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Co-exposure to polystyrene nanoplastics and cadmium induces apoptosis in intestinal cells: Role of the IP3R/Ca²⁺/STAT3 signaling pathway.
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Scientists found that when tiny plastic particles (nanoplastics) and the toxic metal cadmium are present together, they cause more damage to intestinal cells than either pollutant alone. The combination triggers cell death through a specific pathway involving calcium signals in the gut. This matters because both nanoplastics and cadmium are common environmental pollutants that people are regularly exposed to through food and water, suggesting these combined exposures could harm digestive health.
The widespread use of plastic products has elevated nanoplastics (NPs) pollution to a critical global concern, with polystyrene nanoplastics (PS-NPs) and cadmium (Cd) emerging as common environmental contaminants whose co-occurrence and combined toxicity increasingly alarm the scientific community. The intestine, as the main xenobiotic exposure site, is a primary target for PS-NPs and Cd exposure-individually or combined. While PS-NPs and Cd's individual intestinal toxicity mechanisms are well-studied, their combined effects remain poorly understood, especially at the molecular level. This study investigated the combined effects of environmentally relevant concentrations of PS-NPs and Cd on intestinal apoptosis and the regulatory role involving the IP3R/Ca/STAT3 pathway using both C. elegans and Caco-2 cell models. In C. elegans, 72-hour PS-NPs (10μg/L) and Cd (5μg/L) co-exposure induced developmental retardation, intestinal structural abnormalities, and dysregulated expression of apoptosis-related genes along with key components of the IP3R/Ca/STAT3 pathway. Parallel experiments in Caco-2 cells demonstrated that 24-hour co-treatment with PS-NPs (20μg/mL) and Cd (0.25μg/mL) significantly elevated apoptosis rates and triggered endoplasmic reticulum stress. Molecular analyses revealed these effects were mediated through increased IP3R phosphorylation, elevated cytosolic Ca concentrations, and enhanced phosphorylation of the downstream effector STAT3. Notably, pharmacological inhibition of IP3R (2-APB, 10μM), Ca²⁺ chelation (BAPTA, 10μM), or STAT3 phosphorylation (stattic, 5μM) significantly attenuated PS-NPs and Cd-induced apoptosis. These results establish the IP3R/Ca²⁺/STAT3 axis as a pivotal regulatory switch governing intestinal apoptosis under NP-heavy metal co-exposure, providing mechanistic foundations for environmental risk assessment of combined pollutant exposure.
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