We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to Polystyrene Nanoplastics and Cadmium Co-Exposure Accelerates Mitochondrial Autophagy Mediated by HSP60–SIRT3–SOD 2 Signaling Pathway in Primary Duck Embryo Hepatocytes
ClearThe Mechanism of Combined Exposure of Polystyrene Microplastics and Cadmium Inducing Hepatic Injury through the Modulation of PI3K/AKT/mTOR-Mediated Autophagy
Researchers examined liver damage in mice exposed to polystyrene microplastics and cadmium, both alone and in combination, and found that triple exposure to 100-nanometer particles, 1-micrometer particles, and cadmium caused the most severe liver dysfunction. The study suggests that nanoscale microplastics significantly enhance cadmium-induced liver injury through disrupted autophagy via the PI3K/AKT/mTOR signaling pathway.
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.
Liver Injury Induced by Exposure to Polystyrene Microplastics Alone or in Combination with Cadmium in Mice Is Mediated by Oxidative Stress and Apoptosis
Researchers exposed mice to polystyrene microplastics alone and combined with cadmium over eight weeks to study liver damage. Both exposures caused liver injury through oxidative stress and programmed cell death, but the combination of microplastics and cadmium produced more severe effects. The study suggests that microplastics may worsen the toxic impact of heavy metals on the liver when both are present together.
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.
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.
Cadmium and polyvinyl chloride microplastics induce mitochondrial damage and apoptosis under oxidative stress in duck kidney
Researchers exposed Muscovy ducks to cadmium and polyvinyl chloride microplastics, both individually and in combination, and found that each pollutant alone caused kidney damage through oxidative stress and mitochondrial dysfunction. Interestingly, the combined exposure actually reduced some markers of damage compared to single exposures, suggesting complex interactions between the two contaminants. The study demonstrates that microplastics and heavy metals can significantly impair kidney function in waterfowl through apoptosis and disrupted cellular defense pathways.
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.
Microplastics Exacerbate Cadmium-Induced Kidney Injury by Enhancing Oxidative Stress, Autophagy, Apoptosis, and Fibrosis
Researchers exposed mice to microplastics and cadmium for three months and found that microplastics significantly worsened cadmium-induced kidney injury. The combined exposure enhanced oxidative stress, autophagy, cell death, and tissue scarring in the kidneys beyond what cadmium alone caused. The study suggests that microplastics may act as amplifiers of heavy metal toxicity in organ systems.
Synergistic 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.
Molecular regulatory networks of microplastics and cadmium mediated hepatotoxicity from NAFLD to tumorigenesis via integrated approaches
This study mapped out how microplastics and the toxic metal cadmium work together to damage the liver, tracing a progression from fatty liver disease to cirrhosis and eventually liver cancer. Cadmium activates genes linked to cell growth and tumor formation, while microplastics trigger cell death pathways related to inflammation. When combined, the two pollutants accelerate liver damage more than either one alone, raising concerns about real-world exposure where people encounter both simultaneously.
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
Researchers studied the combined effects of polystyrene nanoplastics and cadmium on the ovaries of adolescent rats over 28 days. They found that co-exposure was significantly more harmful than either pollutant alone, causing damage to ovarian structure and hormone disruption through a process called ferroptosis triggered by mitochondrial oxidative stress. The study suggests that nanoplastics may act as a carrier that amplifies heavy metal toxicity to the reproductive system during critical developmental periods.
Co-exposure of polyvinyl chloride microplastics with cadmium promotes nonalcoholic fatty liver disease in female ducks through oxidative stress and glycolipid accumulation
Researchers found that female ducks exposed to both PVC microplastics and cadmium together developed nonalcoholic fatty liver disease, with the combination being worse than either pollutant alone. The co-exposure caused oxidative stress and abnormal fat and sugar buildup in the liver. This study is relevant to human health because people are also exposed to microplastics and heavy metals simultaneously, and the combined effects may be more damaging than exposure to either one individually.
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.
Effects of chronic co-exposure polystyrene nanoplastics and cadmium on liver function in Prussian carp (Carassius gibelio)
Researchers exposed Prussian carp to polystyrene nanoplastics and cadmium, both individually and together, for 21 days and found that the combination caused significantly worse liver damage than either pollutant alone. The nanoplastics enhanced cadmium accumulation in the liver and amplified oxidative stress, tissue damage, and immune gene activation. The findings demonstrate that nanoplastics and heavy metals can have synergistic toxic effects on aquatic organisms.
