Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics

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)....

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Main Authors: Linhong Yan, Zihua Yu, Peichun Lin, Shijie Qiu, Liuying He, Zijie Wu, Lihua Ma, Yanggao Gu, Lei He, Zhenqing Dai, Chunxia Zhou, Pengzhi Hong, Chengyong Li
Format: Article
Language:English
Published: Elsevier 2023-01-01
Series:Ecotoxicology and Environmental Safety
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0147651322012155
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author Linhong Yan
Zihua Yu
Peichun Lin
Shijie Qiu
Liuying He
Zijie Wu
Lihua Ma
Yanggao Gu
Lei He
Zhenqing Dai
Chunxia Zhou
Pengzhi Hong
Chengyong Li
author_facet Linhong Yan
Zihua Yu
Peichun Lin
Shijie Qiu
Liuying He
Zijie Wu
Lihua Ma
Yanggao Gu
Lei He
Zhenqing Dai
Chunxia Zhou
Pengzhi Hong
Chengyong Li
author_sort Linhong Yan
collection DOAJ
description 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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spelling doaj.art-31cb85e9e29d459881f6cf17e443d0082023-01-05T04:30:26ZengElsevierEcotoxicology and Environmental Safety0147-65132023-01-01249114375Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplasticsLinhong Yan0Zihua Yu1Peichun Lin2Shijie Qiu3Liuying He4Zijie Wu5Lihua Ma6Yanggao Gu7Lei He8Zhenqing Dai9Chunxia Zhou10Pengzhi Hong11Chengyong Li12College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Zhanjiang 524088, PR ChinaCollege of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Zhanjiang 524088, PR ChinaSchool of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR ChinaSchool of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR ChinaSchool of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR ChinaCollege of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Zhanjiang 524088, PR ChinaCollege of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Zhanjiang 524088, PR ChinaSchool of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR ChinaSchool of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR ChinaShenzhen Institute of Guangdong Ocean University, Shenzhen 518108, PR China; Corresponding author.College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Zhanjiang 524088, PR ChinaCollege of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Guangdong Provincial Engineering Technology Research Center of Seafood, Zhanjiang 524088, PR ChinaSchool of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR China; Shenzhen Institute of Guangdong Ocean University, Shenzhen 518108, PR China; Corresponding author at: School of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR China.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.http://www.sciencedirect.com/science/article/pii/S0147651322012155NanoplasticsMicroplasticsOkadaic acidCaco-2 cellsEndoplasmic reticulum stressApoptosis
spellingShingle Linhong Yan
Zihua Yu
Peichun Lin
Shijie Qiu
Liuying He
Zijie Wu
Lihua Ma
Yanggao Gu
Lei He
Zhenqing Dai
Chunxia Zhou
Pengzhi Hong
Chengyong Li
Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
Ecotoxicology and Environmental Safety
Nanoplastics
Microplastics
Okadaic acid
Caco-2 cells
Endoplasmic reticulum stress
Apoptosis
title Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
title_full Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
title_fullStr Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
title_full_unstemmed Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
title_short Polystyrene nanoplastics promote the apoptosis in Caco-2 cells induced by okadaic acid more than microplastics
title_sort polystyrene nanoplastics promote the apoptosis in caco 2 cells induced by okadaic acid more than microplastics
topic Nanoplastics
Microplastics
Okadaic acid
Caco-2 cells
Endoplasmic reticulum stress
Apoptosis
url http://www.sciencedirect.com/science/article/pii/S0147651322012155
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