We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Co-exposure to Cadmium and Polystyrene Nanoplastics Intensifies Renal Damage in Mice via the Activation of the PANoptosis Pathway
AI summary Read the abstract
Researchers exposed mice to cadmium and polystyrene nanoplastics individually and together, finding that co-exposure synergistically worsened kidney damage by activating PANoptosis — a coordinated cell death cascade integrating pyroptosis, apoptosis, and necroptosis — with the scaffold protein ASC markedly upregulated as a central driver.
Cadmium (Cd) and Polystyrene Nanoplastics (PS-NPs) are co-occurring environmental pollutants with potential nephrotoxic effects, yet their combined impact and underlying mechanisms remain unclear. This study aimed to investigate whether co-exposure to Cd and PS-NPs exacerbates renal injury in mice and to determine the role of PANoptosis—a coordinated cell death pathway involving Pyroptosis, Apoptosis, and Necroptosis—in mediating this toxicity. Sixty male Kunming mice were divided into four groups (n = 15): control, Cd (1.5 mg/kg/day), PS-NPs (1 mg/kg/day), and Cd + PS-NPs co-exposure. Treatments were administered via intragastric gavage for 35 days. Body weight, kidney index, histopathology (H&E, Masson, PAS), and ultrastructure (TEM) were evaluated. Molecular activation of PANoptosis was assessed by Western blot, qRT-PCR, immunohistochemistry, and immunofluorescence. Co-exposure significantly reduced body weight and kidney index (p < 0.05) and caused severe glomerular atrophy, tubular necrosis, and collagen deposition. Ultrastructural damage, including mitochondrial vacuolation and nuclear degeneration, was most pronounced in the co-exposure group. Mechanistically, co-exposure synergistically upregulated key markers of Pyroptosis (Caspase-1, Pyrin, GSDMD), Apoptosis (Caspase-8, Bax), and Necroptosis (RIPK1, p-RIPK3, MLKL). Notably, the PANoptosis scaffold protein ASC was markedly increased at both protein and mRNA levels (p < 0.001), indicating PANoptosome activation. Co-exposure to Cd and PS-NPs induces synergistic renal damage in mice, primarily through activation of the PANoptosis pathway. This study reveals a novel mechanism of nano-heavy metal co-toxicity, highlighting PANoptosis as a critical target in environmental nephrotoxicity assessment. Co-exposure to Cd/PS-NPs activates PANoptosis in renal tissue Synergistic renal damage exceeds single Cd or PS-NPs toxicity PANoptosis integrates pyroptosis, apoptosis, and necroptosis pathways
More Papers Like This
Nanoplastics Exacerbated Renal Injury amid Hypertension: Rethinking Health Hazards in Disease and Implication of Renal Senescence and EMT Associated with Sirt1 Downregulation
AI summary
This study investigated interactions between silver nanoparticles (AgNPs) and microplastics on Daphnia toxicity, examining whether combined exposure to nano-silver and plastic particles produces additive or synergistic effects. The results demonstrate that microplastics can alter AgNP toxicity by affecting nanoparticle aggregation and bioavailability to zooplankton.
Polystyrene nanoplastics and cadmium co-exposure aggravated cardiomyocyte damage in mice by regulating PANoptosis pathway
AI summary Read the abstract
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.
Effects of Nanoplastic Particles on the Kidney
AI summary Read the abstract
Scientists found that tiny plastic particles (like those from broken-down everyday plastics) can travel through the digestive system and reach the kidneys, where they get absorbed by important filtering cells and change their shape and structure. Using fish and lab-grown human kidney cells, researchers also discovered that if the kidney's filtering system is already damaged, these plastic particles pass through more easily, suggesting people with kidney disease might be more vulnerable to potential harm from microplastic exposure. This early research highlights a new reason to take plastic pollution seriously, though more studies are needed to know exactly how this affects human health long-term
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
AI summary Read the abstract
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.
Cellular and Animal Toxicities of Micro- and Nanoplastics
AI summary Read the abstract
Researchers reviewed evidence from cell and animal studies on the toxic effects of micro- and nanoplastics, finding that these particles can cause inflammation, oxidative stress, and organ damage in laboratory models, raising concern about what chronic low-level human exposure might mean for long-term health.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.