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.
Co-exposure to PVC microplastics and cadmium induces oxidative stress and fibrosis in duck pancreas
Researchers found that exposing ducks to PVC microplastics and cadmium together caused far worse pancreatic damage than either pollutant alone, including severe inflammation, fibrosis, and disrupted organ function. The combined exposure overwhelmed the ducks' antioxidant defenses and caused mitochondrial damage in pancreatic cells. Since waterfowl are highly exposed to both microplastics and heavy metals in contaminated waterways, this study shows how these common pollutants can interact to amplify organ damage.
Micro-/nano-plastics as vectors of heavy metals and stress response of ciliates using transcriptomic and metabolomic analyses
This study examined how polystyrene microplastics and nanoplastics interact with cadmium to affect single-celled marine organisms called ciliates. The combined exposure was more toxic than either pollutant alone, disrupting the organisms' metabolism and stress responses at the genetic level. The findings demonstrate that microplastics can make heavy metal pollution worse by carrying metals into cells, a concern for marine food web contamination that could ultimately affect seafood safety.
CPT1 deficiency blocks autophagic flux to promote lipid accumulation induced by co-exposure to polystyrene microplastic and cadmium
Researchers found that combined exposure to polystyrene microplastics and cadmium in mice led to fat accumulation in the liver by blocking a cellular cleanup process called autophagy. The study identified a specific enzyme, CPT1, whose activation could alleviate both the fat buildup and the blocked autophagy pathway. The findings suggest that microplastics may worsen the toxic effects of heavy metals on liver health through shared metabolic pathways.
Polystyrene nanoplastics and cadmium co-exposure aggravated cardiomyocyte damage in mice by regulating PANoptosis pathway
Researchers gave mice low doses of polystyrene nanoplastics and cadmium (a toxic metal) together and found that the combination caused significantly worse heart damage than either substance alone. The damage involved a newly recognized form of cell death called PANoptosis, which combines multiple destructive pathways in heart cells. This suggests that real-world exposure to nanoplastics alongside common environmental pollutants like cadmium could compound risks to heart health.
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.
Redefining the synergistic toxicity of nano-plastics and cadmium in earthworm coelomocytes: the mechanism of α-amylase molecular docking orientation and energy crisis
Researchers exposed earthworm immune cells (coelomocytes) to polystyrene nanoplastics combined with the heavy metal cadmium, finding that nanoplastics act as carriers that amplify cadmium uptake and worsen oxidative stress, energy metabolism disruption, and enzyme damage beyond what cadmium causes alone.
Combined effect of arsenic and polystyrene-nanoplastics at environmentally relevant concentrations in mice liver: Activation of apoptosis, pyroptosis and excessive autophagy
Researchers investigated the combined toxic effects of arsenic and polystyrene nanoplastics on mouse liver at environmentally relevant concentrations. The study found that co-exposure activated multiple cell death pathways including apoptosis, pyroptosis, and excessive autophagy in liver tissue, suggesting that the interaction between nanoplastics and heavy metals may amplify liver damage.
Exposure to microplastics cause gut damage, locomotor dysfunction, epigenetic silencing, and aggravate cadmium (Cd) toxicity in Drosophila
Researchers used fruit flies as a model to study the effects of microplastics alone and combined with cadmium, a toxic metal commonly used in plastic production. They found that microplastics caused size-dependent gut damage and enhanced cadmium's harmful effects on movement and gene regulation through epigenetic silencing. The study demonstrates that microplastics can amplify the toxicity of co-occurring environmental contaminants and suggests Drosophila as a useful tool for rapid microplastic toxicity screening.
New Evidence for the Mechanisms of Nanoplastics Amplifying Cadmium Cytotoxicity: Trojan Horse Effect, Inflammatory Response, and Calcium Imbalance
Researchers discovered that nanoplastics act as a "Trojan horse" by carrying cadmium (a toxic heavy metal) into liver cells and then releasing it inside, amplifying cadmium's toxicity by over 23%. The combined exposure triggered more severe inflammation and cell death than either pollutant alone, demonstrating how nanoplastics can make other environmental contaminants more dangerous to human health.