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61,005 resultsShowing papers similar to Synergistic effects of PS-NPs and Cd on ovarian toxicity in adolescent rats: Ferroptosis by induction of mitochondrial redox imbalance via the SIRT3-SOD2/Gpx4 pathway
ClearSynergistic effect of PS-MPs and Cd on male reproductive toxicity: Ferroptosis via Keap1-Nrf2 pathway
A mouse study found that microplastics and the heavy metal cadmium work together to cause more severe damage to male reproductive organs than either pollutant alone. The combination triggered a form of cell death called ferroptosis by disrupting a key protective pathway in the body. This is the first study to show this synergistic reproductive harm, suggesting that microplastics can make other environmental toxins more dangerous.
Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney
A mouse study found that combined exposure to cadmium (a toxic metal) and polystyrene nanoplastics caused more kidney damage than either pollutant alone. The combination triggered a harmful chain reaction involving oxidative stress, iron buildup, and excessive breakdown of cellular energy factories called mitochondria. This is significant because people are often exposed to both nanoplastics and heavy metals simultaneously, and their combined effects may be worse than expected.
Maternal Exposure to Combined Cadmium and Polystyrene Nanoplastics Induces Offspring Testicular Dysplasia via Mitochondrial Reactive Oxygen Species Overactivating the Peroxisome Proliferator-Activated Receptor α-Mediated Autophagy Signaling Pathway
Researchers investigated the combined effects of maternal exposure to polystyrene nanoplastics and cadmium on offspring in a mouse model. The study found that co-exposure caused testicular developmental abnormalities in offspring through mitochondrial oxidative stress and disrupted autophagy signaling, suggesting that nanoplastics may amplify the reproductive toxicity of co-occurring environmental contaminants.
Maternal Exposureto Combined Cadmium and PolystyreneNanoplastics Induces Offspring Testicular Dysplasia via MitochondrialReactive Oxygen Species Overactivating the Peroxisome Proliferator-ActivatedReceptor α‑Mediated Autophagy Signaling Pathway
Maternal exposure to combined polystyrene nanoplastics and cadmium during pregnancy caused testicular dysplasia in offspring via mitochondrial reactive oxygen species overactivating the PPARα-mediated autophagy pathway, with combined exposure more harmful than either alone.
Nanoplastic PS and cadmium co-exposure accelerates ferroptosis mediated by HIF-1α-related signaling in spermatogonium
Researchers exposed mouse sperm precursor cells to nanoplastics combined with cadmium and found that co-exposure caused significantly more cell damage than either contaminant alone. The combined treatment triggered a form of cell death called ferroptosis through a specific signaling pathway involving the gene HIF-1a. The study suggests that nanoplastics may worsen the reproductive toxicity of heavy metals commonly found alongside plastic pollution in the environment.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
PS-MPs or their co-exposure with cadmium impair male reproductive function through the miR-199a-5p/HIF-1α-mediated ferroptosis pathway
Researchers found that polystyrene microplastics, especially when combined with cadmium, caused significant reproductive damage in male mice through a cell death pathway called ferroptosis. Smaller microplastic particles were more toxic than larger ones, and the combination of microplastics with cadmium amplified the harm beyond what either caused alone. The study identifies a specific molecular mechanism by which microplastics and heavy metals together may threaten male reproductive health.
Co-exposure of cadmium and polystyrene nanoplastics: Induction pyroptosis and autophagy in mice testis
Researchers investigated the combined effects of cadmium and polystyrene nanoplastics on mouse testicular tissue. The study found that co-exposure produced more severe testicular damage than either substance alone, driven by the interplay between pyroptosis (inflammatory cell death) and autophagy. Inhibiting one of these cellular processes affected the other, suggesting they are closely interconnected in the toxicity response to nanoplastic and heavy metal co-exposure.
Maternal co-exposure to Cd and PS-NPLs induces offspring ovarian inflammatory aging via promoting M1 macrophage polarization
Researchers co-exposed pregnant mice to cadmium and polystyrene nanoplastics during pregnancy and lactation, finding that this combination disrupted sex hormones in female offspring and promoted M1 macrophage polarization in ovarian tissue — a pro-inflammatory state associated with accelerated ovarian aging — via gut microbiota disruption and TLR4 signaling activation.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
Synergistic neurotoxicity of polystyrene nanoplastics and cadmium co-exposure: oxidative stress, mitochondrial dysfunction, and ATF5-mediated mitochondrial unfolded protein response in C. elegans and PC12 cells
This study found that co-exposure to polystyrene nanoplastics and cadmium produced synergistic neurotoxicity in C. elegans and PC12 cells, mediated through oxidative stress, mitochondrial dysfunction, and activation of the ATF5-dependent mitochondrial unfolded protein response pathway.
Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation
Researchers found that polystyrene nanoplastics trigger ferroptosis — a form of iron-dependent cell death driven by fat oxidation — in pig egg cells, disrupting their maturation and reproductive viability. This finding raises concerns about nanoplastic exposure potentially impairing fertility by damaging the eggs needed for reproduction.
Polystyrene Nanoplastics and Cadmium Co-Exposure Accelerates Mitochondrial Autophagy Mediated by HSP60–SIRT3–SOD 2 Signaling Pathway in Primary Duck Embryo Hepatocytes
Scientists found that when tiny plastic particles and the toxic metal cadmium are combined, they cause more damage to liver cells than either pollutant alone. The plastic particles help cadmium get into cells more easily, leading to harmful changes in the cell's powerhouses (mitochondria) and increased cell death. While this study used duck cells, it suggests that the growing presence of microplastics in our environment could make heavy metal pollution more dangerous to human health.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Co-exposure to polystyrene nanoplastics and triclosan induces synergistic cytotoxicity in human KGN granulosa cells by promoting reactive oxygen species accumulation
Researchers found that when human ovarian cells are exposed to both nanoplastics and triclosan (a common antibacterial chemical) at the same time, the toxic effects are worse than either one alone. The combination triggered more cell damage, harmful oxygen molecules, and cell death than individual exposure. This matters because people are typically exposed to multiple pollutants simultaneously, and this synergy could have implications for female reproductive health.
Maternal exposure to nanopolystyrene induces neurotoxicity in offspring through P53-mediated ferritinophagy and ferroptosis in the rat hippocampus
When pregnant and nursing rats were fed nanoplastics, their offspring showed impaired learning and memory due to a specific type of cell death called ferroptosis in the brain's hippocampus. The nanoplastics triggered a chain reaction involving oxidative stress and iron buildup that damaged developing brain cells, suggesting that maternal exposure to nanoplastics during pregnancy and breastfeeding could harm offspring brain development.
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte
Researchers found that polystyrene nanoplastics cause testicular damage in mice through a cell death process called ferroptosis. The nanoplastics triggered the breakdown of iron-storage proteins and reduced levels of a protective mitochondrial protein called CISD1 in sperm cells. The study suggests that nanoplastic exposure may contribute to male reproductive harm by driving excess iron into mitochondria.
Polystyrene nanoplastics disrupt iron homeostasis by promoting FPN1 ubiquitination in GC-2spd(ts) cells
Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production
Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
Co-exposure to polystyrene microplastics and lead aggravated ovarian toxicity in female mice via the PERK/eIF2α signaling pathway
Researchers found that combined exposure to polystyrene microplastics and lead caused more severe ovarian damage in female mice than either pollutant alone. The study showed that co-exposure activated endoplasmic reticulum stress through the PERK/eIF2-alpha signaling pathway, leading to increased cell death in ovarian tissue, but these effects could be alleviated with stress inhibitor or antioxidant treatment.
Combined effect of polystyrene microplastics and cadmium on rat blood-testis barrier integrity and sperm quality
Researchers exposed male rats to polystyrene microplastics and cadmium, both separately and together, and found that both substances damaged testicular tissue, disrupted the blood-testis barrier, and reduced sperm quality. Notably, the combined exposure was less severe than cadmium alone, likely because microplastics absorbed some cadmium in the gut and reduced its bioavailability. The study also found for the first time that microplastics trigger autophagy in reproductive cells as a protective response.
Polystyrene nanoplastics distinctly impact cadmium uptake and toxicity in Arabidopsis thaliana
In a study using the model plant Arabidopsis, polystyrene nanoplastics increased the uptake and accumulation of the toxic heavy metal cadmium in plant roots. The combined stress of nanoplastics and cadmium caused worse oxidative damage and growth problems than either pollutant alone. This is concerning because it means microplastics in agricultural soil could help toxic metals get into crops more easily, potentially increasing human exposure through food.