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Original research — experimental, observational, or case-control study. Direct primary evidence.
Human Health Effects
Nanoplastics
Remediation
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Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
Ecotoxicology and Environmental Safety2022
46 citations
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Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Score: 55
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0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Linhong Yan,
Pei‐Chun Lin,
Lei He,
Chengyong Li
Zhenqing Dai,
Lei He,
Linhong Yan,
Lihua Ma,
Linhong Yan,
Lihua Ma,
Linhong Yan,
Lei He,
Lihua Ma,
Pei‐Chun Lin,
Chengyong Li
Lei He,
Pei‐Chun Lin,
Lei He,
Lei He,
Pei‐Chun Lin,
Pei‐Chun Lin,
Pei‐Chun Lin,
Zihua Yu,
Pei‐Chun Lin,
Lei He,
Lei He,
Lei He,
Lei He,
Zihua Yu,
Lei He,
Pei‐Chun Lin,
Lei He,
Zijie Wu,
Zijie Wu,
Zhenqing Dai,
Chengyong Li
Lei He,
Lei He,
Lei He,
Zhenqing Dai,
Zijie Wu,
Zijie Wu,
Zhenqing Dai,
Lei He,
Lei He,
Zihua Yu,
Pei‐Chun Lin,
Lei He,
Zhenqing Dai,
Chengyong Li
Zihua Yu,
Lihua Ma,
Pei‐Chun Lin,
Lei He,
Zhenqing Dai,
Lei He,
Lei He,
Zhenqing Dai,
Lei He,
Shijie Qiu,
Zhenqing Dai,
Lei He,
Zhenqing Dai,
Linhong Yan,
Zhenqing Dai,
Linhong Yan,
Lei He,
Lei He,
Linhong Yan,
Lei He,
Lei He,
Lei He,
Linhong Yan,
Lei He,
Linhong Yan,
Linhong Yan,
Shijie Qiu,
Chunxia Zhou,
Chengyong Li
Zhenqing Dai,
Liuying He,
Zhenqing Dai,
Zhenqing Dai,
Liuying He,
Lihua Ma,
Zijie Wu,
Zhenqing Dai,
Zhenqing Dai,
Lei He,
Zhenqing Dai,
Lei He,
Lei He,
Zijie Wu,
Lihua Ma,
Chunxia Zhou,
Chunxia Zhou,
Chunxia Zhou,
Chunxia Zhou,
Chunxia Zhou,
Zhenqing Dai,
Chunxia Zhou,
Zhenqing Dai,
Pengzhi Hong,
Zhenqing Dai,
Liuying He,
Zhenqing Dai,
Zhenqing Dai,
Zhenqing Dai,
Zhenqing Dai,
Lei He,
Lei He,
Zijie Wu,
Zhenqing Dai,
Chunxia Zhou,
Pengzhi Hong,
Liuying He,
Pengzhi Hong,
Zhenqing Dai,
Zijie Wu,
Pengzhi Hong,
Pengzhi Hong,
Zhenqing Dai,
Chengyong Li
Chunxia Zhou,
Zhenqing Dai,
Zijie Wu,
Chengyong Li
Zhenqing Dai,
Zhenqing Dai,
Lihua Ma,
Pengzhi Hong,
Pengzhi Hong,
Zhenqing Dai,
Pengzhi Hong,
Zhenqing Dai,
Zhenqing Dai,
Zijie Wu,
Lihua Ma,
Chengyong Li
Yanggao Gu,
Chengyong Li
Zhenqing Dai,
Zhenqing Dai,
Zhenqing Dai,
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Lei He,
Pengzhi Hong,
Pengzhi Hong,
Pengzhi Hong,
Yanggao Gu,
Zhenqing Dai,
Zhenqing Dai,
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chunxia Zhou,
Chunxia Zhou,
Chunxia Zhou,
Pengzhi Hong,
Zhenqing Dai,
Chengyong Li
Zhenqing Dai,
Lei He,
Chengyong Li
Chengyong Li
Chengyong Li
Pengzhi Hong,
Pengzhi Hong,
Zhenqing Dai,
Chunxia Zhou,
Lei He,
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Zhenqing Dai,
Chengyong Li
Pengzhi Hong,
Chengyong Li
Chengyong Li
Chengyong Li
Chunxia Zhou,
Pengzhi Hong,
Chengyong Li
Chengyong Li
Pengzhi Hong,
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
Chengyong Li
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.