Luo Sihuan, Zhao Xiaomei, Wang Yijin, Jiang Miao, Cao Yi
Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical College, University of South China, Hengyang, 421001, China.
Food Chem Toxicol. 2025 Mar;197:115304. doi: 10.1016/j.fct.2025.115304. Epub 2025 Feb 2.
The wide uses of plastics lead to nanoplastic exposure in reality. Previous studies reported that micro- and nano-plastics (MNPs) disrupted metabolism, but few studies investigated lipid profile changes. Hereby, we exposed mice to vehicles (control), 0.05 or 0.5 mg/kg 20 or 100 nm nanoplastics via gavage, once a day, for 14 days. Albeit no obvious tissue damage, lipidomics data revealed 76 up-regulated and 29 down-regulated lipid molecules in mouse intestines. Further analysis revealed that a number of up-regulated lipid molecules belong to glycerophospholipid (GP). Among GP, we noticed an up-regulation of 9 phosphatidylserine (PS) molecules, and we further verified the presence of autophagosomes and co-localization of typical autophagic lipolysis proteins in intestinal sections, as well as decreased lysosomal associated protein 2 (LAMP2) and increased adipose triglyceride lipase (ATGL) in intestinal homogenates, indicating perturbed autophagic pathway. The exposure also up-regulated 9 phosphatidylinositol (PI) molecules, and we verified a significant decrease of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), indicating altered PI3K-signaling pathway. Besides GP, nanoplastics also significantly up-regulated some sphingolipids (SP), such as ceramide (Cer), and some sterol lipids, such as cholesterol derivatives. Combined, these results suggested that oral exposure to nanoplastics altered lipid profiles and related signaling pathway in mouse intestines.
塑料的广泛使用导致现实中纳米塑料的暴露。先前的研究报道，微塑料和纳米塑料（MNPs）会扰乱新陈代谢，但很少有研究调查脂质谱的变化。在此，我们通过灌胃法让小鼠每天一次接触载体（对照）、0.05或0.5毫克/千克的20或100纳米纳米塑料，持续14天。尽管没有明显的组织损伤，但脂质组学数据显示小鼠肠道中有76种脂质分子上调，29种脂质分子下调。进一步分析表明，许多上调的脂质分子属于甘油磷脂（GP）。在GP中，我们注意到9种磷脂酰丝氨酸（PS）分子上调，并且我们进一步证实了肠道切片中自噬体的存在以及典型自噬性脂解蛋白的共定位，以及肠道匀浆中溶酶体相关蛋白2（LAMP2）减少和脂肪甘油三酯脂肪酶（ATGL）增加，表明自噬途径受到干扰。这种暴露还上调了9种磷脂酰肌醇（PI）分子，并且我们证实3-羟基-3-甲基戊二酰辅酶A还原酶（HMGCR）显著降低，表明PI3K信号通路改变。除了GP，纳米塑料还显著上调了一些鞘脂（SP），如神经酰胺（Cer），以及一些甾醇脂质，如胆固醇衍生物。综合起来，这些结果表明口服纳米塑料会改变小鼠肠道中的脂质谱和相关信号通路。
