文献类型： 外文期刊
作者： Zhang, Haiyan 1 ; Ji, Yunyun 1 ; Jiang, Zhongquan 1 ; Yang, Guangxin 1 ; Kong, Cong 1 ; Shen, Zhemin 2 ; Yuan, Tao 2 ; Shen, Xiaosheng 1 ;
作者机构： 1.Chinese Acad Fishery Sci, East China Sea Fisheries Res Inst, Shanghai 200090, Peoples R China
2.Shanghai Jiao Tong Univ, Sch Environm Sci & Engn, Key Lab Environm Hlth Impact Assessment Emerging C, Minist Ecol & Environm, Shanghai 200240, Peoples R China
关键词： Antarctic krill oil; Arsenic species; Caco-2 cells; Oxidative stress; Apoptosis
期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.1； 五年影响因子：6.4 ）
ISSN： 0147-6513
年卷期： 2025 年 289 卷
页码：
收录情况： SCI
摘要： Arsenic is a pervasive environmental pollutant that can bioaccumulate in Antarctic krill through the food chain, posing potential risks to human health. This study investigates the toxic effects of arsenic in Antarctic krill oil (AKO) on Caco-2 cells, focusing on oxidative stress and apoptosis induction. AKO is nutrient-rich and contains various arsenic species, including arsenite (Asa+), arsenate (As5+), dimethyl arsinic acid (DMA), and arsenobetaine (AsB), each exhibiting different toxic potencies. Caco-2 cells were treated with arsenic standards and AKO to assess cell viability, lactate dehydrogenase (LDH) release, oxidative stress markers (superoxide dismutase [SOD], catalase [CAT], malondialdehyde [MDA], and glutathione peroxidase [GSH-Px]), reactive oxygen species (ROS) production, and apoptosis. Results demonstrated dose-dependent cytotoxicity, with Asa + being the most toxic, followed by As5+, DMA, and AsB. After 24 hours of exposure, cell viability in the high-concentration AKO group decreased to 63.95 %. Arsenic exposure elevated ROS levels, disrupted mitochondrial membrane potential, upregulated apoptosis-related genes such as Caspase-3, Caspase-9, and Bax, and downregulated the PI3K/AKT/ mTOR signaling pathway. This study elucidates the mechanisms underlying arsenic toxicity in AKO and underscores its implications for food safety assessments.
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