Zhang Haiyan, Ji Yunyun, Jiang Zhongquan, Yang Guangxin, Kong Cong, Shen Zhemin, Yuan Tao, Shen Xiaosheng
East China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Shanghai 200090, China.
East China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Shanghai 200090, China; Key Laboratory of Environmental Health Impact Assessment of Emerging Contaminants, Ministry of Ecology and Environment, School of Environmental Science and Engineering, Shanghai Jiao Tong University, Shanghai 200240, China.
Ecotoxicol Environ Saf. 2025 Jan 1;289:117680. doi: 10.1016/j.ecoenv.2025.117680. Epub 2025 Jan 10.
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 (As³⁺), 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 As³ ⁺ 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.
砷是一种普遍存在的环境污染物，可通过食物链在南极磷虾体内生物累积，对人类健康构成潜在风险。本研究调查了南极磷虾油（AKO）中的砷对Caco-2细胞的毒性作用，重点关注氧化应激和凋亡诱导。AKO营养丰富，含有多种砷形态，包括亚砷酸盐（As³⁺）、砷酸盐（As⁵⁺）、二甲基胂酸（DMA）和砷甜菜碱（AsB），每种形态的毒性效力不同。用砷标准品和AKO处理Caco-2细胞，以评估细胞活力、乳酸脱氢酶（LDH）释放、氧化应激标志物（超氧化物歧化酶[SOD]、过氧化氢酶[CAT]、丙二醛[MDA]和谷胱甘肽过氧化物酶[GSH-Px]）、活性氧（ROS）产生和凋亡情况。结果显示出剂量依赖性细胞毒性，As³⁺毒性最强，其次是As⁵⁺、DMA和AsB。暴露24小时后，高浓度AKO组的细胞活力降至63.95%。砷暴露会提高ROS水平，破坏线粒体膜电位，上调凋亡相关基因如Caspase-3、Caspase-9和Bax的表达，并下调PI3K/AKT/mTOR信号通路。本研究阐明了AKO中砷毒性的潜在机制，并强调了其对食品安全评估的意义。
