophagy suppression
Researchers found that polystyrene nanoplastics induce premature cellular aging (senescence) in human ovarian granulosa cells by suppressing autophagy, triggering inflammatory signaling and mitochondrial dysfunction, and that restoring autophagy with rapamycin reversed these effects — pointing to a potential mechanism linking nanoplastic exposure to accelerated ovarian aging.
Nanoplastic impact on bone microenvironment: A snapshot from murine bone cells.
This study examined how nanoplastics affect bone cell function in a murine model, investigating effects on osteoblasts and osteoclasts that govern bone formation and resorption in the bone microenvironment. Nanoplastic exposure altered bone cell activity, suggesting that daily plastic particle exposure could have long-term implications for bone health.
Toxicity of microplastics polystyrene to freshwater planarians and the alleviative effects of anthocyanins
Researchers determined the lethal concentration of polystyrene microplastics for freshwater planarians for the first time and found that exposure disrupted their internal balance, caused oxidative damage, and triggered nerve cell changes and cell death. Notably, long-term exposure to low, environmentally relevant concentrations was more harmful than short-term exposure to high doses. The study also found that anthocyanins, natural plant pigments, could effectively reduce the toxic effects of polystyrene on these organisms.
Lipid metabolic dysregulation: A novel developmental toxicity pathway of aged nanoplastics via inhibition of lipophagy in zebrafish
Researchers showed that UV-aged polystyrene nanoplastics cause more severe developmental toxicity in zebrafish larvae than pristine particles by blocking lipophagy — the cellular process of breaking down stored fat via lysosomes — leading to abnormal lipid accumulation and disrupted early development.
Elucidating the underlying toxic mechanisms of nanoplastics on zebrafish hematological and circulatory systems
This study demonstrated that nanoplastics disrupt early embryonic development and impair mitochondrial function in zebrafish by inhibiting PINK1/Parkin-mediated mitophagy, a cellular cleanup process. A mitophagy activator was able to mitigate these effects, pointing to mitochondrial dysfunction as a key mechanism of nanoplastic hematological and circulatory toxicity.
Bridging relevance between microplastics, human health and bone metabolism: Emerging threats and research directions
Researchers reviewed how microplastics — tiny plastic fragments that accumulate in tissues throughout the body — may disrupt bone metabolism by triggering inflammation, oxidative stress, and hormonal interference, raising concern that widespread microplastic exposure could contribute to bone diseases like osteoporosis.
Pharmacological assessment of delphinidin in counteracting polystyrene microplastic induced renal dysfunction in rats
Researchers investigated whether the plant compound delphinidin could protect against kidney damage caused by polystyrene microplastics in rats. They found that microplastic exposure triggered oxidative stress, inflammation, and cell death markers in kidney tissue, while delphinidin treatment significantly restored normal kidney function. The study suggests that delphinidin may have protective properties against microplastic-induced organ damage in animal models.
Aged polystyrene microplastics exposure affects apoptosis via inducing mitochondrial dysfunction and oxidative stress in early life of zebrafish
Zebrafish embryos exposed to UV-aged polystyrene microplastics at environmental concentrations showed more severe developmental problems than those exposed to fresh microplastics. The aged particles caused greater oxidative stress and mitochondrial damage, triggering increased cell death during early development -- suggesting that weathered microplastics in the real environment may be more harmful than the pristine particles typically used in lab studies.
Nanoplastic impact on bone microenvironment: A snapshot from murine bone cells.
Researchers investigated how nanoplastics affect the bone microenvironment using murine bone cell models, examining effects on osteoblast and osteoclast activity that regulate bone formation and resorption. Nanoplastic exposure disrupted bone cell function, raising concerns about skeletal health impacts from daily plastic particle exposure.