Author response for "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"

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

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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

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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.

Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice

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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.

Author response for "Polystyrene Nanoplastic Exposure Promotes Amyloid Misfolding and Metabolic Impairment at Sub-Lethal Doses. A Subcellular Infrared Imaging Study"

Co-exposure to Cadmium and Polystyrene Nanoplastics Intensifies Renal Damage in Mice via the Activation of the PANoptosis Pathway

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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.