We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsMaternal 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.
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.
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.
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 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.
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.
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.
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.
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.
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.
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.
PPARγ mediated lysosomal membrane permeabilization and lipophagy blockage were involved in microplastics and di (2-ethylhexyl) phthalate co-exposure induced immature testis injury
Mice exposed to both polystyrene microplastics and DEHP, a common plastic additive, suffered significantly worse testicular damage than those exposed to either substance alone. The combined exposure disrupted fat metabolism in reproductive cells by damaging lysosomes (cellular recycling centers) and blocking the normal breakdown of lipids. This is especially relevant to human health because people are typically exposed to microplastics and plastic additives like DEHP at the same time through everyday products.
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.
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.
Disturbance of mitochondrial dynamics led to spermatogenesis disorder in mice exposed to polystyrene micro- and nanoplastics
Polystyrene micro- and nanoplastics caused spermatogenesis disorders in mice by disrupting mitochondrial dynamics, triggering excessive mitochondrial fission that activated both apoptosis and pyroptosis pathways in testicular tissue. Nanoplastics caused mitochondrial DNA to leak into the cytoplasm, activating the cGAS-STING inflammatory pathway — a mechanism confirmed by rescue experiments with a mitochondrial fission inhibitor.
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.
A meta-analysis-based adverse outcome pathway for the male reproductive toxicity induced by microplastics and nanoplastics in mammals
This meta-analysis of 39 studies mapped the adverse outcome pathway for microplastic and nanoplastic-induced male reproductive toxicity in mammals. Increased reactive oxygen species triggers a cascade of cellular damage including mitochondrial dysfunction, sperm DNA damage, and disrupted hormone signaling, ultimately leading to reduced sperm quality, impaired spermatogenesis, and decreased testosterone levels.
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.
The simultaneous administration of microplastics and cadmium alters rat testicular activity and changes the expression of PTMA, DAAM1 and PREP
Researchers examined the combined effects of microplastics and cadmium on testicular function in rats. The study found that simultaneous exposure caused testicular damage including impaired tissue structure, increased cell death, reduced testosterone, and altered expression of proteins involved in sperm cell development. The study suggests that microplastics may partially reduce cadmium bioavailability through adsorption, resulting in combined effects that were more severe than microplastics alone but less harmful than cadmium alone.
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.
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.
Polystyrene nanoplastics aggravated dibutyl phthalate-induced blood-testis barrier dysfunction via suppressing autophagy in male mice
In a mouse study, polystyrene nanoplastics combined with dibutyl phthalate (a common plasticizer chemical) caused significantly worse damage to the blood-testis barrier than either substance alone. The nanoplastics carried the phthalate into the reproductive system, where the combination reduced sperm quality, impaired sperm development, and damaged the protective barrier around the testes. This research shows how nanoplastics can make other common plastic chemicals more dangerous to male fertility.
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.