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Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
Summary
Researchers compared how polystyrene nanoplastics and microplastics interact with the marine toxin okadaic acid in human intestinal cells. They found that nanoplastics enhanced the toxicity of okadaic acid significantly more than microplastics, triggering endoplasmic reticulum stress and cell death through calcium overload. The study suggests that smaller plastic particles may amplify the harmful effects of co-occurring environmental toxins in the digestive system.
Microplastics (MPs) are widespread in the environment and can be ingested through food, water, and air, posing a threat to human health. In addition, MPs can have a potential combined effect with other toxic compounds. Polystyrene (PS) has been shown to enhance the cytotoxicity of okadaic acid (OA). However, it remains unclear whether this enhancement effect is related to the size of PS particles. In this study, we investigated the mechanism of the combined effect of PS microplastics (PS-MPs) or PS nanoplastics (PS-NPs) and OA on Caco-2 cells. The results indicated that PS-NPs enhanced the cytotoxicity of OA and induced endoplasmic reticulum (ER) stress-mediated apoptosis in Caco-2 cells, compared to PS-MPs. Specifically, PS-NPs and OA cause more severe oxidative stress, lactate dehydrogenase (LDH) release, and mitochondrial membrane depolarization. Furthermore, it induced intracellular calcium overload through store-operated channels (SOCs) and activated the PERK/ATF-4/CHOP pathway to cause ER stress. ER stress promoted mitochondrial damage and finally activated the caspase family to induce apoptosis. This study provided an indirect basis for the assessment of the combined toxicity of MPs or NPs with OA.