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Dietary Lipids Induce Ferroptosis in Caenorhabditiselegans and Human Cancer Cells.
Developmental Cell ( IF 10.7 ) Pub Date : 2020-07-10 , DOI: 10.1016/j.devcel.2020.06.019
Marcos A Perez 1 , Leslie Magtanong 2 , Scott J Dixon 2 , Jennifer L Watts 1
Affiliation  

Dietary lipids impact development, homeostasis, and disease, but links between specific dietary fats and cell fates are poorly understood. Ferroptosis is an iron-dependent form of nonapoptotic cell death associated with oxidized polyunsaturated phospholipids. Here, we show that dietary ingestion of the polyunsaturated fatty acid (PUFA) dihomogamma-linolenic acid (DGLA; 20:3n-6) can trigger germ-cell ferroptosis and sterility in the nematode Caenorhabditis elegans. Exogenous DGLA is also sufficient to induce ferroptosis in human cells, pinpointing this omega-6 PUFA as a conserved metabolic instigator of this lethal process. In both C. elegans and human cancer cells, ether-lipid synthesis protects against ferroptosis. These results establish C. elegans as a powerful animal model to study the induction and modulation of ferroptosis by dietary fats and indicate that endogenous ether lipids act to prevent this nonapoptotic cell fate.



中文翻译:

膳食脂质在秀丽隐杆线虫和人类癌细胞中诱导铁死亡。

膳食脂质影响发育、体内平衡和疾病,但对特定膳食脂肪与细胞命运之间的联系知之甚少。铁死亡是与氧化多不饱和磷脂相关的铁依赖性非凋亡细胞死亡形式。在这里,我们表明饮食摄入多不饱和脂肪酸 (PUFA) 二高伽玛亚麻酸 (DGLA; 20:3n-6) 可以引发线虫秀丽隐杆线虫的生殖细胞铁死亡和不育。外源性 DGLA 也足以在人类细胞中诱导铁死亡,将这种 omega-6 PUFA 确定为这一致命过程的保守代谢始动因素。在秀丽隐杆线虫和人类癌细胞中,醚-脂质合成可防止铁死亡。这些结果确定了秀丽隐杆线虫 作为研究膳食脂肪诱导和调节铁死亡的强大动物模型,并表明内源性醚脂质可防止这种非凋亡细胞命运。

更新日期:2020-08-24
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