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Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
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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.
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Polystyrene microplastics exacerbated the toxicity of okadaic acid to the small intestine in mice
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Researchers studied the combined effects of polystyrene microplastics and okadaic acid, a marine toxin, on the small intestines of mice. They found that co-exposure significantly worsened intestinal damage compared to either contaminant alone, increasing oxidative stress and disrupting the gut barrier. The study suggests that microplastics may amplify the harmful effects of naturally occurring marine toxins when both are consumed through seafood.
Polystyrene Microplastics Can Aggravate the Damage of the Intestinal Microenvironment Caused by Okadaic Acid: A Prevalent Algal Toxin
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Researchers examined how polystyrene microplastics worsen the intestinal damage caused by okadaic acid, a common algal toxin found in seafood. Using human intestinal cells and gut bacteria experiments, they found that co-exposure disrupted the gut barrier, increased inflammation, and altered the microbial community more severely than either contaminant alone. The findings suggest that microplastics may amplify the health risks of naturally occurring marine toxins in our food supply.
Effects of bisphenol A and nanoscale and microscale polystyrene plastic exposure on particle uptake and toxicity in human Caco-2 cells
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Researchers studied how human intestinal Caco-2 cells take up polystyrene plastic particles of five different sizes ranging from 300 nanometers to 6 micrometers. The study found that smaller particles were taken up at higher rates and that co-exposure with bisphenol A increased cellular toxicity, suggesting that nanoscale plastics may pose a greater risk to human intestinal cells than larger microplastics.
Nanoplastics induce more severe apoptosis through mitochondrial damage in Caco-2 cells compared to sub-micron plastics
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Researchers found that 20 nm polystyrene nanoplastics cause more severe apoptosis in intestinal Caco-2 cells than 200 nm sub-micron plastics, disrupting cell membrane integrity at 80 ug/mL, localizing in lysosomes and mitochondria, and triggering mitochondria-mediated cell death pathways more intensively than larger particles. The study suggests nanoplastic size is a critical determinant of cytotoxicity in the gastrointestinal tract.
Do polystyrene nanoplastics aggravate the toxicity of single contaminants (okadaic acid)? Using AGS cells as a biological model
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Polystyrene nanoplastics and the marine algal toxin okadaic acid were tested in combination against human gastric adenocarcinoma (AGS) cells to determine whether nanoplastics aggravate okadaic acid toxicity. PS nanoplastics enhanced toxicity by increasing reactive oxygen species production, inducing DNA damage, and impairing DNA replication and repair through the Fanconi anemia pathway.
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