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

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

  • Ecotoxicol Environ Saf. 2022 Dec 9;249:114375. doi: 10.1016/j.ecoenv.2022.114375.
Linhong Yan 1 Zihua Yu 1 Peichun Lin 2 Shijie Qiu 2 Liuying He 2 Zijie Wu 1 Lihua Ma 1 Yanggao Gu 2 Lei He 2 Zhenqing Dai 3 Chunxia Zhou 1 Pengzhi Hong 1 Chengyong Li 4
Affiliations

Affiliations

  • 1 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 China.
  • 2 School of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR China.
  • 3 Shenzhen Institute of Guangdong Ocean University, Shenzhen 518108, PR China. Electronic address: daizq@gdou.edu.cn.
  • 4 School of Chemistry and Environment, Guangdong Ocean University, Zhanjiang 524088, PR China; Shenzhen Institute of Guangdong Ocean University, Shenzhen 518108, PR China. Electronic address: cyli@gdou.edu.cn.
Abstract

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.

Keywords

Apoptosis; Caco-2 cells; Endoplasmic reticulum stress; Microplastics; Nanoplastics; Okadaic acid.

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