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Papers
61,005 resultsMaternal 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.
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.
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.
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.
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.
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.
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.
Arsenic and polystyrene-nano plastics co-exposure induced testicular toxicity: Triggers oxidative stress and promotes apoptosis and inflammation in mice.
Combined exposure of mice to polystyrene nanoplastics and arsenic caused greater testicular damage than either pollutant alone, with co-exposure triggering amplified oxidative stress, apoptosis, and inflammatory signaling in testicular tissue, pointing to compounding reproductive toxicity from these co-occurring environmental contaminants.
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.
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.
The 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.
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.
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.
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.
Polystyrene nanoplastics aggravate reproductive system damage in obese male mice by perturbation of the testis redox homeostasis
Researchers found that polystyrene nanoplastics worsened reproductive damage in male mice already fed a high-fat diet, reducing sperm quality and testosterone production beyond what obesity alone caused. The nanoplastics disrupted the protective blood-testis barrier and increased oxidative stress in reproductive tissues. The study suggests that nanoplastic exposure combined with obesity may create compounding risks to male fertility.
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.
Polystyrene nanoparticles enhance the adverse effects of di-(2-ethylhexyl) phthalate on male reproductive system in mice
Researchers investigated the combined reproductive toxicity of polystyrene nanoparticles and the plasticizer DEHP in male mice over 35 days. The study found that co-exposure to nanoparticles and DEHP produced enhanced adverse effects on sperm quality and testicular tissue compared to either substance alone, suggesting nanoplastics may amplify the endocrine-disrupting effects of plasticizers.
Combined exposure to titanium nanoparticles and nanoplastics damages the male reproductive system and sperm activity
This study assessed the effects of combined TiO2 nanoparticles and polystyrene nanoplastics on male reproductive function in animal models, finding that co-exposure caused greater damage to sperm motility, testicular structure, and hormone levels than either material alone. The results raise concerns about combined environmental exposure to two common industrial nanomaterials.
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.
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.
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.
From mothers to offspring: Polystyrene nanoplastics create a hidden toxic legacy via mitochondrial dysfunction
Researchers exposed female zebrafish to polystyrene nanoplastics before mating with unexposed males and found that maternal exposure at 100 μg/L reduced offspring hatching success and caused developmental defects in the F1 generation raised in clean water, demonstrating transgenerational toxicity via mitochondrial dysfunction.
Chronic toxicity effects of sediment-associated polystyrene nanoplastics alone and in combination with cadmium on a keystone benthic species Bellamya aeruginosa
Researchers conducted a 28-day sediment toxicity test to examine the effects of polystyrene nanoplastics alone and combined with cadmium on the freshwater snail Bellamya aeruginosa. The study found that nanoplastics increased cadmium bioavailability and facilitated its accumulation, leading to enhanced oxidative stress and cellular damage. The findings suggest that nanoplastics may amplify the toxicity of co-occurring heavy metal contaminants in freshwater sediments.
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.